Chemical Synapses and Effects of the Neurotransmitter - Essay Example

The process that must occur in the presynaptic axon is a series of events that lead to the release of a neurotransmitter. An action potential in the presynaptic cell causes Ca2+ channels to open. An influx of Ca2+ into the presynaptic terminal causes the neurotransmitter, which is stored in synaptic vesicles, to be released by exocytosis. The neurotransmitter diffuses across the synaptic cleft, binds to receptors on the postsynaptic membrane, and produces a change in membrane potential on the postsynaptic cell. The change in membrane potential on the postsynaptic cell membrane can be either excitatory or inhibitory, depending on the nature of the neurotransmitter released from the presynaptic nerve terminal. If the neurotransmitter is excitatory, it causes depolarization of the postsynaptic cell; if the neurotransmitter is inhibitory, it causes hyperpolarization of the postsynaptic cell.

Local currents depolarize each adjacent region to the threshold. Finally, the presynaptic terminal is depolarized, and this depolarization causes voltage-gated Ca2+ channels in the presynaptic membrane to open. When these Ca2+ channels open, the Ca2+ permeability of the presynaptic terminal increases, and Ca2+ flows into the terminal down its electrochemical gradient. Ca2+ uptake into the terminal causes the release of the neurotransmitter acetylcholine (ACh), which has been previously synthesized and stored in synaptic vesicles. To release ACh, the synaptic vesicles fuse with the plasma membrane and empty their contents into the synaptic cleft by exocytosis. ACh is formed from acetyl coenzyme A (Acetyl CoA) and choline by the action of the enzyme choline acetyltransferase. ACh is stored in vesicles with ATP and proteoglycans for subsequent release. Upon stimulation, the entire content of a synaptic vesicle is released into the synaptic cleft. The smallest possible amount of ACh that can be released is the content of one synaptic vesicle.

Following this ACh diffuses across the synaptic cleft to the postsynaptic membrane. These membranes usually contain receptors for ACh. For ACh, these receptors are nicotinic. ACh binds to the α subunits of the nicotinic receptor and causes a conformational change. It is important to note that the nicotinic receptor for ACh is an example of a ligand-gated ion channel: It also is a Na+ and K+ channel. When the conformational change occurs, the central core of the channel opens, and the permeability of the postsynaptic neuronal membrane to both Na+ and K+ increases.

When these channels open, both Na+ and K+ flow down their respective electrochemical gradients, each attempting to drive the membrane to its equilibrium potential. As a result, the neural membrane is depolarized to a value about halfway between the equilibrium potentials for Na+ and K+, or approximately 0 mV. The content of each synaptic vesicle produces a miniature change in the membrane potential. A collection of these quanta will depolarize the membrane from its resting potential of -90 mV to the threshold potential of -50 mV. This will generate the action potential and it will be fired. These action potentials are propagated down the muscle fiber by a continuation of this process (Hille B., 2001). Read More