SNAB A2 Revision

Notes and
Unit 4: Environment
Survival

Topic 5: On the wild side

4.5.1
A particular species can be identified using the features (the
phenotype) which are characteristic to only that species. Species
with similar phenotypes are likely to be related to each other. A key
of characteristics is used to identify the species
Organisms are classified into families according to similarity of
features. The families start of large, but rapidly become smaller.
This is the basis of a hierarchical classification system
Kingdom
Phylum
Class
Order
Family
Genus
Species

There are 5 kingdoms Animals, Plants, Fungi,

Protoctists, Prokaryotes
You need to know the main characteristics of
each kingdom

Taxonomy: the science of classifying living things.

Biodiversity: the variety of life on our planet, measurable as the
variety within species, between species, and the variety of
ecosystems
If two organisms can interbreed to produce fertile offspring they
are the same species. If not, they are different species
Binomial System:
(2 names)

Felix catus

Genus: tells you what group the

species is from
(has a capital letter)

Italics in print
Underlined in hand

species: tells you the exact

species
(small case letter)

Distinguishing Characteristics of the Kingdoms

Prokaryotes

Microscopic prokaryotic cells (2 - 5m long rather than 10-100m)

Lack of a nucleus (DNA in cytoplasm) and possibly plasmids
Lack of membrane-bound organelles
Presence of 70s ribosomes
No cytoskeleton

Protoctists

Eukaryotic cell structure

Simple body form, either unicellular, filamentous (chains), colonial (ball) or
macroscopic (large and visible)

The Proctoctists kingdom tends to be full of organisms that do not fit into any
other Kingdom e.g. algae and yeast
Fungi

Heterotrophic nutrition (get food from eating, unlike plants)

Made of a network of Hyphae, which form a 3D structure called a Mycelium.
(look up Module 1 notes)
Call walls containing chitin

Plants
The distinguishing features of the Plants are;

Multicellular with eukaryotic structure

Cell walls containing cellulose
Complex body form
Photoautotrophic nutrition (make food themselves through P/S)
Presence of photosynthetic cells with chloroplasts
2 stages in the life cycle: a diploid spore-producing stage and a haploid
gamete-producing stage.

Animals
The distinguishing features of the Animals are;

Multicellular with eukaryotic cell structure

Cells without cell walls
Heterotrophic nutrition
Highly organised organs and tissues including nervous co-ordination

The only haploid cells

Genetic diversity

they have are gametes

4.5.2
Individuals in the same species look different (have different
phenotypes). This is called variation
Variation is caused by;
1. The genotype of the individual (i.e. which alleles they have)
2. The environment
Genetic diversity describes the range of different genotypes
within a species. If there are few genotypes the genetic diversity is
small. If there are lots of genotypes the genetic diversity is large.

Advantages of little genetic diversity

Advantages of wide genetic diversity

All individuals have a preferential

phenotype

Less chance of genetic disease

Less chance of extinction when faced with

disease (i.e. some individuals will have a
phenotype that allows them to survive)

Environment has less effect on phenotype

Species more likely to survive environment

change

Species more likely to colonise

Allows access to more niches, therefore

less interspecific competition

Natural selection & speciation can occur

Causes of Genetic Diversity:

1. Independent Assortment
2. Mutation
3. Random fusion

4. Crossing Over
Independent Assortment = which allele of each pair goes into
which gamete. This is caused by the orientation of homologous
pairs of chromosomes during metaphase 2 of meiosis
Changes in the sequence of bases in codons (mutation) cause
genetic variation. This usually occurs by DNA being improperly
copied or damaged. Chemicals (mutagens) and radiation can do
this.
Each gamete is different. Therefore, by combining different
gametes new variation occurs (random fusion).
During meiosis sections of DNA are swapped between homologous
chromosomes (pairs of chromosomes). This creates more
variation by creating new combinations of alleles (crossing over)

Dihybrid Cross

4.5.3

Dihybrid Crosses are for crosses involving two different genes

(2 loci).
A = Purple stem,

a = Green Stem, D = Big Leaves,

leaves

Parents Phenotype:

Purple stem &

Big Leaves

Purple Stem &

Big Leaves

Parents Genotype:

AaDd

AaDd

Gametes:

F1 Genotype:

d = little

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aD

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aD

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aD

ad

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AAD D

AAD d

AaDD

AaDd

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AAD d

AAd d

AaDd

Aadd

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AaDD

AaDd

aaDD

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AaDd

Aadd

aaDd

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4.5.4
F1 Phenotype:

Ecological Sampling Techniques

9:3:3:1
A_B_ : A_bb : aaB_ : aabb
Purple & Big : Purple & Little : Green & Big : Green & Little

Biotic Factor: A living variable within the ecosystem, which affects the survival
of organisms. Examples include predation, competition, and pollution from
excreted waste.
Abiotic Factor: A non-living variable within the ecosystem, which affects the
survival of organisms. Examples include temperature, light, and water.
Random Sampling (quadrats placed at randomly generated intervals)
Used where habitat is uniform
Removes observer bias
Used in a large area
Used if time is limited
Systematic Sampling (quadrats placed at regular intervals)
Used to show zonation
Used where there is continuous variation
Used to sample linear habitats (e.g. a roadside)
2 types of systematic sampling technique;
Line Transect:
Used where time is limited
Used to visually illustrate how species change along a line
Belt Transect:
Produces more data, gives detail about species abundance down the line
as well as range
Shows species dominance down the line
What interval should be used?
Transects can either be continuous with the whole length of the line being
sampled, or samples can be taken at particular points along the line
For both line and belt transects, the interval at which samples are taken will
depend on the individual habitat, as well as on the time and effort which can be
allocated to the survey.

4.5.5

Too great an interval may mean that many species actually present are
not noted, as well as obscuring zonation patterns for lack of observations.

Too small an interval can make the sampling time consuming, as well as
yielding more data than is needed.

An example of a Named Environment

Is the British Rocky Seashore

Abiotic Factors have more

effect going up the beach

Biotic Factors have more

effect going down the beach

Abiotic Factors include; dessication, salinity, wave action, temperature, water

availability, substrate, aspect, pH etc
Biotic Factors include; interspecific competition, intraspecific competition,
predation, food availability, presence of excreted wastes

Species living in the Rocky Sea shore

Splash Zone: Lichen can survive dessication & temp variation, requires little
nutrient
Upper Shore: Black Tar Lichen can survive long periods without water, grows
slowly, but is less tolerant to dessication than lichen.
Middle Shore: Eggwrack More water availability, less temp range, but more
predation from herbivores and carnivores
Lower Shore: Kelp constant environment, usually submerged, lower light levels,
intense competition from same and other species
Limpet: (Shore
Common
Oystercatcher:
Crab: ):
Micro-algae
Bladderwrack
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4.5.6 on a different habitat. Learn this study
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4.5.7

Dont learn this case study if your teacher gave you notes
on a different habitat. Learn this study if youre desperate

Light Dependent Step of Photosynthesis

Light Dependent Step:

1. Chlorophyll absorbs light (remember chlorophyll is the trap in the
bottom of the photosystem)

2. Chlorophyll emits electrons

3. Electrons are received by electron carrier proteins in the thylakoid
membrane (electron transport chain)
4. Electron transport chain uses high energy electrons to power the
following conversions;
ADP + Pi
ATP and NADP + H+ +
eNADPH
5. Water is split (photolysis) to produce replacement electrons for
the photosystems, H+ for the reduction of NADP and O 2 which is
excreted.
The purpose of the light dependent step is to produce ATP and NADPH.
ATP provides the energy for converting CO 2 into glucose and NADPH
provides the H for glucose.

4.5.8

Light Independent Step of Photosynthesis

CO2
GP

RuBP
ADP + P

ATP

ATP
NADPH

ADP + P
NADP

GALP
Glucose
There are three steps in the Calvin Cycle;
1. Carboxylation: RuBP fixes CO2to form GP. This reaction is
catalysed by the enzyme Rubisco

2. Reduction: In a series of reactions GP reacts with ATP and NADPH

reduced GP to form GALP (by reducing GP the NAHPH itself is
oxidised, reverting to NADP)
3. Regeneration: Some GALP is converted back into RuBP so the Calvin
Cycle can continue. The rest of GALP is converted into glucose in a
series of reactions.

A glucose molecule is generated every 6 turns of the Calvin Cycle

4.5.9

4.5.10
Thylakoid membrane = location of photosystems & electron transport chain
Stroma = site of Calvin Cycle & photolysis of water

Grana provide large surface area for absorbtion of light

NPP = GPP R
NPP = Net Primary Productivity (amount of stored chemical energy the
plant has to use for growth. This is directly proportional to biomass)
GPP = Gross Primary Productivity (amount of stored chemical energy the
plant earns through photosynthesis)
R = Respiration (amount of energy lost through respiration, i.e. heat, lost
as CO2 etc)
Best analogy is a salary. GPP is the amount of stored chemical energy the
plant earns through photosynthesis. R is like income tax. The plant has to
pay respiration tax because it cant photosynthesis at night & not all
parts of the plant are capable of photosynthesis. NPP = disposable
income: what the plant has to spend after paying tax.

