In a type of short-term plasticity that is observed in a number of systems, synaptic transmission is potentiated by depolarizing changes in the membrane potential of the presynaptic neuron prior to spike initiation. This digital-analog form of plasticity is graded. The more depolarized the neuron, the greater the increase in the efficacy of synaptic transmission. In a number of systems, including the system under investigation here, this type of modulation is calcium dependent, and its graded nature is presumably a consequence of a direct relationship between the [Ca+2]i and the effect on synaptic transmission. It is therefore of interest to identify factors that determine the magnitude of this type of calcium signal. Here we study a synapse in Aplysia and demonstrate that there can be a contribution from currents activated during spiking. When neurons spike there are localized increases in the [Ca+2]i that directly trigger neurotransmitter release. Additionally, spiking can lead to global increases in [Ca+2]i that are reminiscent of those induced by subthreshold depolarization. We demonstrate that these spike induced increases in [Ca+2]i result from the activation of a current not activated by subthreshold depolarization. Importantly, they decay with a relatively slow time constant. Consequently, with repeated spiking, even at a low frequency, they readily summate to become larger than increases in [Ca+2]i induced by subthreshold depolarization alone. When this occurs, global increases in [Ca+2]i induced by spiking play the predominant role in determining the efficacy of synaptic transmission.
- transmitter release
- synaptic plasticity
- Copyright © 2017, Journal of Neurophysiology