Voluntary Nicotine Consumption Triggers In Vivo Potentiation of Cortical Excitatory Drives to Midbrain Dopaminergic Neurons

• Published in: The Journal of neuroscience 2009-08, Vol.29 (33), p.10410-10415
• Main Authors: Caille, Stephanie, Guillem, Karine, Cador, Martine, Manzoni, Olivier, Georges, Francois
• Format: Article
• Language: English
• Subjects: Animals; Brief Communications; Cerebral Cortex - drug effects; Cerebral Cortex - physiology; Excitatory Postsynaptic Potentials - drug effects; Excitatory Postsynaptic Potentials - physiology; Life Sciences; Male; Mesencephalon - drug effects; Mesencephalon - physiology; Neural Pathways - drug effects; Neural Pathways - physiology; Neurons - drug effects; Neurons - physiology; Neurons and Cognition; Nicotine - administration & dosage; Psychology and behavior; Rats; Rats, Sprague-Dawley; Self Administration
• ISSN: 0270-6474; 1529-2401
• DOI: 10.1523/JNEUROSCI.2950-09.2009

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.