4.5.11
Energy in Primary Consumer
Lost energy
NPP in plant
Lost energy
Energy in
Sunlight

Energy is lost between trophic levels. Energy is lost in the following ways;
in respiration (mostly lost through heat), energy still present in egested
food, through movement, through digestion, energy still present in
excreted materials etc

Of the 100% sunlight energy that reaches plants, ~3% is converted into
NPP. Energy is lost in the following ways; reflected light, light of
wavelengths not useful to plants, passes through leaves, lost in
respiration, lost as heat etc

4.5.12
Evolution: the idea that one species changes into another over time
Natural Selection: Darwins suggestion for the process by which evolution
might occur
Evolution by Natural Selection (Darwinian Evolution)
1. There is variation in a species
2. More individuals are born than the environment can sustain, so
some individuals must die.
3. The individuals that survive tend to be those that have alleles
which give them a selective advantage in their environment (i.e.
they are the best adapted to their environment, e.g. camouflaged).
These are the fittest
4. The fittest survive long enough to reproduce and pass their alleles
onto the next generation.
5. Over a few generations the frequency of fit alleles increases and
the frequency of unfit alleles decreases
6. Soon all / most individuals have the fit phenotype and the unfit
phenotype is eradicated
7. This process continues over many generations
8. Over this time new mutations occur, which give new even better
alleles
9. Over time the mutations accumulate in the phenotype until the
organism is unable to reproduce (i.e. produce fertile offspring) with
the original organisms. At this point a new species has been
produced (speciation)

This process is speeded up by isolation (see 4.5.14) because this stops the
influx of alleles from outside and allows new mutations to accumulate in
the genotype more quickly

4.5.13
1798 Malthus publishes paper on population growth. Malthus noticed that
the human population was expanding exponentially. He thought that the
human population would outgrow its resources and that this would lead to
famine and war.
Darwin was influenced by this idea, because he noticed that animal
populations grow exponentially and then plateau when they reach the
limits the environment can sustain (i.e. the population size is determined
by the environment)

1809 Lamarck publishes a mechanism for evolution based on two laws

Law 1: Organs / structures grow if they are used. This means that the
environment determines the phenotype of an organism
Law 2: Changes are passed on to the next generation
So a blacksmith, who uses his muscles all day, will grow bigger muscles.
This works! But, will the bigger muscles be passed onto his children? No,
so Lamarcks theory is easy to falsify.

1859 Darwin publishes the Origin of species by means of Natural

Selection. He publishes with Wallace who wrote to Darwin to discuss his
own ideas about evolution. They were very similar to Darwins and this
prompted Darwin to publish.

4.5.14
Isolation is important for evolution because it decreases the size of the
gene pool. This stops new alleles coming in from breeding with original

alleles and speeds the accumulation of new mutations (which is what leads
to speciation)
The different types of isolation.

Method of isolation
Ecological isolation
Temporal isolation
Behavioural isolation
Physical incompatibility
Hybrid inviability
Hybrid sterility

Description
The species occupy different parts of the
habitat
The species exist in the same area, but
reproduce at different times
The species exist in the same area, but do not
respond to each others courtship behaviour
Species coexist, but there are physical reasons
which stop them from copulating
In some species, hybrids are produces but they
do not survive long enough to breed
Hybrids survive to reproductive age, but cannot
reproduce

4.5.15
Evolution is a theory, not a fact. Many people believe that species were
created (creationism). Other people believe in evolution, but by
mechanisms other than Natural Selection. You should respect the opinions
of other people, even if you do not necessarily agree with them.

4.5.16
Primary succession is the first stage of the ecological succession of plant
life from abiotic land with no soil to fully support plant ecosystems (e.g., a
forest). In primary succession, pioneer plants like mosses and lichen,
start to "normalize" the habitat, creating rudimentary soil from their
dead matter. These pioneer plants create conditions for the start of
plant growth and so more complex plants like grasses and shrubs begin to
colonise the area.
Over time the grass area is colonised by small woody plants, which give
way to small trees and finally, after a few hundred years, large trees
take over. The large trees represent the climax community because
succession stops at this point.

A good example of primary succession takes place after a volcano has

erupted. The barren land is first colonised by simple pioneer plants which
pave the way for more complex plants, such as hardwood trees by
creating soils and other necessities. Unlike secondary succession, which
refers to succession after an environmental disaster (such as a forest
fire) primary succession occurs on the geologic timescale, over thousands
of years

4.5.17
Parents Phenotype:

Red

Red

Zoos can
play a large roleRr
in conserving endangered
species by;
Parents
Genotype:
Rr
1. Conducting research

Gametes:
2. Running captive breeding programmes
3. Reintroducing species into the wild
4. Educating people
Research enables scientists to understand the role of a species in an
ecosystem.
F1
Genotype:By understanding the niche, food web, reproductive behaviour,
habitat, feeding relationships etc scientists can suggest effective
methods of conserving species.
Captive breeding programmes are used to reintroduce species to the
wild, build up population numbers and maintain genetic diversity. In a small
population many alleles are lost between generations because an individual
only passes on 50% of their alleles. E.g.

R = Red,

R
F1 Phenotype:

r = white

9:3:3:1
A_B_ : A_bb : aaB_ : aabb
Purple & Big : Purple & Little : Green & Big : Green & Little

If the parents only have 2 children and they are both Red (RR) then the r
allele has been lost. This is genetic drift and is a big cause of the loss of
genetic diversity in an endangered species.
To avoid this studbooks are kept (basically, a family tree for the captive
animals) so that only non-related animals are bred with each other. This
decreases the change of genetic drift and also decreases the change of
genetic disease.
Wild animals are often introduced to captive breeding programmes to
avoid these problems
Reintroducing species into the wild has some success, but depends
greatly on the species. As a general rule of thumb, the more advanced the
species the more difficult reintroduction is. This is because animals need
to learn specific behaviours e.g. how to hunt, how to reproduce, how /
where to find shelter, group behaviours. Breeding animals in captive
environments that mimic the wild has more success because it allows some
of these behaviours to be learned in captivity. Feeding the animals in the
wild also helps survival rates.
Educating people is essential to conservation. Often just doing something
slightly differently will have a big impact on conserving a species e.g.
building roads with tunnels under them for badgers.

4.5.18
If you get a question on this in the exam youll need to think. There are no
set facts to learn.

4.5.19
If you get a question on this in the exam youll need to think. There are no
set facts to learn.

SNAB A2 Revision
Notes
Unit 4: Environment and
Survival

Topic 6: Infection, Immunity & Forensics

4.6.1
Time of death can be measured using the following factors;

o
o
o
o

Body temperature
Extent of rigor mortis
Level of decomposition
Forensic entomology

Body temperature:
A body cools following an S-shaped
(sigmoid) curve. The initial plateau at
37C lasts 30 60 min, then the body
cools quickly to ambient temperature.
After 24hrs a body has usually
finished cooling and temperature is no
longer useful.
Temperature is measured using a long
thermometer with a wide range.
Temperature is usually taken rectally
or using an abdominal stab.

The rate of cooling depends on the situation the body is found in e.g.

Clothing slows cooling

Found in water speeds cooling
Found indoors slows cooling
Air movements speed cooling
Extent of rigor mortis:
Temperature of body
Warm
Warm
Cold
Cold

Stiffness of body
Not stiff
Stiff
Stiff
Not stiff

Approx time since death

No more than 3 hrs
3 8hrs
8 36hrs
> 36 48hrs

Rigor mortis is the stiffening of joints and muscles. Small muscles stiffen
first and unstiffen last.
Muscles stiffen because they run out of ATP, causing the actin and
myosin muscle fibres to stick permanently to each other. Muscles
unstiffen because the muscle fibres begin to break down.
On page 80 of your text book is a little more detail about the sequence of
events that causes muscles to run out of ATP.
Level of decomposition:
Autolysis is the break down of body tissues using the bodys own enzymes
from the digestive system and from lysosomes
After this, bacteria from the gut invade tissues and release more
enzymes. This tends to happen in anaerobic conditions, which favours the
growth of anaerobic bacteria
Greenish discolouration of abdomen (36hrs)

Spreads across rest of body (36 72hrs)

Discolouration darkens to reddish green (36 72hrs)

Discolouration darkens to purple-black (72hrs)

Body becomes bloated with gas (one week)

Gas is released, body deflates & shrinks (one week +)

Autolysis is increased by mild heat and slowed by intense heat. Humidity

has a big involvement as well dry conditions slow autolysis and, in some
cases (e.g. mummies) stop it completely.
The presence of wounds, the clothing the person was wearing and the
combination of gases released during decomposition also have an effect.
Forensic entomology:
The insects found in a dead body can help identify time of death in 3
ways;
1. If the temperature of the body has remained relatively constant
the age of the maggots growing in it can be determined by their
starting length and the temperature of the part of the body they
grew in.

Corpse succession:

e.g. a maggot 3mm long found growing at 28C will be roughly 0.3 days (8
hrs old)
2. Using the life-cycle of the maggot to identify age
3. If maggots are taken from the body, allowed to grow and the time
taken to pupate is recorded; it is sometimes possible to work
backwards from the pupation date and work out hold the maggots
must have been when they were taken from the body. This works
because maggots of different species usually take a fixed number
of days to pupate.

4.6.2
The identity of a dead person can be ascertained by;
1. Identity papers
2. Fingerprints
3. Dental records
4. Genetic Fingerprint
Identity Papers: This is very obvious, think about it.
Fingerprints: The skin on fingers, toes etc is ridged into specific
patterns (arches, tented arches, whorls & loops). Sweat and sebum oil is
left behind from our fingers on the things we touch. Using aluminium
powder or protein stain (e.g. ninhydrin) fingerprints are revealed.
Fingerprints are unique and can be used to identify people.
Dental Records: Can be used to identify age and to identify a person
based on their dentists record of their teeth. This is usually used when
the body is damaged (e.g. a corpse from a fire)
Genetic Fingerprint: Used because DNA is unique to individuals (except
identical twins and clones grown by mad scientists). Genetic fingerprinting
looks for the presence of repeated sequences of bases in the non-coding
sections of DNA (introns). The repeated sequences are called satellites
and can be 2 4 bases long (Micro-satellite) or 5 20 bases long (Minisatellite). The satellites are repeated anything from 5 500 times and
this produces a unique DNA signature.
Fingerprinting process:
1. A sample of DNA is copied using PCR
2. Sample is cut using a restriction enzyme
3. Sample is run on an electrophoresis gel, often using a DNA sample
of known length to act as a standardization.

