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

Joanna H. Schaffhausen, Thomas M. Fischer, Thomas Carew

Research output: Contribution to journalArticle

Abstract

Recent studies in Aplysia have revealed a novel postsynaptic Ca2+ component to posttetanic potentiation (PTP) at the siphon sensory to motor neuron (SN-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 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 Ca2+ for 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 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 Ca2+ sensitivity to PTP. Finally, the postsynaptic Ca2+ 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 Ca2+ contribution summates with the conventional presynaptic mechanisms to yield an enhanced form of PTP.

Original languageEnglish (US)
Pages (from-to)1739-1749
Number of pages11
JournalJournal of Neuroscience
Volume21
Issue number5
StatePublished - Mar 1 2001

Fingerprint

Aplysia
Synapses
Motor Neurons
Tail
Long-Term Synaptic Depression
Excitatory Postsynaptic Potentials
Interneurons
N-Methyl-D-Aspartate Receptors

Keywords

  • Aplysia
  • Postsynaptic Ca
  • Posttetanic potentiation
  • Sensory neurons
  • Short-term facilitation
  • Synaptic plasticity

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Contribution of postsynaptic Ca2+ to the induction of posttetanic potentiation in the neural circuit for siphon withdrawal in Aplysia. / Schaffhausen, Joanna H.; Fischer, Thomas M.; Carew, Thomas.

In: Journal of Neuroscience, Vol. 21, No. 5, 01.03.2001, p. 1739-1749.

Research output: Contribution to journalArticle

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