I.

Audition
a.
1. environmental stimuli
i. sound waves
1.
compressed air at peak
2.
rarified air at trough
3.
intensity determines volume
4.
frequency determines pitch
b.
2. reception
i. outer ear
1.
pinna, auditory canal
ii. middle ear
1.
tympanic membrane
eardrum vibrates
2.
ossicles malleus, incus,
stapes
3.
footplate of stapes vibrates
at oval window
4.
attenuation reflex loud
sounds make muscles tense up
to prevent damage
iii. inner ear
1.
cochlea
a.
scala vestibuli
continuous w/ scala timpani
b.
scala media

c.

c.
perilymph found in
vestibuli & timpani, similar
to other brain fluids
d.
endolymph found in
scala media, high
concentration of potassium
e.
helicotrema where
vestibuli becomes timpani
f. round window pressure
released from sound wave
g.
basilar membrane
separates vestibuli from
timpani
i. rigid and narrow at base,
floppy and wide at apex
ii. low frequency waves
vibrate the base, high
frequency waves vibrate
the apex
h.
organ of corti sits on
basilar membrane
i. outer and inner hair cells
ii. tectorial membrane
move hair cells against
stereocilia
3. transduction

i. basilar membrane moves up and

down to move stereocilia back and
forth
ii. stereocilia have K+ channels on
tips movement closes and opens
channels
iii. kinocillium tallest stereocilium
iv. surrounded by endolymph (high
K+)
v. open channels, K+ flows in,
depolarizes, triggers NT release
(glutamate), synapses onto
auditory nerve fiber, goes to brain
vi. inner hair cells one row, synapse
onto multiple spiral acoustic
ganglia
vii. outer hair cells multiple rows,
many synapse onto one spiral
acoustic ganglion
viii. fibers come from brain and
synapse onto outer hair cells to
provide regulatory info
d.
4. transmission
i. tonotopy map of frequency
ii. DVSLIM

1.
dorsal/ventral cochlear
nuclei
2.
superior olive
3.
lateral limniscus fibers
4.
inferior colliculus
5.
medial geniculate nucleus
(MGN)
iii. sometimes SL is skipped over
iv. DVSLIM goes to A1 (primary
auditory cortex), specifically
Herschls Gyrus
II. Music and the Brain
a.
pitch perception
i. fundamental lowest tone
ii. harmonics tones higher by
multiples of the fundamental
b.
pitch and timbre
i. pattern of harmonics differs
c.
the brain stuff
i. each hair cell vibrates at a different
frequency
ii. fundamental represented by
inferior colliculus neurons and
above
iii. A1 (temporal lobe) planum
temporale processes pitch
d.
stream segregation

i. auditory object perception

ii. sound broken down by frequencies,
put into different streams,
separated by the brain
iii. location, time, timbre, frequency
grouped
e.
music and emotion
i. pleasure of music
1.
smth about dopamine
ii. perceived emotion
1.
tempo, mode, loudness
changes, timbre
III. Attention
a.
Attention is the process by which
info is selected to process further
b.
FILTER MODEL
i. inputs (attended and unattended)
sensory store selective filter
(based on certain physical
properties) bottleneck
(unattended info is discarded)
higher level processing working
memory
c.
ATTENUATION MODEL
i. inputs (attended and unattended)
sensory store attenuating

filter bottleneck (both kept and

integrated) hierarchy of
analyzers working memory
d.
Properties of Attention
i. limited and specific (space or
feature)
e.
Kinds of attention
i. spatial vs. featural
ii. endogenous vs. exogenous
1.
endogenous goal directed
or top down
2.
exogenous something
grams attention, bottom up
iii. overt vs. covert
1.
overt paying attention to
where youre looking
2.
covert paying attention
w/o eye contact
f. behavioral effects of attention
i. better perceptual discrimination
ii. improved detection
iii. faster detection
iv. specific to feature/location being
attended
g.
Physiological effects of attention
i. fixation and attention = more
action potentials spatial

ii. activate specific areas if looking for

featural changes
h.
Control of attention
i. bottom up
1.
saliency
2.
unexpected
3.
potentially
harmful/threatening
ii. top down
1.
expectation based on past
experiences
i. neural networks
i. parietal lobe
1.
DISORDER: hemispatial
neglect
ii. BOTTOM UP
1.
V1V4Parietal
cortexhigher order structures
in prefrontal cortex (some info
back down to sensory areas)
iii. TOP DOWN
1.
PFCParietal cortexV4
and pulvinarV1
iv. DISORDER: Balint Syndrome
1.
damage to both parietal
cortices

