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Synaptic Plasticity

Historically, it was generally thought that the role of the synapse was to simply transfer information between one neuron and another neuron or between a neuron and a muscle cell. In addition, it was thought that these connections, once established during development, were relatively fixed in their strength, much like a solder joint between two electronic components. One exciting development in neurobiology over the past twenty years is the realization that most synapses are extremely plastic; they are able to change their strength as a result of either their own activity or through activity in another pathway. Many think that this synaptic plasticity is central to understanding the mechanisms of learning and memory.

There are two general forms of synaptic plasticity, intrinsic and extrinsic. Intrinsic mechanisms, also known as homosynaptic mechanisms, refer to changes in the strength of a synapse that are brought about by its own activity. (Homo from the Greek meaning the same.) Extrinsic plasticity, or heterosynaptic plasticity, is a change in the strength of a synapse brought about by activity in another pathway.

Homosynaptic Plasticity. There are two types of intrinsic or homosynaptic plasticity, synaptic depression and synaptic facilitation. Synaptic depression and facilitation are not always found at the same synapse. Some synapses exhibit one but not the other, whereas some synapses exhibit both. Figure 7.1B illustrates homosynaptic plasticity at the synapse between a 1A afferent fiber and a spinal motor neuron. An action potential in the sensory neuron produces an EPSP in the motor neuron. A second action potential in the sensory neuron, 200 msec after the first, produces an EPSP that is smaller than that produced by the first action potential. This phenomenon is called synaptic depression. The efficacy of synaptic transmission is not constant; it varies depending upon the frequency of stimulation. The mechanisms of synaptic depression vary but one common mechanism is depletion of the available transmitter. The second of two action potentials will release less transmitter because less transmitter is available to be released. (See Figure 7.2A)

The figure at left illustrates the second form of homosynaptic plasticity, synaptic facilitation. This particular example is known as paired-pulse or twin-pulse facilitation. Two action potentials in the presynaptic cell produce two EPSPs in the postsynaptic cell. The first action potential produces a 1 mV EPSP, but the second action potential, which occurs about 20 msec after the first, produces an EPSP that is larger than the EPSP produced by the first. In this example, it is twice as large as the first one. This doubling of the EPSP represents the synaptic facilitation. The net EPSP is 3 mV. Through the process of temporal summation the second EPSP (2 mV) adds to the amplitude of the first EPSP (1 mV).

One mechanism contributing to twin pulse facilitation is residual calcium. An action potential leads to the opening of Ca²⁺ channels and the influx of Ca²⁺, which leads to the release of transmitter. Now consider the fate of the calcium after the first action potential (Figure 7.2B). Ca²⁺ levels will decline back to their initial level, but this recovery will not occur instantaneously. Thus, if a second action potential is initiated at a time during which the calcium has not yet recovered to its basal level, the calcium influx associated with the second spike will add to the "residual calcium" that is left over from the first. The net effect is that the total concentration of calcium will be greater after the second spike than it was after the first, and more transmitter will be released.

Another intrinsic type of synaptic plasticity is called post-tetanic potentiation (PTP). It is an extreme example of facilitation defined as a relatively persistent (minutes) enhancement of synaptic strength following a brief train of spikes (a tetanus).