The distribution of mRNA encoded by a new member of the neuronal nicotinic acetylcholine receptor gene family (α5) in the rat central nervous system
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Cited by (225)
Linking the CHRNA5 SNP to drug abuse liability: From circuitry to cellular mechanisms
2021, NeuropharmacologyAlterations in nicotinic receptor alpha5 subunit gene differentially impact early and later stages of cocaine addiction: a translational study in transgenic rats and patients
2021, Progress in NeurobiologyCitation Excerpt :The VTA, dorsal prefrontal cortex and NAcc shell are crucial to cocaine-induced reinstatement while the central nucleus of the amygdala and bed nucleus of the stria terminalis are necessary for stress-induced reinstatement (Kalivas and McFarland, 2003). In this line, α5 is expressed at relatively high levels in the VTA and NAcc, but absent in the amygdala (Wada et al., 1990). The lack of effect of Chrna5 deletion on cue- and stress-induced relapse seems in accordance with the physiological absence of α5 containing nAChRs in brain areas specifically involved in these modalities of relapse.
Genetic susceptibility to nicotine addiction: Advances and shortcomings in our understanding of the CHRNA5/A3/B4 gene cluster contribution
2020, NeuropharmacologyCitation Excerpt :Taken together, these preclinical results fit well with the human situation where the α5SNP is associated with an increased risk for NA, lower ratings of aversive effect, and delayed smoking cessation (Bierut et al., 2008; Chen et al., 2015; Jensen et al., 2015; Saccone et al., 2007). The α5 nAChR subunit is expressed in discrete regions of the rodent central nervous system (CNS), including the striatum where it regulates DA transmission (Exley et al., 2012), the cerebral cortex, cerebellum, thalamus, hippocampus, substantia nigra (SN), VTA and mHb, with the highest concentration found in the IPN (Forget et al., 2018; Hsu et al., 2013; Marks et al., 1992; Sheffield et al., 2000; Wada et al., 1990). According to the databases listed in part 2.1.1, rodent Chrna5 expression partly follows human CHRNA5 expression, with an overall higher expression in the hindbrain (notably the cerebellum) than in the forebrain, but with constantly detectable (although lower) expression in the cortex and in the thalamus.
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Present address: Laboratory of Neurochemistry, NINDS, NIH, Bldg. 36, Room 4D20, Bethesda, MD 20892, U.S.A.
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Present address: Department of Pharmacology, Washington University School of Medicine, St. Louis, MO 63110, U.S.A.
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Present address: Baylor College of Medicine, Division of Nueroscience, One Baylor Plaza, Houston, TX 77030, U.S.A.