Implication of dopaminergic modulation in operant reward learning and the induction of compulsive-like feeding behavior in Aplysia.

A. Bedecarrats, C. Cornet, J. Simmers, R. Nargeot
Learning & Memory. 2013-05-16; 20(6): 318-327
DOI: 10.1101/lm.029140.112

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1. Learn Mem. 2013 May 16;20(6):318-27. doi: 10.1101/lm.029140.112.

Implication of dopaminergic modulation in operant reward learning and the
induction of compulsive-like feeding behavior in Aplysia.

Bédécarrats A(1), Cornet C, Simmers J, Nargeot R.

Author information:
(1)Institut de Neurosciences Cognitives et Intégratives d’Aquitaine-INCIA,
Université de Bordeaux, UMR 5287, F-33000 Bordeaux, France.

Feeding in Aplysia provides an amenable model system for analyzing the neuronal
substrates of motivated behavior and its adaptability by associative reward
learning and neuromodulation. Among such learning processes, appetitive operant
conditioning that leads to a compulsive-like expression of feeding actions is
known to be associated with changes in the membrane properties and electrical
coupling of essential action-initiating B63 neurons in the buccal central pattern
generator (CPG). Moreover, the food-reward signal for this learning is conveyed
in the esophageal nerve (En), an input nerve rich in dopamine-containing fibers.
Here, to investigate whether dopamine (DA) is involved in this learning-induced
plasticity, we used an in vitro analog of operant conditioning in which
electrical stimulation of En substituted the contingent reinforcement of biting
movements in vivo. Our data indicate that contingent En stimulation does, indeed,
replicate the operant learning-induced changes in CPG output and the underlying
membrane and synaptic properties of B63. Significantly, moreover, this network
and cellular plasticity was blocked when the input nerve was stimulated in the
presence of the DA receptor antagonist cis-flupenthixol. These results therefore
suggest that En-derived dopaminergic modulation of CPG circuitry contributes to
the operant reward-dependent emergence of a compulsive-like expression of
Aplysia’s feeding behavior.

DOI: 10.1101/lm.029140.112
PMID: 23685764 [Indexed for MEDLINE]

Auteurs Bordeaux Neurocampus