THE ROLE OF CALCIUM IN NERVE TRANSMISSION

SGD KUB 3

1. Nia Fransiska (1502005054)

2. Vivi Paula Putri (1502005056)
3. I Komang Bintang Satria Mahaputra (1502005072)
4. Made Nindya Prahasari Wismawan (1502005073)
5. I Putu Hendri Aryadi (1502005077)
6. Ida Ayu Dewi Dhyani (1502005081)
7. Made Karina Duta Dwijayanti (1502005082)
8. Astari Rahayu Dewi (1502005084)
9. Joshua Erza Ronaldo Bayak (1502005089)
10. Septendinova Julife F. Correia (1502005111)
11. Pavitra Loganathan (1502005192)
12. Theivya Subramanian (1502005193)

FACULTY OF MEDICINE
UDAYANA UNIVERSITY
2015
 CHAPTER I
INTRODUCTION

Information is coded in the brain as patterns of electrical impulse that are transmitted
along nerve procces. These impulse are passed from one neuron to the next primarily at the
chemical synapse where the electrical event is converted to the release of a neurotransmitter
substance that activates the next neurin in the pathway. Calcium, a positively charged
molecule, is useful many places within the human body. The role of calcium inside the
nervous system extends from the initiation of a nerve signal to the action taking place.
Calcium signals an impulse to a muscle cell and continues to be useful until the contraction is
complete. But there is only little information about the relationship between the quantity of
calcium and the amount of neurotransmitter that being released (Physol, 1970 : Sukardi,
1984).
Role of calcium in nerve transmission is begin in the impuls transfer in the synapse
(Delaney, 2009). Neurotransmitter formed in the pre-synaptic elemen or bouton synaptic.
Dale principle said that one neuron can only form one kind of neurotransmitter. The
forming of neurotransmitter can undergo one or three steps. Every steps in the forming of
neurotransmitter is using one kind of enzyme. After the neurotransmitter is made, it will be
collect in a synaptic vesicle. This synaptic vesicle will protect the neurotransmitter from the
enzyme around them. When an impulse arrive on the bouton synaptic, it will trigger the
synaptic vesicle to release the neurotransmitter into the synaptic cleft. The release of
neurotransmitter into the synaptic cleft is controlled by calcium ion. As the impulse pass
through bouton synaptic, the permeability between bouton synaptic and calcium ion. The
amount of calcium ion that pass through bouton synaptic will also increase the amount of
neurotransmitter that being released by the synaptic vesicle (Sukardi, 1984).
The neurotransmitter that have been released will travel the cleft between pre- and
post-synaptic and the neurotransmitter will make an interaction with special receptor that
exist in the receiver post-synaptic membrane. Interaction between neurotransmitter and the
receptor will cause some chain reaction. This interaction can cause post-synaptic to undergo
an excitation and inhibition. In other word, this reaction will cause a specific physiologic
reaction.
 CHAPTER II
CONTENT

1. Definition of Calcium, Nerve, and Nerve Impulse

Calcium
Calcium is a chemical element, atomic number 20, atomic weight 40.08.Calcium is the
most abundant mineral in the body. In combination with phosphorus it forms calcium
phosphate, the dense, hard material of the bones and teeth. It is an important cation in
intracellular and extracellular fluid and is essential to the normal clotting of blood, the
maintenance of a normal heartbeat, and the initiation of neuromuscular and metabolic
activities. Within the body fluids calcium exists in three forms. Protein-bound calcium
accounts for about 47 per cent of the calcium in plasma where most of it in this form is bound
to albumin. Another 47 percent of plasma calcium is ionized. About 6 per cent is complexed
with phosphate, citrate, and other anions. Ionized calcium is physiologically active. One of its
most important physiological functions is control of the permeability of cell membranes.
Parathyroid hormone, which causes transfer of exchangeable calcium from bone into the
blood stream, maintains calcium homeostasis by preventing either calcium deficit or excess.
Nerve
Nerve is a bundle of fibres that uses electrical and chemical signals to transmit
sensory and motor information from one body part to another. The fibrous portions of
a nerve are covered by a sheath called myelin and a membrane called neurilemma.
Nerve Impulse
A nerve impulse is an electrical signal that travels along an axon. There is an
electrical difference between the inside of the axon and its surroundings, like a tiny
battery. When the nerve is activated, there is a sudden change in the voltage across the
wall of the axon, caused by the movement of ions in and out of the neuron. This
triggers a wave of electrical activity that passes from the cell body along the length of
the axon to the synapse.

