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" Mechanisms of Short-Term Synaptic Facilitation " To understand the complex dynamics exhibited by biological neural networks, it is important to understand the dynamics of synaptic interactions between neurons. Transmission of activity across a synapse is not a static process, but constantly varies in response to changes in the afferent activity. Long-term plasticity of synaptic strength is believed to underlie different forms of learning and memory. Much more prevalent are the transient, short-term plasticity (STP) effects, which play a role in regulating the neural dynamics on short time scales. In this talk we will explore the mechanisms of short-term facilitation (STF), a common form of STP. STF has been shown to depend on the accumulation of residual calcium (Ca) in the presynaptic terminal. However, it is known that the residual free Ca levels are tiny in comparison to the high Ca concentration near an open Ca channel, required for the release of neurotransmitter. Several explanations have been proposed to resolve this issue: (1) according to the "bound calcium hypothesis", STF is not caused by the rise in free residual Ca, but by the increase in the Ca-bound, activated state of the neurotransmitter release machinery; (2) it was also suggested that the Ca sensor responsible for STF is located further away from the Ca channel, where the residual free Ca is comparable to the peak Ca achieved during an action potential; (3) finally, it has been proposed that the peak Ca transients themselves may increase, due to the saturation of endogenous Ca buffers, even when the Ca influx remains constant from one stimulus to the next. Using computer simulations, we have examined these putative STF mechanisms, and in this talk we will describe the constraints that the observed properties of STF impose on these models. |