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Many synapses exhibit temporally complex forms of activity-dependent short-term synaptic plasticity. The diversity of these phenomena reflects the evolutionary specialization of synapses within networks. We examined the properties of transmission and plasticity, in vivo, at an identified, specialized axo-axonic nicotinic synapse between the goldfish Mauthner cell and one of its targets, the cranial relay neuron (CRN), using intracellular paired recordings and low frequency (0.33-2 Hz) train stimulations. Depression of successive excitatory postsynaptic potentials (EPSPs), which dominates short-term plasticity, had two components. A fast component reduced the amplitude of EPSP(2), to less than 50% of EPSP(1). A slow component produced an additional 10-30% of amplitude reduction and developed with a time constant of tens of seconds. The latencies of the later depressed responses were ∼0.1 ms longer than that of EPSP(1), suggesting a reduced release probability. The Ca(2+) chelators EGTA and BAPTA, injected presynaptically, reduced all EPSPs and slowed development of the second component of depression. Interestingly, spike broadening, produced by injecting K(+) channel blockers, reduced release, but accelerated the kinetics of the slow component. Finally, Ba(2+) in the external medium enhanced release, and reduced the first component and slowed the development of the second component of depression. Taken together, these last two results, which are in contrast to observations at other synapses, and the two-component depression suggest atypical release properties at the output synapses of the Mauthner cell, which triggers an escape behavior. We suggest that the second component of depression provides an additional safety factor to prevent repetitive firing of the CRN.

Atypical properties of release and short-term depression at a specialized nicotinic synapse in the Mauthner cell network