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The Cellular Basis of Cs-Us Pairing Efficacy for Classical Conditioning of Aplysia's Withdrawal Reflex: Potential Contribution of a Hebbian Mechanism

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For more content, see Archives Néerlandaises de Zoologie (Vol 1-17) and Animal Biology (Vol 53 and onwards).

The marine snail Aplysia californica exhibits a simple form of associative learning-classical conditioning of its defensive withdrawal reflex. Previous cellular analyses of this form of learning have suggested that it is due to a presynaptic neuronal mechanism-activity-dependent presynaptic facilitation of the monosynaptic connections between the sensory and motor neurons which mediate the reflex. Classical conditioning of Aplysia's withdrawal reflex shares with many vertebrate conditioning preparations the property of temporal contiguity: conditioning is best when the conditioned stimulus (CS) precedes the unconditioned stimulus (US) by a small temporal interval. The temporal contiguity of conditioning in Aplysia has been accounted for by a molecular model. Specifically, it has been proposed that Aplysia sensory neurons possess an adenylyl cyclase that is dually regulated by Ca2+ which is elevated in the sensory neuron by the occurrence of the CS-and the facilitatory transmitter serotonin (5-HT)-whose release is stimulated by the occurrence of the US. It has been further suggested that the activation of the adenylyl cyclase exhibits a temporal requirement: the elevation of Ca2+ within the sensory neuron must precede the 5-HT stimulation for optimal activation of the cyclase. Recent data from our laboratory suggest that a postsynaptic mechanism-Hebbian potentiation of sensorimotor synapses-may mediate classical conditioning of Aplysia's withdrawal reflex. Here we summarize these data and suggest how Hebbian potentiation of sensorimotor synapses may play a role in the temporal contiguity of conditioning in Aplysia.

Affiliations: 1: Department of Physiological Science, University of California, Los Angeles, California 90024, U.S.A, Brain Research Institute, University of California, Los Angeles, California 90024, U.S.A.; 2: Department of Physiological Science, University of California, Los Angeles, California 90024, U.S.A

10.1163/156854293X00377
/content/journals/10.1163/156854293x00377
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/content/journals/10.1163/156854293x00377
1993-01-01
2016-12-09

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