4. A southern blot is taken

5. DNA is labeled using a DNA probe specific to the satellite
6. An X-ray is taken to reveal the location of the bands of DNA
The fingerprint is the pattern of bands on the electrophoresis gel.
Assuming the original DNA sample has not been contaminated (by e.g. a
hair from the pathologist) the fingerprint will be exact.

4.6.3
Succession on corpses:
The idea that as each organism or group of organisms feeds on a body, it
changes the body. This change in turn makes the body attractive to
another group of organisms, which changes the body for the next group,
and so on until the body has been reduced to a skeleton. This is a
predictable process, with different groups of organisms occupying the
decomposing body at different times. This technique allows you to tell, by
the age and specific species living on a corpse, how old the corpse is.
Succession and forensic entomology also show if the body has been
moved.

4.6.4

A typical prokaryote

Ribosomes. Same function as eukaryotic cells (protein synthesis),

but are smaller (70s rather than 80s).
Nuclear Zone. The region of the cytoplasm that contains DNA.
There is no nuclear membrane.
DNA. Always circular, and not in chromosome form.
Plasmid. Very small circles of DNA, containing non-esential genes.
Can be exchanged between different bacterial cells.
Cell membrane. made of phospholipids and proteins, like eukaryotic
membranes.
Mesosome. Tightly-folded region of the cell membrane containing all
the proteins required for respiration and photosynthesis.
Cell Wall. DIFFERENT from plant cell wall. Made of murein (a
protein). There are two kinds of cell wall, which can be distinguished
by a Gram stain:
A: Gram positive bacteria have a thick cell wall and stain
purple
B: Gram negative bacteria have a thin cell wall with an outer
lipid layer and stain pink.
Capsule (or Slime Layer). Thick polysaccharide layer outside of the
cell wall. Used for;
1. Sticking cells together
2. As a food reserve

3. As protection against desiccation (drying out) and chemicals, and

as protection against phagocytosis (being broken down by a white
blood cell).

Flagellum. A rotating tail used for propulsion.

Prokaryotic Cells

Eukaryotic cells

Small cells (< 5 mm)

Larger cells (> 10 mm)

Always unicellular

Often multicellular

No nucleus or any membrane-bound

organelles

Always have nucleus and other

membrane-bound organelles

DNA is circular, without proteins

DNA is linear and associated with

proteins to form chromatin

Ribosomes are small (70S)

Ribosomes are large (80S)

No cytoskeleton

Always has a cytoskeleton

Cell division is by binary fission

Cell division is by mitosis or meiosis

Reproduction is always asexual

Reproduction is asexual or sexual

A typical virus

Viruses have a wide range of different structures. Some viruses are

about 100nm in diameter, whilst others can range from 20
3000nm.
All viruses have a protein coat (the capsid), which contains genetic
material. The genetic material is either DNA or RNA, and can be
single or double-stranded.
The virus genetic material (the viral genome) contains only a few
genes, from about 20 in the polio virus to more than 200 in the
herpes virus (human genome contains ~80,000 genes). The viral
genome codes for the proteins required to manufacture the virus.
The

protein capsid is made from identical subunits (called

capsomeres). The capsomeres can be arranged into an icosahedral
shape (e.g. polio & herpes), or a cylindrical shape (e.g. TMV &
rabies) or a loose containment structure (e.g. measles &
influenza).

In addition, some viruses also have an outer membrane envelope, which

allows the virus to penetrate the host cell membrane by
endocytosis. Influenza, HIV and measles virus all have membrane
envelopes.

(ligands)

Viral Damage What do Viruses actually do to us?

Like bacteria, viruses have protein ligands on their capsid that

attach to ligand receptors on eukaryotic cells. After a virus ligand
attaches to a host cell ligand receptor it becomes anchored to the
host cell. The virus attempts to get its viral genome into the host
cell, usually through endocytosis using its lipid membrane. Viruses
without lipid membranes may have specialised proteins designed to
help inject the viral genome into the cell cytoplasm.
(i)
(ii)
(iii)

Virus RNA enters host cell

Virus may also inject RNA Polymerase into host cell as well.
Viral RNA and RNA Polymerase enter host cell nucleus via
nuclear pores
(iv) Viral RNA is copied in nucleus
(v)
Viral RNA is transcribed using viral RNA Polymerase
(vi) Viral mRNA is translated in the cytoplasm
(vii) New Virus proteins formed
(viii) Viral proteins associate with copied RNA forming new
complete viruses
(ix) New viruses leave host cell to infect other cells
Viruses that have a DNA code instead of an RNA code often insert
their viral DNA into the host cells DNA. Other RNA viruses inject
the enzyme Reverse Transcriptase, which makes a cDNA copy of
the viral RNA. The cDNA copy is then inserted into the host cells
DNA. Other viruses (e.g. HIV) also inject the enzyme integrase,
which helps insert the viral cDNA into the hosts DNA
Be sure you can recall what the 3 viral enzymes do;
DNA Polymerase:
RNA Transcriptase:
Integrase:
Some viruses target specific tissues (e.g. Poliomyelitis virus targets
motor neurones, HIV targets helper T cells, Influenza targets
epithelial cells & rabies virus targets specific brain cells). If lots of
new virus is being made, these host cell may lyse (burst) and die.

4.6.5 & 4.6.6

Course of infection for Tuberculosis:
Tuberculosis (TB) is caused by the Mycobacterium tubercolusis
bacterium.
1. Mycobacterium tuberculosis is inhaled into the lungs in
droplets of water & mucus from another persons lung (droplet
infection)
2. TB begins to reproduce in the lungs.
3. The bacteria produce toxins, which damage lung tissue &
cause coughing, increasing the transmission of the disease.
4. The body launches an immune response to the TB bacterium.
5. Histamine release and inflammation occur (see 4.6.7)
6. Macrophages enter the lungs in large numbers.
7. The macrophages engulf the TB bacteria in large groups,
forming a mass of tissue called a granuloma. The inside of the
granuloma is starved of oxygen, which kills the bacteria.
8. Once the bacteria are dead, the lung heals
BUT
9. TB bacteria can survive inside macrophages as the cell wall of
the bacterium is very thick and waxy and is resistant to the
macrophage enzymes.
10.The bacterium can survive and reproduce inside the
macrophage for many years without causing infection. When
the immune system is weakened (by stress, malnutrition, or
another disease HIV is a common cause) the TB bacterium
breaks out and re-infects the body.
11. The bacteria reproduce too rapidly for the body to destroy
12. The lungs are progressively damaged, which eventually leads
to death.
13.TB can also spread to the lymph nodes in the body, where it
reproduces causing the disease scrofula
Course of infection for Tuberculosis:

HIV is the Human immunodeficiency Virus, which eventually leads to

Acquired Immunodeficiency Syndrome (AIDS)
HIV is spread by direct contact i.e. through sexual intercourse,
blood-to blood transfer (tattoos, needle sharing, piercing & cut-tocut transfer).
Once inside the bloodstream an HIV infection occurs in 3 distinct
phases;
1. The acute phase. HIV virus has a ligand (GP120), which
attaches to a receptor (CD4) on the membrane of a type of
white blood cell called a Helper T cell. HIV rapidly infects
Helper T cells and the virus population increases quickly. At
the same time the population of Helper T cells falls rapidly.
The acute phase ends when the Killer T cells begin to
recognise infected Helper T cells and kill them, which slows
the replication of the virus.
2. The chronic phase. This can last for many years. The virus
continues to replicate, but the Killer T cells keep the numbers
in check. However, because the immune system is weakened
other bacteria and viruses are more likely to infect the
person (TB may reactivate at this point)
3. The disease phase. As the numbers of virus increase and the
numbers of Helper T cell fall the immune system becomes
weaker and weaker. Eventually a second pathogen will infect
the person (an opportunistic infection) which cannot be
fought off. The person will die quickly from the secondary
infection and this is the AIDS disease state.
The huge problem with HIV is that it mutates very quickly. Once
inside the body the viral antigens change and the (already
damaged ) immune system cant keep pace with the changes.
Another problem is that HIV attacks Helper T cells, which are
crucial for activating the B cells and also play a role in activating

Killer T cells. With low numbers of Helper T cell, the immune system
cannot communicate effectively and this increases the ability of
HIV to survive in the body.

4.6.7
Non-specific immune responses:
Inflammation: damaged white blood cells and mast cells release
histamine at the site of infection. Histamine causes local arterioles
to vasodilate, increasing the blood supply to the area. It also causes
holes to open between endothelial cells in capillary walls. This causes
local oedema (the swelling associated with inflammation). It allows
monocytes and neutrophils into the infected area, which engulf and
destroy foreign bodies and pathogens. Eventually phagocytes arrive
and complete the job. Dead monocytes and pathogen form pus.
Lysozyme: an enzyme that breaks down bacterial cell walls, causing
them to lyse and die. Lysozyme is made in lysosomes inside
phagoctyes and is responsible for digesting engulfed bacteria.
Lysozyme is also made by the skin, epithelial cells, and is present in
tears
Interferon: a protein made by virus-infected cells. It blocks RNA
synthesis and therefore stops virus replication
Phagocytosis: the process in which a pathogen is engulfed and
destroyed. Macrophages engulf pathogens using pseudopodia (fake
feet). The bacterium is taken into the macrophage by endocytosis
and enters the macrophage inside a vacuole. Lysosomes containing
lysozyme fuse with the vacuole and digest the bacterium inside.

