Is synaptic facilitation caused by presynaptic spike broadening?

Abstract

FACILITATION is a characteristic of many synapses whereby the efficacy of synaptic transmission increases following presynaptic activity. This form of neuronal plasticity has been implicated in behavioural modifications such as habituation¹ and learning². Facilitation has been shown to be due to a presynaptic increase in transmitter release³, but its biophysical mechanism remains obscure. Although it is often suggested that facilitation is due to the action of a residual increase in intracellular free calcium⁴, an alternative hypothesis, that facilitation may be caused by action potential prolongation, has recently been proposed^5–7. In molluscan neural somata, spike broadening occurs in a train of impulses, due to non-inactivating calcium channels and cumulatively inactivating potassium channels⁷. This might result in an increased calcium influx associated with prolonged spikes⁸, which would lead immediately to facilitated transmitter release⁹. We show here that at crustacean neuromuscular junctions, spike broadening is not primarily responsible for facilitation.