E4 Chemical synaptic transmission

Topic

Chemical synapses convert the presynaptic action potential—already described in the action potential model—into an input for the postsynaptic neuron through three successive steps: calcium-dependent neurotransmitter release, diffusion of the neurotransmitter across the synaptic cleft, and activation of postsynaptic receptors by the neurotransmitter.

Within the chemical synapse, calcium influx into the presynaptic terminal controls—in a highly cooperative manner—both the probability of neurotransmitter release and the number of vesicles actually released; the greater the calcium influx, the higher the release probability and the greater the number of vesicles released. Crucially, this relationship is not merely proportional but far more pronounced than a simple proportional increase in calcium would predict, precisely because the process is highly cooperative.

The released neurotransmitter binds reversibly to the chemical synapse's postsynaptic receptors, alternating between bound and unbound states according to two-state kinetics. In the case of ionotropic receptors specifically, this binding opens a channel; the resulting conductance rises rapidly upon opening and subsequently decays more slowly, generating a postsynaptic current that depolarizes or hyperpolarizes the postsynaptic neuronal membrane, depending on the channel's reversal potential.

In the short term, the efficacy of a chemical synapse can be facilitated or depressed based on its recent history of presynaptic activity: the level of recent presynaptic activity determines whether synaptic efficacy increases or decreases—depending on the balance between facilitation and depression—a phenomenon captured by synaptic resource models of the type proposed by Tsodyks and Markram. This model of the chemical synapse reuses the same variables already defined for the resting neuronal membrane and for impulse propagation along the axon: observed membrane potential, membrane capacitance, the conductance of each ion channel, the Nernst potential of each ion, and membrane resistance. Ultimately, it is this chemical synapse—spanning the process from calcium entry at the presynaptic terminal to the postsynaptic current resulting from the opening of ionotropic receptors—that converts the presynaptic action potential into a signal capable of depolarizing or hyperpolarizing the postsynaptic neuron, with an efficacy that can also change in the short term based on recent presynaptic activity.

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