Voluntary nicotine consumption triggers in vivo potentiation of cortical excitatory drives to midbrain dopaminergic neurons.
Journal of Neuroscience. 2009-08-19; 29(33): 10410-10415
DOI: 10.1523/jneurosci.2950-09.2009
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1. J Neurosci. 2009 Aug 19;29(33):10410-5. doi: 10.1523/JNEUROSCI.2950-09.2009.
Voluntary nicotine consumption triggers in vivo potentiation of cortical
excitatory drives to midbrain dopaminergic neurons.
Caillé S(1), Guillem K, Cador M, Manzoni O, Georges F.
Author information:
(1)Inserm U862, Neurocentre Magendie, Pathophysiology of Synaptic Plasticity
Group, University of Bordeaux, and Centre National de la Recherche Scientifique
(CNRS) UMR 5227, Neuropsychopharmacology of Addiction Group, University of
Bordeaux, Bordeaux, France.
Active response to either natural or pharmacological reward causes synaptic
modifications to excitatory synapses on dopamine (DA) neurons of the ventral
tegmental area (VTA). Here, we examine these modifications using nicotine, the
main addictive component of tobacco, which is a potent regulator of VTA DA
neurons. Using an in vivo electrophysiological technique, we investigated the
role of key components of the limbic circuit, the infralimbic cortex (ILCx) and
the bed nucleus of the stria terminalis (BNST), in operant behaviors related to
nicotine reward. Our results indicated that nicotine self-administration in rats,
but not passive delivery, triggers hyperactivity of VTA DA neurons. The data
suggest that potentiation of the ILCx-BNST excitatory pathway is involved in
these modifications in VTA DA neurons. Thus, recruitment of these specific
excitatory inputs to VTA DA neurons may be a neural correlate for the learned
association between active responding and the reward experience.
DOI: 10.1523/JNEUROSCI.2950-09.2009
PMID: 19692616 [Indexed for MEDLINE]