作者: Beatriz Antolin-Fontes , Jessica L. Ables , Andreas Görlich , Inés Ibañez-Tallon
DOI: 10.1016/J.NEUROPHARM.2014.11.019
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摘要: Abstract Progress has been made over the last decade in our understanding of brain areas and circuits involved nicotine reward withdrawal, leading to models addiction that assign different addictive behaviors distinct, yet overlapping, neural ( Koob Volkow, 2010 ; Lobo Nestler, 2011 , Tuesta et al., Volkow ). Recently habenulo-interpeduncular (Hb-IPN) midbrain pathway re-emerged as a new critical crossroad influences response nicotine. This area is particularly enriched nicotinic acetylcholine receptor (nAChR) subunits α5, α3 β4 encoded by CHRNA5-A3-B4 gene cluster, which associated with vulnerability tobacco dependence human genetics studies. finding, together studies mice involving deletion replacement nAChR subunits, investigations circuitry, cell types electrophysiological properties, have begun identify molecular mechanisms take place MHb–IPN underlie aspects dependence. In current review we describe anatomical functional connections system, well contribution specific nAChRs subtypes nicotine-mediated behaviors. Finally, discuss properties neuronal populations how exposure alters their cellular physiology, highlighting unique role context aversion withdrawal. article part Special Issue entitled ‘The Nicotinic Acetylcholine Receptor: From Molecular Biology Cognition’.