4.6.8
Pathogens have proteins on their surface that our immune system
has learned to recognise as foreign. These proteins are called
antigens. T cells, B cells & Macrophages all have the ability to
recognise an antigen and once this has happened, they will trigger an
immune response.
In addition to this, macrophages have the ability to present foreign
antigens to T and B cells. Once a pathogen has been engulfed and
destroyed MHC proteins inside the Macrophage stick to the
pathogenic antigen. They are then incorporated into the cell
membrane of the Macrophage, so it can present the foreign antigen
and activate the T and B cells responses.
Antibodies (also called Immunoglobulins) are proteins produced by B
cellls. They are found in blood plasma, lymph, tissue fluid, tears,
mucus and milk.

Antigen-binding site

Variable
Region

Disulphde
Bridges
Constant
Region

Each B cell produces a different immunoglobulin molecule which

recognises and binds to a specific antigen. There are over a million
different B cells in your body, therefore you have the ability to
recognise and react to a million different antigens.
The variable region of the immunoglobulin protein is what
recognises & binds to the antigen. Each variable region is different,
hence the name.
There are 5 different families of immunoglobulin molecule in the
human body (G, M, A, D & E. IgG - also known as -globulin). The
families can be distinguished from each other by slight differences
in the constant region of the protein
Each antobody molecule contains two pairs of proteins;
- Two heavy chains
- Two light chains
Each pair of chains is held together by disulphide bridges (hydrogen
bonds would be too weak).
Each immunoglobulin molecule has 2 antigen binding sites and can,
therefore, bind 2 antigens at one time. This means that a single

antibody molecule can bind to 2 pathogens at the same time, which

causes pathogens to clump together and form the Antibody-Antigen
Complex.

Antibody
Pathogen

Antigen

The formation of the Antibody-Antigen Complex is important

because it;
- Isolates pathogens so they cannot infect other host cells
- Makes it easier for macrophages to engulf & destroy the
pathogens.
- Stops the pathogen from entering a host cell
- Makes it easier for T cell activation as more antigens are
presented in one area

4.6.9
There are two different types of Immune Response;
A
B
NB:

Cell-mediated Immune Response

Antibody-mediated Immune Response.
Isolated viruses do not present antigens and therefore
do not trigger either the Cell- or Antibody-mediated
immune Response. However, when viruses invade host

cells, viral proteins are expressed which become

incorporated into the host cell surface membrane via
MHC. These proteins are recognised as antigens.
Cell-Mediated Immune Response:
1. Competent T Cells recognise a specific foreign antigen using its T
cell receptor.
2. Activated T Cell undergoes rapid mitosis forming a large number
of identical clone T
3. Cloned T Cells differentiate into Killer, Helper, Memory or
Suppressor T Cells.
4. Killer and Helper Cells migrate to the site of infection
Killer T Cells: attach to the infected / foreign cell and release the
enzyme Perforin, which makes holes in the pathogens cell membrane
causing it to die
Helper T Cells: stimulate B cells to start producing antibody and
attract macrophages to the site of infection
Memory T Cells: remain in the lymph nodes. They will respond
rapidly if the same pathogen invades the body again, because they
have the right T cell receptor to recognise the pathogen. This
means that the body can mount an immune response before
infection becomes serious
Suppresor T Cells: stop the immune reaction after about a week
Antibody-mediated Immune Response:
1. B cells are recognise a specific foreign antigen using the
antibody molecules on their surface. B cells can also be activated
by macrophages & Helper T cells. When a macrophage digests a
pathogenic cell antigens from the cell membrane get stuck in the

macrophages membrane; any B Cells which come into contact

with the antigen will then be activated
2. The activated B cell undergoes rapid mitosis and lots of clone B
cells are produced
3.

Cloned B Cells differentiate into either Plasma or Memory cells

Plasma Cells

Memory Cells

a) Plasma cells antibody, which

specific for one antigen only

is

b) Antibody is transported via the

lymph to the site of infection
c) Antibody attaches to the specific
antigen
d) An antigen-antibody
formed

Memory Cells continue to secrete

antibody for many years, so that if
the body is infected by the same
pathogen the Memory B cells can
produce an instant supply of antibody
before the infection becomes serious

complex is

4.6.10
Negative feedback systems aim to keep something (e.g. blood
[glucose] or body temperature) at a constant level.
Negative feedback works as follows;
1. Signal causes action
2. Action has effect
3. Effect removes original
E.g.
1. High [glucose] in blood causes insulin release
2. insulin stimulates liver to take up glucose & convert it into
glycogen stores

3. [glucose] falls

4.6.11
Homeostasis is the maintenance of the bodys internal environment.
This is carefully controlled by a series of systems, which aim to
keep conditions at a stable controlled level.
Body Temperature:
Body temperature is carefully regulated to maintain a steady
37.5C, which is the optimum temperature for human enzymes.
Sensors (thermoreceptors) in the hypothalamus continually monitor
blood temperature and activate warming / cooling processes to keep
the temperature as stable as possible.

Body temperature is normal

Exercise

Body temperature rises

Detected by thermoreceptors in hypothalamus

Hair erector muscles

cause body hairs to lie
flat

Peripheral arterioles
vasodilate

Sweat glands release

sweat onto skin

More heat radiated

away from skin

Sweat evaporates
carrying heat away

Less insulating air

trapped next to skin

Body temperature returns to normal

Tuberculosis bacterium (Mycobacterium tuberculosis) causes fever.

How does fever work?
All white blood cells communicate with each other and the rest of
the immune system using a class of hormones called cytokines. The
cytokines have hundreds of different roles and many more are yet
to be discovered. One class of cytokine is the hormone interleukin,
which causes fever.
Fever can be induced by many factors. The general class of
hormones that lead to fever are called pyrogens (interleukin is a
natural pyrogen). However, bacterial toxins, viral proteins and
substances produced by necrotic tissue may also trigger fever.
Pyrogens travel in the blood to the hypothalamus in the brain. They
bind to receptors there and trigger a complex set of reactions that
lead to the production of PGE2 hormone, which elevates the
thermoregulatory set point, i.e. it re-sets the bodys natural
thermostat to a higher temperature.
The hypothalamus now thinks body temperature is too low and
triggers a system of responses which aim to generate heat
(thermogenesis) and raise body temperature. These mechanisms
include; shivering, increased muscle tone, vasoconstriction and the
production of thyroxine hormone (which makes respiration less
efficient, therefore producing more heat).

4.6.12

Barrier Mechanisms include;

Skin
Stomach Acid
Normal Flora
Epithelial cells
Skin Adaptations for defence:

The skin is made from 2 layers;

- Outer epidermis layer
- Inner dermis layer
The epidermis provides a physical barrier to invading pathogens.
There are 2 layers in the epidermis;
A

Outer cornified layer, composed of compacted dead dry

cells filled with indigestible keratin protein (which also
forms nails and hair)

Inner Malpighian layer, site of rapid mitosis and

keratinisation.

The skin also has chemical defence mechanisms;

- sweat & sebaceous glands secrete sebum, which is an oil
with pH 3 5. This makes the skin acidic
- sebaceous glands also secrete the enzyme lysozyme, which
is a natural antibiotic. Lysozyme destroys bacterial cell
walls.
Stomach Acid:
Is made from HCl at pH 1 2. it is a very effective barrier.
Normal Flora:
The skin, respiratory tract and gut are covered with commensual
bacteria, which are part of the normal flora of the body.
Commensual bacteria are adapted to live the environment of the
skin and the gut and the and compete with invading pathogens for
the limited supply of nutrients.

Epithelial cell Adaptations for defence:

1. Epithelial cells are closely packed & connected by tight
junctions forming a continuous impermeable layer
2. Epithelial cells have cilia, which form a direct physical barrier
preventing pathogen attachment
3. Cilia beat in waves, which helps clear bacteria out of the
lungs and into the throat, where they are swallowed. Ingested
bacteria are quickly killed by the low stomach pH and
digestive proteases. Cilia also beat in the GI tract.

4. Epithelial cells secrete mucus, which is trapped by cilia. Mucus

also directly prevents pathogen attachment
5. Mucus contains lysozyme

4.6.13
Both T and B Cells differentiate into Memory Cells, which remain in
our lymph nodes and wait until we are re-exposed to the same
pathogen.
When the Memory B cell is activated by the old antigen it makes
large quantities on antibody quickly and kills the pathogen before it
can infect us properly. The memory cells provide active immunity.
When we are exposed to a new antigen it takes us about a week to
be able to make new antibody. However, a second exposure to
antigen produces a much faster response, and several orders of
magnitude higher levels of antibody are produced.

Plasma B cells make

lots of antibody on
re-exposure
Antibody made by
memory B cells
provides active
immunity

Without immunity the

level of antibody
produced by plasma
cells is much less

Passive Immunity is immunity to a pathogen without Memory cells.

It can occur through antibody injection or from drinking breast milk
(breast milk contains high [antibody])
Active Natural Immunity the process above
Passive Natural Immunity beastfeeding (antibody in milk)
Artificial Active Immunity - vaccination
Artificial Passive Immunity antibody injection

4.6.14
We have evolved a very effective immune system, consisting of
barriers, non-speficif defence mechanisms and specific ones. If
were so good at fighting infections, why do we still get ill?
Answer: pathogens are evolving as well.
So how has TB evolved to beat us?
1. It is spread by droplet infection, which is the most effective
method of infection
2. It specifically targets epithelial cells, which means that, when
inhaled, it is exactly where it wants to be
3. It does not kill immediately. This means that it has a large window
of opportunity to spread to others
4. It has a very thick waxy cell wall, which means it is partially
protected against lysozyme
5. It can survive inside macrophages and lie dormant until the immune
system is weakened, when it can re-infect.
So how has HIV evolved to beat us?

