Journal of Neuroscience, Vol 14, 2444-2454, Copyright © 1994 by Society for Neuroscience
Distributed input to the tail-siphon withdrawal circuit in Aplysia from neurons in the J cluster of the cerebral ganglion
JL Raymond and JH Byrne
Department of Neurobiology and Anatomy, University of Texas Medical School, Houston 77225.
Plasticity in the circuits for the withdrawal reflexes has been correlated
with several simple forms of nonassociative and associative learning in
Aplysia, and biochemical, biophysical, and molecular mechanisms of
plasticity in these circuits have been described. In order to examine
network features of this plasticity, we identified and characterized a
component of the modulatory circuitry for the tail- siphon withdrawal
circuit. Activation of mechanoafferent neurons in the J cluster of the
cerebral ganglion produced strong and distributed input to the tail-siphon
withdrawal circuit. Stimulation of the J cells led to excitatory and
inhibitory effects in the sensory neurons in the pleural ganglion, the tail
motor neurons in the pedal ganglion, and several classes of interneurons in
the pleural ganglion, including the multifunctional neuron LPI17.
Activation of the J cells produced both fast and slow post-synaptic
potentials in neurons of the tail-siphon withdrawal circuit. Of particular
interest was the ability of the J cells to produce slow EPSPs in the
pleural sensory neurons. These slow EPSPs were associated with an increase
in the excitability of the sensory neurons, but no effect of the J cells on
spike duration in the sensory neurons was observed. The J cells appear to
mediate both sensory and modulatory inputs to the circuit for tail
withdrawal.