Neuron 2

B1 Fast EPSP


Neuron 1

B2 Slow EPSP


Neuron 2

FIGURE 24 Fast and slow synaptic potentials. (A) Two neurons (1 and 2) make synaptic connections with a common postsynaptic follower cell (Post). (B1) An action potential in neuron 1 leads to a conventional fast EPSP with a duration of about 30 msec. (B2) An action potential in neuron 2 also produces an EPSP in the postsynaptic cell, but the duration of this slow EPSP is more than three orders of magnitude greater than that of the EPSP produced by neuron 1. Note the change in calibration bar.

potentials are not observed at every postsynaptic neuron, but Fig. 24A illustrates an idealized case in which a postsynaptic neuron receives two inputs, one that produces a conventional fast EPSP and the other that produces a slow EPSP. An action potential in neuron 1 leads to an EPSP in the postsynaptic cell whose duration is approximately 30 msec (Fig. 24B1). This is the type of potential that might be produced in a spinal motor neuron by an action potential in an afferent fiber. Neuron 2 also produces a postsynaptic potential (Fig. 24B2), but its duration (note the calibration bar) is more than three orders of magnitude longer than that of the EPSP produced by neuron 1.

How can a change in the postsynaptic potential of a neuron persist for many minutes as a result of a single action potential in the presynaptic neuron? Possible answers to this question include a prolonged presence of the transmitter due to continuous release, slow degradation, or slow re-uptake of the transmitter; but the mechanism here involves a transmitter-induced change in metabolism of the postsynaptic cell. Figure 25 compares the general mechanisms for fast and slow synaptic potentials. Fast synaptic potentials are produced when a transmitter substance binds to a channel and produces a conformational change in the channel, causing it to become permeable to one or more ions (both Na+ and K+ in Fig. 25A). The increase in permeability leads to a depolarization associated with the EPSP (Fig. 25A3). The duration of the synaptic event is critically dependent on the amount of time the transmitter substance remains bound to the receptors. The transmitters that have already been mentioned (ACh, glutamate, and glycine) remain bound for only a very short period of time. These transmitters are either removed by diffusion, enzymatic breakdown, or re-uptake into the presynaptic cell; therefore, the channel closes rapidly.

One mechanism for a slow synaptic potential is shown in Fig. 25B. In contrast to the fast PSP for which the receptors are actually part of the ion-channel complex, the channels that produce the slow synaptic potentials are not directly coupled to the transmitter receptors. Rather, the receptors are physically separated and exert their actions indirectly through changes in the metabolism of specific second messenger systems. Figure 25B illustrates one type of response that involves the cyclic adenosine monophosphate (cAMP)-protein kinase A system, but other slow PSPs use other second messenger-kinase systems (e.g., the protein kinase C system). In the case of cAMP-dependent slow synaptic responses, transmitter binding to membrane receptors activates G proteins and stimulates an increase in the synthesis of cAMP. Cyclic AMP then leads to the activation of

20 msec

20 sec lonotropic

A1 Closed Na+

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