Contribution of postsynaptic Ca2+ to the induction of post-tetanic potentiation in the neural circuit for siphon withdrawal in Aplysia.

Recent studies in Aplysia have revealed a novel postsynaptic Ca(2+) component to posttetanic potentiation (PTP) at the siphon sensory to motor neuron (SN-MN) synapse. Here we asked whether the postsynaptic Ca(2+) component of PTP was a special feature of the SN-MN synapse, and if so, whether it reflected a unique property of the SN or the MN. We examined whether postsynaptic injection of BAPTA reduced PTP at SN synapses onto different postsynaptic targets by comparing PTP at SN-MN and SN-interneuron (L29) synapses. We also examined PTP at L29-MN synapses. Postsynaptic BAPTA reduced PTP only at the SN-MN synapse; it did not affect PTP at either the SN-L29 or the L29-MN synapse, indicating that the SN and the MN do not require postsynaptic Ca(2+) for PTP with all other synaptic partners. The postsynaptic Ca(2+) component of PTP is present at other Aplysia SN-MN synapses; tail SN-MN synapses also showed reduced PTP when the MN was injected with BAPTA. Surprisingly, in both tail and siphon SN-MN synapses, there was an inverse relationship between the initial size of the EPSP and the postsynaptic component to PTP; only the initially weak SN-MN synapses showed a BAPTA-sensitive component. Homosynaptic depression of initially strong SN-MN synapses into the size range of initially weak synapses did not confer postsynaptic Ca(2+) sensitivity to PTP. Finally, the postsynaptic Ca(2+) component of PTP could be induced in the presence of APV, indicating that it is not mediated by NMDA receptors. These results suggest a dual model for PTP at the SN-MN synapse, in which a postsynaptic Ca(2+) contribution summates with the conventional presynaptic mechanisms to yield an enhanced form of PTP.