The Journal of Neuroscience, March 1, 2001, 21(5):1739-1749
Contirbution of Postsynaptic Ca2+ to the Induction of
Posttetanic Potentiation in the Neural Circuit for Siphon Withdrawal in
Aplysia
Joanna H.
Schaffhausen1,
Thomas M.
Fischer2, and
Thomas J.
Carew3
1 Department of Psychology, Yale University, New Haven,
Connecticut 06520, 2 Department of Psychology, Wayne State
University, Detroit, Michigan 48202-3900, and 3 Department
of Neurobiology and Behavior, University of California at Irvine,
Irvine, California 92697-4550
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.
Key words:
synaptic plasticity; Aplysia; postsynaptic Ca2+; posttetanic potentiation; sensory
neurons; short-term facilitation
Copyright © 2001 Society for Neuroscience 0270-6474/01/2151739-11$05.00/0
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