1. It weakens the immune system to increase its chance of survival

2. It stays in the body for years, so it can spread
3. It specifically targets Helper T cells
4. It is spread by sexual contact, so it is easily spread

4.6.15
Antibiotics work by targeting prokaryotic features not found in
eukaryotic cells, e.g. penicillin targets the cell wall and breaks it
down. Penicillin can be taken in large doses by humans because it has
no effect on our cells (we have no cell walls).
Bacteriostatic antibiotics stop bacteria reproducing, they do not
kill bacteria
Bacteriocidal antibiotics kill bacteria

4.6.16
The effectiveness of antibiotics can be measured using a disc
diffusion technique.
1.

A bacterial lawn is grown on an agar plate (either by

spreading the bacteria over the plate, or by using a pour
plate).

2. A disc of blotting paper is soaked in antibiotic of known

concentration and placed in the centre of the plate.
3. A clear circle of dead bacteria will form around the disc

4. The diameter / radius of the circle of dead bacteria is

proportional to the effectiveness of the antibiotic
5. This can be compared to other antibiotics, as long as the
same concentration of antibiotic is used. In addition, one
can also compare the effectiveness of an antibiotic with a
disinfectant or sanitiser (e.g. Phenol coefficient)
4.6.17
Bacteria are becoming resistant to antibiotics. Bacteria develop
resistance through mutation. A bacteria can mutate and develop
resistance by;
1. Having an enzyme that breaks the antibiotic down
2. Having a protein which pumps antibiotic out of the cell
3. Mutating the structure of the bacterium so that the
antibiotic no longer works

This problem is very serious. Bacteria become resistant because;

1. Bacteria mutate very easily. One in every million bacteria contains a
mutation. That might sound like a small amount, but consider that
one E coli bacterium can reproduce to form a colony of 2 million
bacteria in two hours. Over weeks, months and years thats a lot of
mutations, some of which will be beneficial
2. Bacteria reproduce very quickly (they divide every 20min) so a
bacterium with a beneficial mutation will spread quickly
3. Bacteria have the ability to pass copies of plasmids from one to
another (conjugation). So a mutation in one bacterium can quickly
be copied to others, even others in different species.

4. The use of antibiotics speeds the rise of immunity. If a bacterial

population is continually exposed to antibiotic all bacteria will die.
As soon as a bacterium mutates the rest of the bacteria will be
killed off by the latest dose of antibiotic; now the field is open for
the mutated bacterium to grow without competition.
5. Humans have been reckless with use of antibiotics. They are often
given to people who dont need them (i.e. they have viral infections)
or to people who dont bother to complete the course of antibiotic.

4.6.18
The evolutionary arms race between bacteria and drug developers
is, at the moment, tipped against humans. There are over 100
different types of antibiotic and in the 40years since their
development 4 species of bacterium have developed resistance
against all of them. E.g. Methicillin Resistant Staphyloccus Aureus
(MRSA) has been named the Superbug, because we have do drugs
left that can kill it.
Unless drug developers discover another branch of antibiotics were
not currently using (i.e. another way of targeting prokaryotic

SNAB A2 Revision
Notes

structures without damaging eukaryotic ones) there may well be a

global pandemic of resistant bacteria.

Unit 5: Energy, Exercise and

Coordination
Topic 7: Run for your life
5.7.1

Cartilage: a tissue made from collagen, which protects bone ends

A muscle: an organ that produces movement by contraction
A joint:
the junction between two bones
A tendon: joins muscle to bone
A ligament: joins bone to bone to stabilise a joint
Muscles work in pairs. One muscle produces the opposite movement
from the other muscle, therefore, the pairs are called antagonistic
pairs.
Muscles which cause a joint to extend are called extensors, muscles
which cause a limb to retract are called flexors.
A Synovial Joint
Bone
Ligament
Muscle
Cartilage

Synovial Fluid
Synovial membrane

Tendon

5.7.2
Muscles are made from muscle fibres arranged into bundles. Each
fibre is made from bundles of myofibrils, which are extremely long,
cylindrical muscle cells.
Arrangement of myofibrils into a muscle fibre

Muscle cells (Myofibrils)

Muscle Fibre
1. A nerve impulse arrives at the
neuromuscular junction
2. The muscle cell is depolarised
3. Ca2+ is released from the
sarcoplasmic reticulum inside
muscle cells

The functional unit of contraction is the4.sarcomere.

Muscle cells
Ca2+ bids to Troponin protein in the
contain many sarcomeres arranged in parallel.thin
Thefilament.
muscle cell takes
on a characteristic banded appearance because of the regular
5. Troponin
protein and Tropomyosin
arrangement of the sarcomeres. This is called
striation.
protein move position in the thin
filament

6. Myosin binding sites are exposed

A sacromere.
Note the striated
on the thin filament

appearance of the muscle

7. Myosin heads of the thick filament

stick to actin

Cross-Bridge Cycling:

The8. sarcomere
overlapping
ATP (alreadycontains
bound to the
myosin
head)myosin.
is hydrolysed
causingisthe
actin and
The myosin
often
headfilament
to pivot forwards
called myosin
the thick
because inthe
powerstroke
myosintheheads
make it appear thick.
The9. actin
the thin
As the is,
headtherefore,
pivots the thick
filament
filament moves across the thin

filament muscle contraction

The process by which the thin filaments are pulled
in towards each other by
occurs

the myosin is called cross-bridge cycling. It is how muscles contract.

10. ADP diffuses away from the

myosin head leaving the ATPbinding site empty
11. New ATP binds & the myosin head
& causes the myosin head to
detach from the actin.
12. The myosin head re-cocks
13. The head rebinds further up the
myosin.
14. Repeat stages 7 to 13 until the
[Ca2+] falls too low, when
contraction stops

Key Point: ATP is required to release myosin

from actin. If ATP levels drop (assuming Ca 2+ is
present) the myosin stays attached to the
actin and the muscle stays permanently
5.7.3 This is what causes rigor mortis
contracted.
Adenosine TriPhosphate (ATP) is made from three components;
- Ribose (the same sugar that forms the basis of DNA).
- A base (a group consisting of linked rings of carbon and
nitrogen atoms); in this case the base is adenine.
- Up to 3 phosphate groups. These phosphates are the key
to the activity of ATP
Adenine base
3 x phosphate
Ribose

The energy used in all cellular reactions comes from ATP. By

breaking the 3rd phosphate from the ATP molecule energy is
released, which can be used to power intracellular reactions. The
ATP is then regenerated by recombining the phosphate and ADP in
respiration (or another process e.g. photosynthesis).
The recycling of ATP is crucial for life. For example a runner uses
~84kg of ATP in a marathon (more than their total body weight),
yet there are only 50g of ATP in the entire body! This means each
that each molecule of ATP has been recycled 1676 times during the
race!

Adenosine

ATP = one adenosine

molecule
with
3
phosphate
groups
attached

Energy rich bond

Less energy rich bond(30.6kJ/mol)
(13.8kJ/mol)

Energy rich bond

ATP + H2O ADP

+ Pi
(30.6kJ/mol)

How the energy in ATP is liberated:

Energy
Adenosine ADP
P + H2O AMP + Pi
Energy
Adenosine P
AMP + H2O Adenosine + Pi

Energy
Adenosine

Normally, as soon as ATP has been converted into ADP + P i

it is converted back into ATP using energy from
Step respiration.
Reactants
Summary
However, Products
during exercise ADP
may be
converted into AMP or even Adenosine to provide energy.

1.
Glycolysis

1 x Glucose
2 x ATP

2 x Pyruvate
4 x ATP
2 x NADH

A 6C glucose molecule is split

into two 3C pyruvate molecules.
Some ATP is used to split the
glucose molecule in the first part
of glycolysis

1 x Pyruvate
1 x CoA

1 x Acetyl CoA
1 x CO2
1 x NADH

3C Pyruvate is split into a 2C

molecule, which is attached to a
CoA enzyme to form Acetyl CoA.
The remaining carbon atom is
used to form CO2

(cytoplasm)
2.
Link Reaction
(mitochondria
matrix)
3.
Krebs Cycle

1 x Acetyl CoA

4.
Oxidative
Phosphorylation

10 x NADH
2 x FADH2
6 x O2

Respiration

1 x CoA
CoA enzyme gives its 2C atoms
1 x ATP
to a 4C molecule to form a
x CO
temporarybond
6C molecule.
Respiration: a process2 in
which
the chemical
energy In
in a
2
(mitochondria
3 x to
NADH
steps theinto
6C molecule
glucose molecules is used
convert 38series
ADP of
molecules
38
matrix)
1 xis
FADH
releases
the Dioxide
two C atoms
2
ATP molecules. Oxygen
required
and
Carbon
andas CO2
Water are produced as waste products.eventually re-forming the
starting 4C compound. The cycle
is then ready to repeat itself. As
Respiration occurs in 4 distinct steps;
the cycle turns ATP, NADH &
FADH2 are formed

(mitochondria
christae)

34 x ATP
6 x H2O

The electron transport chain

uses the NADH and FADH2 made
in previous steps to make lots of
ATP

5.7.4

Respiration: Step 1 - Glycolysis

Glucose

Glyceraldehyde
Phosphate

2ATPs are required

Glyceraldehyde
Phosphate
2ATPs are made (4 overall)
1 NADH is made (2 overall)

Pyruvate

Pyruvate

Glycolysis takes place in the cytoplasm of a cell

In Glycolysis a Glucose molecule (6C) is split into 2 molecules
of Glyceraldehyde Phosphate (3C). 2ATPs are required for
this to happen.
Then, each 3C Glyceraldehyde Phosphate molecule is converted
into a 3C Pyruvate molecule. In the process of converting one
Glyceraldehyde Phosphate to one Pyruvate, enough energy is
released to convert one NAD molecules into one NADH
molecules and also to make two ATP molecules.
Overall; 4ATP are made, 2NADH are made and 2ATPs are used.
In anaerobic conditions [H+] rises in the mitochondria as there are no available oxygen
molecules to mop it up with and form water. This leads to saturation of the electron
transport chain and a build-up of NADH and FADH2. This means [NAD] falls, which stops
the Krebs Cycle. Acetyl CoA levels build-up, [CoA] falls and the Link Reaction stops.
Pyruvate levels start to rise
Muscle cells turn pyruvate into lactate to stop rising [pyruvate] from stopping Glycolysis
(remember, enzyme controlled reactions are reversible and depend on [reactants] and
[products]).