2. Overview of the function of the calcium in the nerve transmission

The simplest neural pathways have at least two neurons and one connection between
the neurons. Other neural pathways can involve thousands of neurons and their
connections as an impulse travels from the origin of the stimulus, through the sensory
neurons to the brain, and back through motor neurons to the muscles or glands. The
connection between two neurons, or a neuron and an effector, is called a synapse. A
neuromuscular junction is a synapse between a motor neuron and a muscle cell. An
impulse travels the length of the axon until it reaches the far end, called the synaptic
terminal. Most neurons are not directly connected, but have a gap between them
called the synaptic cleft. These neurons are not close enough for the impulse to jump
from one to the other (Coulborne et al., 2007).
At chemical synapses, this synaptic cleft separates the presynaptic axon terminal from
the postsynaptic cell. The presynaptic terminal is packed with vesicles containing
chemical neurotransmitters that are released into the synaptic cleft when an action
potential enters the terminal. Once released, the chemical neurotransmitter diffuses
across the synaptic cleft and binds to receptors on the postsynaptic cell. The binding
of the transmitter to its receptor leads to the opening (or closing) of specific ion
channels, which, in turn, alter the membrane potential of the postsynaptic cell. The
release of neurotransmitters from the presynaptic terminal begins with the invasion of
the action potential into the axon terminal. The depolarization of the terminal by the
action potential causes the activation of voltage-gated Ca2+ channels. The
electrochemical gradients for Ca2+ result in forces that drive Ca2+ into the terminal.
This increase in intracellular ionized calcium causes a fusion of vesicles, containing
neurotransmitters, with the presynaptic membrane at active zones. The
neurotransmitters are then released into the cleft by exocytosis. Increasing the amount
of Ca2+ that enters the terminal increases the amount of transmitter released into the
synaptic cleft. The number of transmitter molecules released by any one exocytosed
vesicle is called a quantum, and the total number of quanta released when the synapse
is activated is called the quantum content. Under normal conditions, quanta are fixed
in size but quantum content varies, particularly with the amount of Ca2+ that enters the
terminal. The way in which the entry of Ca2+ leads to the fusion of the vesicles with
the presynaptic membrane is still being elucidated. It is clear that there are several
proteins involved in this process. One hypothesis is that the vesicles are anchored to
cytoskeletal components in the terminal by synapsin, a protein surrounding the
vesicle. The entry of Ca2+ ions into the terminal is thought to result in phosphorylation
of this protein and a decrease in its binding to the cytoskeleton, releasing the vesicles
so they may move to the synaptic release sites. Other proteins (rab GTP-binding
proteins) are involved in targeting synaptic vesicles to specific docking sites in the
presynaptic terminal. Still other proteins cause the vesicles to dock and bind to the
 presynaptic terminal membrane; these proteins are called SNARES and are found on
both the vesicle and the nerve terminal membrane (called v-SNARES or t- SNARES,
respectively). Tetanus toxin and botulinum toxin exert their devastating effects on the
nervous system by disrupting the function of SNARES, preventing synaptic
transmission. Exposure to these toxins can be fatal because the failure of
neurotransmission between neurons and the muscles involved in breathing results in
respiratory failure. To complete the process begun by Ca2+ entry into the nerve
terminal, the docked and bound vesicles must fuse with the membrane and create a
pore through which the transmitter may be released into the synaptic cleft. The vesicle
membrane is then removed from the terminal membrane and recycled within the
nerve terminal (Rhoades et al., 2009).

