Contirbution of postsynaptic Ca2+ to the induction of posttetanic potentiation in the neural circuit for siphon withdrawal in Aplysia

Recent studies in Aplysia have revealed a novel postsynaptic Ca2+ component to posttetanic potentiation (PTP) at the siphon sensory to motor neuron (S N-MN) synapse. Here we asked whether the postsynaptic Ca2+ component of PTP was a special feature of the SN-MN synapse, and if so, whether it reflecte d a unique property of the SN or the MN. We examined whether postsynaptic i njection of BAPTA reduced PTP at SN synapses onto different postsynaptic ta rgets 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 sy napse, indicating that the SN and the MN do not require postsynaptic Ca2+ f or PTP with all other synaptic partners. The postsynaptic Ca2+ component of PTP is present at other Aplysia SN-MN synapses; tail SN-MN synapses also s howed reduced PTP when the MN was injected with BAPTA. Surprisingly, in bot h 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 t he initially weak SN-MN synapses showed a BAPTA-sensitive component. Homosy naptic depression of initially strong SN-MN synapses into the size range of initially weak synapses did not confer postsynaptic Ca2+ sensitivity to PT P. Finally, the postsynaptic Ca2+ component of PTP could be induced in the presence of APV, indicating that it is not mediated by NMDA receptors. Thes e results suggest a dual model for PTP at the SN-MN synapse, in which a pos tsynaptic Ca2+ contribution summates with the conventional presynaptic mech anisms to yield an enhanced form of PTP.