Net gain: 2ATP and 2NADH

Pyruvate

NADH

Lactate

NAD

In the liver the lactate is converted back into pyruvate. This requires
oxygen, which is the basis of the Oxygen Debt

Respiration: Step 2 Link Reaction

Pyruvate
1 NADH is made (2 overall)
1 CO2 is made (2 overall)
CoA enzyme

Acetyl CoA

Link Reaction takes place in the matrix of the mitochondria

In the Link Reaction a Pyruvate molecule (3C) is split into a 2C
molecule and a CO2. The 2C molecule is attached to a CoA
enzyme, forming Acteyl CoA.
Remember, two molecules of Pyruvate were made at the end of
Glycolysis, therefore the Link Reaction happens twice.

5.7.5

Overall; 2NADH and 2 CO2 are

made.

Respiration: Step 3 Krebs Cycle

Net gain: 2NADH

CoA enzyme

2 NADH are made (4 overall)

1 ATP is made (2 overall)
1 FADH2 is made (2 overall)
2 CO2 are made (4 overall)

Krebs Cycle takes place in the matrix of the mitochondria

In the Krebs Cycle the Acetyl CoA gives its 2C atoms to a 4C

molecule (Oxaloacetate) forming an unstable 6C molecule
(Citric Acid). The 6C molecule breaks down into a 4C compound
(Succinyl CoA) releasing enough energy to make one NADH.
The two spare C atoms are released as two CO2 molecules.
Succinyl CoA is converted back into Oxaloacetate and this
releases enough energy to make one NADH, one FADH 2 and one
ATP. The Oxaloacetate can then be used in the cycle again.
Remember, two molecules of Acetyl CoA were made at the end
of the Link Reaction, therefore
the Krebs Cycle happens twice.
5.7.6

Respiration:
Step 24
Oxidative
Phosphorylation
Overall;
4NADH, 2FADH
, 2CO
2 and 2ATP are made.
Oxidative Phosphorylation uses the NADH and FADH 2
produced in the previous steps of respiration to make ATP.
Each NADH makes 3ATP and each FADH2 makes 2 ATP.

ATP

FADH2

ADP

ADP

NADH

H2O
H+ Carrier

H+ Carrier

e- Carrier

e- Carrier

NAD

e- Carrier

O2 + 2H+

ATP

FADH

2e

ATP

ATP

Oxidative Phosphorylation takes place using enzymes embedded in

the inner membrane of cristae of the mitochondria
Hydrogen atoms from the NADH and the reduced FADH 2 are
passed onto 2 the first 2 enzymes of the Electron Transport
Chain. These enzymes are Hydrogen Carriers and they accept
the H atoms from the NADH and the FADH2.
Electrons, which made up the chemical bond between the
hydrogen atoms and the NADH / FADH 2 are passed onto 3
Electron Carrier enzymes further down the Electron
Transport Chain.
At the end of the Electron Transport Chain, the electrons are
recombined with the H+ atoms and oxygen, to form water. This
is the only, but crucial, part of respiration to involve oxygen.

NADH starts at the first Hydrogen Carrier and has enough

energy to phosphorylate 3ADP. FADH2 has less energy and
starts at the second Hydrogen Carrier, it generates 2 ATPs

Where does the 38 ATP come from?

Glycolysis produces;
Link Reaction produces;
Krebs Cycle produces;
2ATP
Total

2ATP
2NADH
2NADH
6NADH
2 FADH2

4 ATP

10NADH

2 FADH2

Each NADH produces 3ATP total production is 30ATP from

NADH
Each FADH2 produces 2ATP total production is 4ATP from
FADH2

Grand Total

4ATP +

30ATP + 4ATP

= 38ATP

Chemiosmosis of H+ ions
from
the
mitochondrial
envelope into the matrix
through ATP Synthetase
proteins is what actually
generates
the ATP in
respiration

The electron transport chain uses the process of chemiosmosis

(the diffusion of ions across a membrane). H+ ions are actively
pumped into the mitochondrial envelope. This is done by the
proteins in the electron transport chain, using the energy
stored in NADH and FADH2.

The [H+] builds up to very high levels in the envelope. However,

H+ cannot escape because it is charged (hydrophilic) and
therefore cannot move through the phospholipid bilayer in the
envelope membranes.
Special proteins called ATP Synthetase do allow H+ to pass
through them and escape into the mitochondrial matrix.
Whenever an H+ ion moves through the ATP Synthetase protein
an ADP is phosphorylated by the ATP Synthetase.
In summary;
1. NADH and FADH2 contain stored chemical energy
2. The energy is used to pump H + into the mitochondrial
membrane against the concentration gradient
3. H+ trapped in one place represents a store of potential
energy
4. H+ ions leave the envelope through ATP Synthetase
proteins.
5. The potential energy of the H+ is used to phosphorylate
ATP as the H+ moves out of the envelope
5.7.7
In anaerobic respiration lactate is taken via the blood to the liver,
where it is broken down into pyruvate using oxygen and NADH.

5.7.8
c h e m o r e c e p t o r s in
a o r t ic a n d c a r o tid
b o d ie s

c h e m o r e c e p t o r s in
m e d u lla

s tr e tc h r e c e p to r s
in m u s c le s

c o r te x
( v o lu n t a r y c o n t r o l)

R E S P IR A T O R Y
CENTR E
in m e d u lla o f b r a in

p h r e n ic
n e rv e

in t e r c o s t a l
n e rv e

vagus
n e rv e

s tr e tc h
re c e p to rs

in t e r c o s t a l
m u s c le s

d ia p h r a g m

p re s s u re
r e c e p t o r s in a o r tic
a n d c a r o t id
b o d ie s

c h e m o r e c e p to r s in
a o r t ic a n d c a r o tid
b o d ie s

te m p e r a tu r e
r e c e p to rs in
m u s c le s

s tr e tc h r e c e p to r s
in m u s c le s

C A R D IO V A S C U L A R
CENTR E
in m e d u lla o f b r a in
p a r a s y m p a t h e t ic
n e rv e
( in h ib it o r )

s y m p a th e tic
n e rv e
( a c c e le r a t o r )
s in o a tr ia l
node

5.7.9

v a s o c o n s t r ic tio n
and
v a s o d ila t io n

TV

A spirometer is used to plot breathing patterns

Vital Capacity:

The maximum amount of air a person can exhale

after inhaling the maximum possible volume of
air

Tidal Volume:

The volume of air inhaled & exhaled in one

breath

Basal Metabolic Rate:

The rate of respiration

The spirometer can be used to plot VC and TV directly. BMR can be

worked out if a CO2 scrubber is used. The spirometer has fixed volume
and is filled with 100% O 2 before the experiment begins. As the person
respires, O2 is replaced proportionally with CO 2. The total volume should
stay constant. However, if CO2 is removed, the total volume will slowly fall
as O2 is used. The rate at which the volume decreases is proportionaly to
BMR.
You are not expected to know how the spirometer works although its not
very difficult to understand.

5.7.10 & 5.7.11

Sprinters need lots of fast twitch muscle, joggers need slow twitch.
Therefore, the muscle type of a cheetah or a gazelle will be
predominantly fast twitch, whereas the muscle of a camel or an elephant
will be predominantly slow twitch.
Muscle type in humans is predominantly one or the other due to inherited
alleles. However, different training programmes can cause the % of
either type to change slightly.

Slow twitch fibres

Red (lots of myoglobin)
Many mitochondria
Little sarcoplasmic reticulum
Low glycogen content
Numerous capillaries
Fatigue resistant

Fast twitch fibres

White (little myoglobin
Few mitochondria
Lots of sarcoplasmic reticulum
Lots of glycogen
Few capillaries
Fatigue quickly

5.7.12
See 4.6.11 for mechanisms of thermoregulation.
The thermoregulatory process (and most homeostatic systems) are
controlled by negative feedback processes. If a system changes, it
is detected, a homeostatic response is activated, which aims to
return the system to its original level. Negative feedback,
therefore, holds systems at a set point, in this case 37.5C.

5.7.13

A moderate level of exercise

improves health & well-being.
However, over-training can result
in the opposite effect. This is the
phenomenon known as burn-out

Positive effects of exercise include;

1.
2.
3.
4.

