Acute effects of nicotine amplify accumbal neural responses during nicotine-taking behavior and nicotine-paired environmental cues.

Karine Guillem, Laura L. Peoples
PLoS ONE. 2011-09-22; 6(9): e24049
DOI: 10.1371/journal.pone.0024049

PubMed
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1. PLoS One. 2011;6(9):e24049. doi: 10.1371/journal.pone.0024049. Epub 2011 Sep 22.

Acute effects of nicotine amplify accumbal neural responses during
nicotine-taking behavior and nicotine-paired environmental cues.

Guillem K(1), Peoples LL.

Author information:
(1)Université de Bordeaux, Institut des Maladies Neurodégénératives, Bordeaux,
France.

Nicotine self-administration (SA) is maintained by several variables, including
the reinforcing properties of nicotine-paired cues and the nicotine-induced
amplification of those cue properties. The nucleus accumbens (NAc) is implicated
in mediating the influence of these variables, though the underlying
neurophysiological mechanisms are not yet understood. In the present study,
Long-Evans rats were trained to self-administer nicotine. During SA sessions each
press of a lever was followed by an intravenous infusion of nicotine (30 µg/kg)
paired with a combined light-tone cue. Extracellular recordings of single-neuron
activity showed that 20% of neurons exhibited a phasic change in firing during
the nicotine-directed operant, the light-tone cue, or both. The phasic change in
firing for 98% of neurons was an increase. Sixty-two percent of NAc neurons
additionally or alternatively showed a sustained decrease in average firing
during the SA session relative to a presession baseline period. These session
decreases in firing were significantly less prevalent in a group of neurons that
were activated during either the operant or the cue than in a group of neurons
that were nonresponsive during those events (referred to as task-activated and
task-nonactivated neurons, respectively). Moreover, the session decrease in
firing was dose-dependent for only the task-nonactivated neurons. The data of the
present investigation provide supportive correlational evidence for two
hypotheses: (1) excitatory neurophysiological mechanisms mediate the NAc role in
cue-maintenance of nicotine SA, and (2) a differential nicotine-induced
inhibition of task-activated and task-nonactivated neurons mediates the NAc role
in nicotine-induced amplification of cue effects on nicotine SA.

DOI: 10.1371/journal.pone.0024049
PMCID: PMC3178519
PMID: 21961032 [Indexed for MEDLINE]


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