The Journal of Neuroscience, November 15, 2001, 21(22):8990-9000
Combined Effects of Intrinsic Facilitation and Modulatory
Inhibition of Identified Interneurons in the Siphon Withdrawal
Circuitry of Aplysia
Adam S.
Bristol1,
Thomas M.
Fischer2, and
Thomas J.
Carew3
1 Department of Psychology, Yale University, New Haven,
Connecticut 06520-8205, 2 Department of Psychology, Wayne
State University, Detroit, Michigan 48202, and 3 Department
of Neurobiology and Behavior, University of California, Irvine, Irvine,
California 92697-4550
Synaptic plasticity can be induced through mechanisms intrinsic to
a synapse or through extrinsic modulatory mechanisms. In this study, we
investigated the relationship between these two forms of plasticity at
the excitatory synapse between L29 interneurons and siphon motor
neurons (MNs) in Aplysia. Using isolated ganglia, we
confirmed that the L29-MN synapses exhibit a form of intrinsic facilitation: post-tetanic potentiation (PTP). We also found that L29-MN synapses are modulated by exogenous application of 5-HT: they are depressed after 5-HT exposure. We next investigated the functional relationship between an intrinsic facilitatory process (PTP)
and extrinsic inhibitory modulation (5-HT-induced depression). First,
we found that application of 5-HT just before L29 activation results in
a reduction of PTP. Second, using semi-intact preparations, we found
that tail shock (TS) mimics the effect of 5-HT by both depressing L29
synaptic transmission and by reducing L29 PTP. Third, we observed a
significant correlation between L29 activity during TS and subsequent
synaptic change: low-responding L29s showed synaptic depression after
TS, whereas high-responding L29s showed synaptic facilitation. Finally,
we found that we could directly manipulate the sign and magnitude of
TS-induced synaptic plasticity by controlling L29 activity during TS.
Collectively, our results show that the L29-MN synapses exhibit
intrinsic facilitation and extrinsic modulation and that the sign and
magnitude of L29-MN plasticity induced by TS is governed by the
combined effects of these two processes. This circuit architecture,
which combines network inhibition with cell-specific facilitation, can
enhance the signal value of a specific stimulus within a neural network.
Key words:
information processing; neural network; posttetanic
potentiation; serotonin; synaptic plasticity; withdrawal reflex
Copyright © 2001 Society for Neuroscience 0270-6474/01/21228990-11$05.00/0
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