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.
Department of Psychology, Yale University, New Haven, Connecticut 06520, USA.
J H
JH
Schaffhausen
T M
TM
Fischer
T J
TJ
Carew
D015763:2-Amino-5-phosphonovalerate / Q000008:administration & dosage; D000818:Animals; D001048:Aplysia; D002118:Calcium / Q000378:metabolism*; D002614:Chelating Agents / Q000008:administration & dosage; D004305:Dose-Response Relationship, Drug; D004533:Egtazic Acid / Q000008:administration & dosage / Q000031:analogs & derivatives; D018691:Excitatory Amino Acid Antagonists / Q000008:administration & dosage; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D017774:Long-Term Potentiation / Q000187:drug effects / Q000502:physiology*; D008845:Microinjections; D009415:Nerve Net / Q000187:drug effects / Q000378:metabolism*; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D009475:Neurons, Afferent / Q000187:drug effects / Q000502:physiology; D010477:Perfusion; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors; D013569:Synapses / Q000187:drug effects / Q000378:metabolism*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology
D002614:Chelating Agents; D018691:Excitatory Amino Acid Antagonists; D016194:Receptors, N-Methyl-D-Aspartate; D004533:Egtazic Acid; D015763:2-Amino-5-phosphonovalerate; C025603:1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid; D002118:Calcium