The synaptic connections between neurons and between neurons and muscles permit the high-speed transmission of information in an animal's body. Truly fast interneuronal communication is accomplished by electrical synapses. Here the action currents associated with action potentials pass conductively from the pre- to postsynaptic neuron membranes, depolarizing the postsynaptic neuron Vm toward its firing threshold. There are few factors that can alter the electrical synapse coupling.
Chemical synapses, on the other hand, offer a variety of interesting plastic behaviors. All chemical synapses release neurotransmitter molecules when stimulated by the arrival of a presynaptic action potentials. As has been seen, the neu-rotransmitter quickly diffuses across the synaptic cleft to receptor molecules on proteins protruding through the postsynaptic membrane. There they combine with receptor sites and initiate, depending on the transmitter/receptor variety, transient conductance increases for specific ions. Once in the cleft, the neurotransmitter is quickly destroyed (in milliseconds) by enzymatic hydrolysis or some other process so that each arriving spike will produce a new result. If the transmitter is not destroyed, the postsynaptic conductance increases will not die out, and the nervous system ceases to function normally. A class of poisons known as cholinesterase inhibitors have this effect on the common neurotransmitter, ACh.
Depending on the ions, the voltage across the ssm can depolarize, producing an epsp, or hyperpolarize, giving an ipsp. In some cases, an inhibitory synapse can cause a general conductance increase in the SSM receptors that effectively clamps the subsynaptic Vm to a level below the firing threshold, effectively inhibiting the postsynaptic neuron from firing. If the clamping potential equals the resting potential, one does not see a postsynaptic potential.
A question often asked is why does a presynaptic neuron need so many synapses to drive the dendrites of the postsynaptic neuron. There are several answers to this question. One is redundancy; if synapses are damaged by disease or injury, there is ample backup. Another is to reduce the effect of synaptic noise by spatiotemporal averaging over the dendritic field. (Synaptic noise arises from the random release of neurotransmitter from vesicles.) Still another is to provide a large area of dendritic membrane where interaction with other excitatory and inhibitory synapses can take place. Since synapses release their transmitter in an all-or-none manner at the arrival of a presynaptic spike, some factor that deletes synapses could serve to weaken the functional coupling between two neurons. A factor that stimulates the regrowth of synapses thus could strengthen interneuronal coupling. Such modulation of the strength of coupling could be associated with reflex conditioning, or "learning."
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