Increased BMR
Decreased blood pressure
Increased HDL
Decreased LDL

5. Maintaining healthy BMI

6. Decreased risk of diabetes
7. Increased bone density
8. Improved well being
9. Decreased adrenaline levels
10.Less stress
11. Decreased risk of CHD
12.Moderate exercise increases levels of Natural Killer cells,
which secrete apoptosis-inducing chemicals in response to
non-specific viral or cancerous threat
Negative effects of exercise (over-training) include;
1. Decreased levels of Natural Killer Cells, Phagoctyes and B & T
Cells. This decreses immune response.
2. Increased muscle inflammation
3. Muscle tears and sprains
4. Increased adrenaline levels
5. Increased cortisol levels, which also decreases the immune
response
6. Increased stress
7. Damaged cartilage
8. Tendinitis
9. Ligament damage
10.Swollen bursae

5.7.14
Key-hole surgery is a technique which allows doctors to conduct
surgery with the minimum possible damage to the patient. The
surgeon makes a small incision (a key-hole) and uses a fibre-optic
camera to view the damaged area. If required, the surgeon can
make a second incision and use a number of small, remote operated
tools to repair the damage. Because the incisions are small and only
the damaged area is targeted, the patient recovers quickly. There is
also less chance of infection.

Unfortunately, the procedure requires a high degree of training,

expensive equipment and can only be used on certain types of
surgery.
Prosthetics allow people with amputations to participate in many
activities, including sports.

5.7.15
Drug

Effect on physiology

Effect on performance

Erythropoietin EPO causes the bone marrow Extra blood cells mean the
(EPO)
to generate extra red blood blood can carry extra oxygen.
cells.
This increases the level of
work the body can sustain
through aerobic respiration
(aerobic threshold).
Creatine
Creatine
combines
with Because ATP is re-generated
phosphate to form Creatine without using the respiratory
Phosphate (CP). CP can pathways,
theoretically
it
phosphorylate
ADP,
re- should increase the maximum
generating ATP.
power of muscles and decrease
recovery time
Testosterone Binds to androgen receptors Muscle mass increases, which
in target cells and increases makes the athlete more
transcription of anabolic powerful. It also decreases
proteins (growth proteins) recovery time.
such as actin & myosin.

Side-effects
Increased haemocrit
increases
blood
viscosity. This causes
strain on the heart
and
can
lead
to
infarction
Diarrhoea , vomiting,
liver
damage
and
kidney damage.

Agression, decreased
sex drive, infertility,
skin problems, acne,
shrunken testicles

Why should we allow use of drugs;

Gives people a chance to be as good as their potential allows

Removes unfair genetic advantages
Controlled use of drugs is less risky
People should have the right of choice
Legalising drugs makes their distribution controllable (no use
by under-age, infirm etc)

Arguments for not using drugs;

Dangerous (obviously)
May be pushed onto athletes by trainers
Effects are permanent

 Not used under doctors supervision

Often cut with other drugs
Exposes athletes to criminals (danger of using other drugs)
The list goes on, just think for yourself in the context of the
question. You can argue the toss either way, but make sure you can
back up your opinion with some sensible, logical arguments.

SNAB A2 Revision
Notes
Unit 5: Energy,
Exercise and
Coordination

Topic 8: Grey matter

5.8.1
Sensory nerve:

carries electrical message from receptor to spine

Motor nerve:

carries electrical message from spine to effector

Relay nerve:

connects sensory and motor nerves. Also relays

message to the brain.

Schwann cells:

wrap around the axon of the long nerves, creating

a thick layer of membrane, which insulates the
nerve and allows for much faster conduction
speed. The thick layer of membrane has gaps in it
between adjacent Schwann cells, these are called
Nodes of Ranvier.

5.8.2

Low light intensity

High light intensity

Circular muscles: contracted
Radial muscles: relaxed
Pupil diameter: small

Circular muscles: relaxed

Radial muscles: contracted
Pupil diameter: large

5.8.3
The Action Potential
Voltage-Gated K+
Channels open

Voltage-Gated Na+
Channels open

Nerve is
hyperpolarised and
inactive (refractory
period)

Sequence of events in an action potential;

1. Nerve is at resting membrane potential (-70mV)

2.

A stimulus depolarises the nerve to threshold (-50mV)

3.

Voltage-gated Na+ Channels open

4. Sodium floods into the cell and the membrane potential

depolarises to +30mV
5.

Voltage-gated K+ Channels open

6. Potassium floods out of the cell and the membrane potential

falls to -90mV
7. The nerve is in the refractory period and cannot conduct
another action potential
8.

The 3Na+/2K+ ATPase (Na+/K Pump)

concentrations

restores the ion

9. The nerve is ready to fire again

As one part of the nerve fires off, Na + diffuses into the next
section of the nerve, which depolarises the nerve to threshold. This
sequence is repeated like a tiny Mexican wave down the axon of the
nerve.
Nodes of Ranvier speed this conduction process up. When one node
depolarises it induces the next section of the nerve to depolarise by
forming a mini-circuit between nodes. This causes the action
potential to jump between nodes of ranvier, making conduction
speed much faster.

5.8.4
A synapse is the junction between two nerves. It is also a verb, i.e.
one nerve synapses with another (meaning, passes a message to
another).
The neurotransmitter on your syllabus is Ach, but over 2000 other
transmitters have been discovered

3
1
2

5
7

1. The wave of depolarisation arrives at the synaptic knob. The

membrane in the presynaptic neuron is depolarised to 50mv
(threshold potential) and the voltage-gated Na + channels
open, letting Na+ into the cell.
2. The membrane is depolarised to +30mV and voltage-gated K +
channels open. The membrane potential falls to 90mV and
the cell goes into its refractory period, where the 3Na +/2K+ATPase restored the ion concentrations.
3. Unlike axons, presynaptic nerves also contain a Voltagegated Ca2+ channel. As the presynapstic membrane
depolarises these channels open and let Ca2+ into the cell.

4. The Ca2+ causes vesicles in the presynaptic nerve to migrate

and fuse with the presynaptic membrane, where they spill
neurotransmitter chemical into the synaptic cleft.
5. The neurotransmitter (Acetyl Choline) diffuses across the
cleft and binds to receptors on the postsynaptic membrane.
6. The receptors let a little Na+ into the postsynaptic neuron,
which is enough to initiate another action potential in the
postsynaptic nerve.
7. The ACh is broken down by an enzyme called Acetyl Choline
Esterase (AchE), which allows the postsynaptic receptors to
be freed ready for a second synapse.
In a neuromuscular junction the sequence of events in the
synapse is exactly the same. The only difference is that the
posysynaptic nerve is a muscle cell and, instead of being flat,
the postsynaptic membrane has deep grooves (t tubules) which
allow the depolarisation to spread quickly through the muscle
so all parts of the muscle contract at the same time.
Some neurotransmitters can hyperpolarise postsynaptic
nerves, which essentially switches them off. An example of
this type of inhibitory neurotransmitter is GABA
5.8.5
Visual transduction is the process by which light initiates a nerve
impulse. The structure of a rod cell is:

The detection of light is carried out on the membrane disks in the

outer segment. These disks contain thousands of molecules of
rhodopsin, the photoreceptor molecule. Rhodopsin consists of a
membrane-bound protein called opsin and a covalently-bound
prosthetic group called retinal. Retinal is made from vitamin A, and
a dietary deficiency in this vitamin causes night-blindness (poor
vision in dim light). Retinal is the light-sensitive part, and it can
exists in 2 forms: a cis form and a trans form:
In

the dark retinal is in the cis form, but when it absorbs a photon of
light it quickly switches to the trans form. This changes its shape
and therefore the shape of the opsin protein as well. This process is
called bleaching. The reverse reaction (trans to cis retinal) requires
an enzyme reaction and is very slow, taking a few minutes. This
explains why you are initially blind when you walk from sunlight to a
dark room: in the light almost all your retinal was in the trans form,
and it takes some time to form enough cis retinal to respond to the
light indoors.
Rod cell membranes contain a special sodium channel that is
controlled by rhodopsin. Rhodopsin with cis retinal opens it and
rhodopsin with trans retinal closes it. This means in the dark the
channel is open, allowing sodium ions to flow in and causing the rod
cell to be depolarised. This in turn means that rod cells release
neurotransmitter in the dark!
However the synapse with the bipolar cell is an inhibitory synapse,
so the neurotransmitter stops the bipolar cell making a nerve
impulse. In the light everything is reversed, and the bipolar cell is
depolarised and forms a nerve impulse, which is passed to the
ganglion cell and to the brain.

Summary for light;

1. Photon hits rhodopsin
2.

Bleaching occurs and trans retinal is formed

3.

Trans retinal blocks Na+ channels

4. The rod is hyperpolarised and stops releasing inhibitory

neurotransmitter
5. The bipolar cell is no longer inhibited and depolarises
6. The ganglion cell is activated, which carries the message to
the brain
Cones work in exactly the same way, except that they contain the
pigment Iodopsin, which is found in 3 different forms; redsensitive, blue-sensitive and green-sensitive. This gives us colour
vision.

5.8.6

Homeostasis is the maintenance of the internal environment.

- Nerve reflexes give immediate responses
- Hormone responses give responses over weeks months
Hormones are released from glands, which release hormone into the
blood. The hormone is carried all over the body. It binds to hormone
receptors on cell membranes and initiates responses in those cells.

5.8.7

Midbrain
Cerebrum

Cerebellum
Medulla

Hindbrain

Brainstem

Brainstem Uppermost part of the spine, where the spine joins the
brain
Medulla - controls vital housekeeping functions, such as heartbeat,
blood pressure and peristalsis.
Cerebellum - controls muscle co-ordination & learns motor
programmes (e.g. like how to ride a bike, or write).

