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The Journal of Neuroscience, December 1, 1999, 19(23):10595-10602
Cellular Analog of Differential Classical Conditioning in
Aplysia: Disruption by the NMDA Receptor Antagonist
DL-2-Amino-5-Phosphonovalerate
Geoffrey G.
Murphy1 and
David L.
Glanzman2
1 Interdepartmental Graduate Program in Neuroscience,
School of Medicine, and 2 Departments of Physiological
Science and Neurobiology and the Brain Research Institute, University
of California, Los Angeles, California 90095-1761
We previously showed that the associative enhancement of
Aplysia siphon sensorimotor synapses in a cellular analog of
classical conditioning is disrupted by infusing the
Ca2+ chelator
1,2-bis(2-aminophenoxy)ethane-N,N-N',N'-tetraacetic acid
into the postsynaptic motor neuron before training or by training in
the presence of the NMDA receptor antagonist
DL-2-amino-5-phosphonovalerate (APV). Our earlier
experiments with APV used a nondifferential training protocol, in which
different preparations were used for associative and nonassociative
training. In the present experiments we extended our investigation of
the role of NMDA receptor type potentiation in learning in
Aplysia to differential conditioning. A cellular analog of
differential conditioning was performed with a reduced preparation that
consisted of the CNS plus two pedal nerves. A siphon motor
neuron and two siphon sensory neurons, both of which were
presynaptically connected to the motor neuron, were impaled with sharp
microelectrodes. One sensorimotor synapse received paired stimulation
with a conditioned stimulus (brief activation of a single sensory
neuron) and an unconditioned stimulus (pedal nerve shock), whereas the
other sensorimotor synapse received unpaired stimulation. Training in
normal artificial seawater (ASW) resulted in significant differential
enhancement of synapses that received the paired stimulation. Training
in APV blocked this differential synaptic enhancement. A comparison of
the present data with the data from earlier experiments that used
nondifferential training is consistent with the possibility that
differential training comprises competition between the presynaptic
sensory neurons. Synaptic competition may contribute significantly to the associative effect of paired stimulation in the differential training paradigm.
Key words:
Aplysia californica; classical conditioning; learning and memory; long-term potentiation (LTP); NMDA; synaptic
plasticity; synaptic competition
Copyright © 1999 Society for Neuroscience 0270-6474/99/192310595-08$05.00/0
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