Picture 1. The release of

neurotransmitter (Rhoades et al., 2009)

3. Diseases in the nerve transmission

 Huntington’s chorea
Huntington’s chorea is a hereditary disease which first comes as painful then
flicking of joins of the extremities. It even continues to distortions by
dementia and motor dysfunction, and cases are often found on people on their
thirties or forties, which is caused by loss of the cells producing γ-
aminobutyric acid (GABA), the most common inhibitory neurotransmitter of
CNS. The dementia shows up due to loss of cells secreting acetylcholine.
 Alzheimer disease
Alzheimer is the disease that dominates the dementia and is characterized by a
gradual memory loss premortemly. Glutamate is known as multifunctional
neurotransmitter in the central nerve system which includes learning and
memory. One of the family of glutamate is calcium permeable. Elevated Ca2+
levels lead to death of neuron which can ends in neuronal loss through
apoptosis or necrosis. This disturbance of formation of Ca2+ leads to
Alzheimer disease.
 Parkinson disease
Parkinson disease affects both central and peripheral nervous systems, in
which causes a motor error on Parkinson disease patients. Pathology of
Parkinson disease is not just as simple as neuronal loss and are caused by
some factors, including low intrinsic calcium buffering capacity and poorly
myelinated, highly-branched axons.
 CHAPTER III
CONCLUSION

Role of calcium in nerve transmission is begin in the impuls transfer in the synapse.
Neurotransmitter formed in the pre-synaptic elemen. The depolarization of the terminal by
the action potential causes the activation of voltage-gated Ca2+ channels. The electrochemical
gradients for Ca2+ result in forces that drive Ca2+ into the terminal. This increase in
intracellular ionized calcium causes a fusion of vesicles, containing neurotransmitters, with
the presynaptic membrane at active zones. The neurotransmitters are then released into the
cleft by exocytosis. Increasing the amount of Ca2+ that enters the terminal increases the
amount of transmitter released into the synaptic cleft. The neurotransmitter that have been
released will travel the cleft between pre and post-synaptic and the neurotransmitter will
make an interaction with special receptor that exist in the receiver post-synaptic membrane.
Interaction between neurotransmitter and the receptor will cause some chain reaction. This
interaction can cause a specific physiologic reaction. Therefore, in short, influx of calcium
ions through selective voltage-sensitive ion channels (calcium channels) plays a key role to
link the action potential to the triggering of secretory vesicle discharge.
There are some diseases that could happen in the nerve transmission such as Huntingon’s
chorea which shows up due to loss of cell secreting acetylcholine, Alzheimer which
characterized by a gradual memory loss premortemly, and Parkinson which affects both
central and peripheral nervous systems which causes a motor error.
 REFERENCES

Colbourne H, Constantin B, Dobell D. 2007. Inquiry of Biology. 2nd ed. Canada: McGraw-
Hill, p.378.
Gartner LP, Hiatt JL. 2011. Concise Histology. 1st ed. Philadelphia: Saunders, p.121.
Giacomello M, Oliveros JC, Naranjo JR, Carafoli E. 2013. Neuronal Ca2+ dyshomeostatis in
Huntington disease. Prion 7(1):76-84.
Revett TJ, Baker GB, Jhamandas J, Kar S. 2013. Glutamate system, amyloid β peptides and
tau protein: functional interrelationships and relevance to Alzheimer disease pathology. J
Psychiatry Neurosci 38 (1): 6-18.
Rhoades RA, Bell DR. 2009. Medical Physiology: Principle for Clinical Medicine. 3rd ed.
China: Wolters Kluwer, p.47.
Surmeier DJ, Sulzer D. 2013. The pathology roadmap in Parkinson disease. Prion 7(1): 85-
91.