Midbrain:
Thalamus a relay station that carries sensory information from
the sense organs to the correct part of the cortex and
hypothalamus. The thalamus contains the Superior Collicului, which
control the initial processing of visual information. The Superior
Colliculi control object tracking, spatial position and partial
recognition (i.e. whether a stimulus is food or a threat)
Hypothalamus receives sensory information from the thalamus.
Contains homeostatic centres, which control factors like body
temperature and blood osmolarity. The hypothalamus is connected
to the Pituitary gland and therefore the hypothalamus can stimulate
the release of a great number of pituitary hormones

Forebrain:
Cortex processes sensory information and controls the bodys
voluntary behaviour, i.e. learning, personality and memory.
This is the part of the brain that actually thinks. The cortex is
very large in humans and is folded to increase the surface area
further. Other animals have roughly similar size hind- and
midbrains. However, their cortex is much, much smaller.

(Speech
Premotor
Auditory
motor
area)association area

Somatosensory
Visual
association area

(Understanding language)

Occipital lobe - processes & interprets information from the

eyes
Temporal lobe - processes & interprets information from the
ears and processes language and the meaning of words
Parietal lobe processes and interprets information about
touch, taste, pressure, pain, heat and cold. Also initiates motor
commands.
Frontal lobe - plans and organises thought, is involved with
short term memory and puts speech together.
5.8.8

Technique

Surgery

C T Scan

MRI Scan

fMRI Scan

5.8.9

How it works
During brain surgery a local
anaesthetic is often used. This
allows the surgeon to ask the
patient
questions
as
he
operates on their brain
Thousands of narrow-beam Xrays pass through the patients
head from a rotating source.
The rays are collected on the
other side of the head and
their strength measured. The
density of the tissue the Xray
passes through decreases the
strength of the signal, and
therefore, lets us work out
what type of tissue is in the
brain.
Magnetic fields are used to
align protons in water molecules
in the patients brain. When the
fields are switched off, the
protons give out a little energy,
which can be detected.

Very similar to above, except

that the magnetic fields are
tuned to excite deoxygenated
haemoglobin. This shows up all
the areas in the brain where
oxygen is being used

What it allows us to see

The patient can tell the doctor
what he/she is feeling as the
doctor stimulates parts of
his/her brain. This can tell us a
lot about the function of the
brain.
CT Scans show brain structures,
not brain activity. They also only
give
frozen
still
images.
However, they are very useful
for picking up diseases, such as
cancer, stroke and oedema.

By recording the energy given

out by protons we can build up a
sequence of thin pictures of the
types of tissues inside the brain.
This can be fed into a computer,
which uses the picture to build up
a 3D image of the inside of the
head
As above, but the doctor not only
knows what the tissues look like,
but whether they are active.
This is the only technique, that
shows brain activity.

How to process stimuli correctly must be learned. The cortex is

split into column of cells. When we are born, the columns overlap
and are tangled. As we learn to process stimuli, the cells organise
themselves into discrete columns, which no longer overlap. There is
a critical window for this to happen (usually before puberty,
younger for visual processing). If we miss the window, our brains will
become fixed with tangled columns and wont be able to process
stimuli properly.
Hubel & Wiesels experiments prove this.

5.8.10
The Muller-Lyer illusion;

Lines A and B are the same length, yet look different why? The
answer is that you have learned to process this kind of stimuli in a
certain way. We live in a carpentered world of straight lines and
we interpret line B as a corner (therefore larger than it appears,
because it must be far away) and line A as a corner (therefore,
smaller than it appears, because it must be close).
These optical illusions do not work on Zulus, which proves the
illusion is caused by learned visual processing, rather than an innate
function of the eye / brain.

5.8.11
Association (classical conditioning):
US UR

(Food Salivation)

Over time, if a neutral stimulus (CR) is played with the US, it

becomes associated with the US and begins to elicit the same
response. Eventually, the animal learns
CS CR

(Bell Salivation)

Pavlovian conditioning occurs by synapses between nerves growing

together. This means that the sensory nerve carrying the message
of the CS will always lead to the firing of the motor nerve, which
triggers the CR.
Operant Conditioning:
This is very similar to classical conditioning except the animal learns
by doing something i.e. it learns that an action has a certain
outcome
AO

(pushing a level food)

Habituation:
If the neutral stimulus is continuously present (not just before the
US), but all the time, the animal learns to ignore the CS. The animal
learns the bell signals nothing and it ignores the CS totally. This is
called habituation.
If a nerve is frequently stimulated, the amount of Ca 2+ that enters
the pre-synaptic nerve gradually diminishes, until it is no longer
enough to trigger vesicles to fuse with the pre-synaptic membrane.
This means no neurotransmitter is released, which results in no

post-synaptic depolarisation. The effect is, essentially, that the

stimulus is ignored.
Insight Learning:
In the early 1900s, Wolfgang Kohler performed insight experiments
on chimpanzees. Kohler showed that the chimpanzees sometimes
used insight instead of trial-and-error responses to solve problems.
When a banana was placed high out of reach, the animals discovered
that they could stack boxes on top of each other to reach it. They
also realized that they could use sticks to knock the banana down.
In another experiment, a chimp balanced a stick on end under a
bunch of bananas suspended from the ceiling, then quickly climbed
the stick to obtain the entire bunch intact and unbruised (a better
technique than the researchers themselves had in mind). Kohler's
experiments showed that primates can both see and use the
relationships involved to reach their goals.
This type of learning is very difficult to explain using the Pavlovian
model of conditioning. It is also difficult to explain using neuronal
models of learning (i.e. synapses growing together through use)
developed through studies on Aplysia. How insight learning occurs is
unknown at the moment.

5.8.12
Pavlovs Dogs
Pavlov had observed that an unconditioned stimulus causes an
unconditioned response, i.e. food causes salivation. This is not
learned and is, therefore, unconditioned.
What Pavlov discovered was that if a neutral stimulus, such as a bell
is rung just before the food is given for a few occasions, the dog
will salivate every time the bell is rung, even if no food is presented.
In this case, the dog has learned that the bell signals food. The
food is, therefore, a conditioned stimulus and it prompts a
conditioned response.

US UR
US + CS UR
Eventually, CS CR
Hubel & Wiesel

Permanently
blind
monkeys?

Hubel & Wiesel investigated

the critical window.
They used monkeys and kittens
in their studies
Their work permanently blinded
some animals and can be argued
to be unethical.

Hubel & Wiesels Method:

1. Raise monkeys from birth in three groups for 6 months
2. Group 1 are the control (no blindfold), Group 2 are blindfolded
in both eyes, Group 3 are blindfolded in one eye (monocular
deprivation)
3. Test the monkeys to see whether they can see using each eye
4. Test the sensitivity of retinal cells
5. Test the activity of nerves in the visual cortex in response to
stimuli
The results:

Monkeys in Group 2 (both eyes blindfolded) had impaired

vision

Monkeys in Group 3 (monocular deprivation) were blind in the

deprived eye
Retinal cells were responsive in all groups
Cortical activity was reduced in parts of the brain that
process information from the deprived eye
Adults undergoing the same tests showed no difference
between groups. All could see.

The Conclusion:
There is a critical window for visual neural development, which
requires stimulus from the eye. If this window is missed the monkey
is blind, because of events happening in the brain, not the eye.
You need to know about these experiments because they all use
animals
Clinical Trials Stage 1 involves animals.
5.8.13
WhyArguments
not use computer
Arguments
Against simulations in
Without animals we
would notFor
be able
Clinical trials instead?
to discover new drugs
Animal physiology is different to human
Animal testing is better than nothing
physiology. Animal testing is, therefore,
and does, in some cases, avert
unhelpful
potential loss of human life
Utilitarian argument: Animal testing
Animals have rights too.
is for the greater good
Machines like the MRI were unvested
using animals.
Animal testing has advanced our
understanding of human physiology

5.8.14

Animals have no informed consent

Testing on animals when the potential
side-effects are unknown is immoral.
Animals cant tell you when they are
suffering
Animals are often poorly cared for in
labs

In Parkinsons disease neurons in the brain die. All these neurons

secrete dopamine neurotransmitter, which causes difficulty in
movement and limb shaking.
In depression neurons in the brain that secrete serotonin
neurotransmitter stop working properly and serotonin levels fall.
In both cases treatments that increase the levels of
neurotransmitter might prove successful in relieving the symptoms
of these diseases

5.8.15
Drugs that affect synapses can drastically alter the functioning of
the brain;
MDMA:
Active ingredient in ecstasy. This binds to protein pumps on the
pre-synaptic membrane of nerves that secrete serotonin. The
pumps would normally take serotonin up after it had been released,
therefore reducing firing in post-synaptic nerves. BUT, when these
channels are blocked, serotonin builds up in the cleft, giving greater
post-synaptic activation and a sense of euphoria.
L-Dopa:
This is a precursor of dopamine. When given to Parkinsons
sufferers it is turned into dopamine, which helps alleviate some of
the symptoms of the disease.

5.8.16
Continuous variation: there is a wide range of phenotypes (e.g.
height)
Discontinuous variation: phenotypes fall into discrete categories
(e.g. blood type)

Discontinuous variation tends to be coded for by one gene with a

few different alleles. However, continuous variation is more
complex. This is usually coded for by many genes (polygenes), with
many alleles, which produces the much greater range of possible
phenotypes.
Polygenes can give rise to susceptibility to disease, usually with an
environmental trigger. Diseases that are both genetic and
environmental are called multifactorial

5.8.17
Brain development is a combination of nature and nurture.