Abstract
Some synapses show two forms of short-term plasticity, homosynaptic facilitation, and a plasticity in which the efficacy of transmission is modified by subthreshold changes in the holding potential of the presynaptic neuron. In a previous study we demonstrated a further interactive effect. We showed that depolarizing changes in the presynaptic holding potential can increase the rate at which facilitation occurs. These experiments studied synaptic transmission between an Aplysia sensory neuron (B21) and its postsynaptic follower, the motor neuron (B8). We have also shown that subthreshold depolarizations of B21 produce widespread increases in its [Ca(2+)](i) via activation of a nifedipine-sensitive current. To determine whether it is this change in 'background' calcium that modifies synaptic transmission we compared the facilitation observed at the B21-B8 synapse under control conditions to the facilitation observed in nifedipine. Nifedipine had a depressing effect. Other investigators studying facilitation have focused on Ca(res) (i.e., the calcium that remains in a neuron after spiking). Our results indicate that facilitation can also be impacted by calcium channels opened before spiking begins.