2.
can only see one object at a
time (simultagnosia)
IV. Development of the Brain
a.
1. Neurulation
i. ectoderm neural plate neural
tube (CNS)
ii. when neural tube closes, neural
crest (PNS) is pinched off
iii. prosencephalon (diencephalon and
telencephalon), mesencephalon
(midbrain), rhombencephalon
(pons, medulla)
b.
2. Cell Proliferation
i. ventricular zone new neurons
formed
ii. marginal zone
iii. pial surface (facing the skull)
iv. radial glial cells produce neurons,
provide scaffolding
v. nucleus moves to pial surface,
replicates DNA, returns to
ventricular surface and divides
1.
symmetrical 2 new radial
glial cells, happens first
2.
asymmetrical 1 new radial
glial cell, 1 neural precursor

vi.
c.
i.

ii.

iii.
iv.
d.
i.

ii.

cell, happens second, decided

by transcription factors Notch-1
and Numb
DISORDER: microencephaly not
enough neurons
3. Cell Migration
Migrating neurons move up the
processes of the radial glial cells
into correct layers (there are 6
layers)
cortical plate becomes each
progressive layer migration
destination
subplate disappears after all layers
are established
reelin layers reversed
4. Neuronal Differentiation
semaphorin 3A differentiation
agent for pyramidal neurons
1.
attracts apical dendrite,
repels axon (polarity)
growth cones end of axon,
explores environment for facts that
attract or repel microtubules and
actin filaments

iii. chemoaffinity hypothesis

direction of growth shaped by
chemical cues
iv. axonal decussation at midline,
there is lots of slit; lots of netrin
receptors (attracted to slit)
expressed on growth cone; after
crossing midline, axon expresses
robo (repelled by slit)
v. topography gradients on the
surface of certain receptors
respond to gradient of factor
1.
EXAMPLE: retina to tectum
connections nasal side of
retina has less eph receptors
(repelled by ephrin), while
posterior side of tectum has a
lot of ephrin, and vice versa, so
connections are established
correctly
vi. axon guidance
1.
fasciculation one pioneer
axon finds target, subsequent
axons follow
2.
adhere to each other via
CAMs (cell adhesion molecules)

e.

5. Synapse formation
i. dendrite forms filopodium, sends it
towards axon target
ii. axon forms vesicles and
presynaptic active zone
iii. dendrite forms postsynaptic
receptor cluster
iv. many disorders of synapse function
exist
f. 6. Synaptic Pruning
i. selective cell death
ii. cells that fire together, wire
together; cells out of sync lose
their link Hebbian modification
g.
7. Apoptosis
i. lots of pathways with life and death
factors
h.
8. Myelination
i. happens after neurons have lost
their plasticity cements them in
place
ii. prefrontal cortex myelinated last,
doesnt end until mid to late 20s
V. Neurodegeneration
a.
Apoptosis vs. Necrosis

i. apoptosis is regulated and clean

prevents macrocephaly
ii. necrosis is messy and causes
neural degeneration
b.
Modes of Degeneration
i. Oxidative stress
1.
ROS=reactive oxygen
species
2.
AOX=antioxidants
3.
depleted AOX can lead to
cell damage/death
ii. DISORDER: Parkinsons Disease
1.
hypokinesia (lack of
movement), bradykinesia
(slowness of movement),
rigidity, tremor, postural
instability and gait, cognitive
symptoms
2.
affects the direct pathway
substantia nigra
3.
genetic and environmental
facs lead to oxidative stress
4.
treatment: L-DOPA, deep
brain stim, possibly stem cells
iii. DISORDER: Huntingtons Disease

1.
chorea (excess/uncontrolled
movements), motor
impersistence, cognitive
(working memory), psychiatric
(irritability, depression)
2.
indirect pathway striatum
degradation
3.
increased CAG repeats in
the Hungington gene lead to
mutated huntingin
4.
treatment: specific
symptom treatment, DOPA
suppressant, stem cells?
iv. DISORDERS: dementia and
Alzheimers
1.
progressive and disabling
memory loss and decline in
cognitive function
2.
Alzheimers is most
common form of dementia
3.
cause unknown most of the
time
4.
generalized neuron loss
larger sulci and ventricles
5.
hippocampus and temporal
lobe massively degenerate

6.
amyloid plaques buildup of
A peptides
7.
treatment: cholinesterase
inhibitors, NMDA inhibitors,
inhibition of cell death
mechanisms
VI. Neural Differences and Disorders
a.
neurodiversity vs. disability
b. Autism Case Study