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Volume 17, Number 8,
Issue of April 15, 1997
pp. 2886-2899
Copyright ©1997 Society for Neuroscience
A Simplified Preparation for Relating Cellular Events to
Behavior: Mechanisms Contributing to Habituation, Dishabituation, and
Sensitization of the Aplysia Gill-Withdrawal Reflex
Received Sept. 20, 1996; revised Jan. 2, 1997; accepted Jan. 31, 1997.
Tracey E. Cohen1,
Saul W. Kaplan1,
Eric R. Kandel1, 2, 3, and
Robert D. Hawkins1, 2
1 Center for Neurobiology and Behavior,
College of Physicians and Surgeons of Columbia University,
2 New York State Psychiatric Institute, and
3 Howard Hughes Medical Institute, New York,
New York 10032
To relate cellular events to behavior in a more rigorous fashion,
we have developed a simplified preparation for studying the
gill-withdrawal reflex of Aplysia, in which it is
relatively easy to record the activity of individual neurons during
simple forms of learning. Approximately 84% of the reflex in this
preparation is mediated through the single motor neuron LDG1, so that
changes in the firing of LDG1 can account for most of the changes in
behavior. We have used this preparation to investigate cellular
mechanisms contributing to habituation, dishabituation, and
sensitization by recording evoked firing, the complex postsynaptic
potential (PSP), and the monosynaptic component of the complex PSP in
LDG1. Our results suggest that habituation is largely attributable to depression at sensory neuron synapses. By contrast, dishabituation and
sensitization involve several mechanisms at different loci, including
facilitation at sensory neuron synapses, enhancement in the periphery
(perhaps attributable to post-tetanic potentiation at the neuromuscular
junction), and both facilitation and inhibition of excitatory and
inhibitory interneurons. Moreover, these different mechanisms
contribute preferentially at different times after training, so that
information processing in the neuronal circuit for the reflex is
distributed not only in space but also in time. Nonetheless, our
results also suggest that the neuronal circuit is not a highly
distributed neural network. Rather, plasticity of the reflex can
evidently be accounted for by several specific mechanisms and loci of
plasticity in a defined neural circuit, including a limited number of
neurons, some of which make a large contribution to the behavior.
Key words:
Aplysia;
gill-withdrawal reflex;
motor neuron;
habituation;
dishabituation;
sensitization;
learning
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