title: Modulation of ventral tegmental area dopamine receptors inhibit nicotine-induced anxiogenic-like behavior in the central amygdala.
abstract: Nicotine, the major addictive substance in tobacco, increases the activity of the central amygdala (CeA). Amygdala is directly implicated in anxiety modulation and sends projections to the vicinity of the midbrain dopamine neurons, including the ventral tegmental area (VTA) which is a key area that controls nicotine dependence processes. In this study, the role of dopamine D(1) and D(2)/(3) receptors of the VTA on anxiogenic-like behavior induced with intra-CeA injection of nicotine has been investigated. Male Wistar rats with cannula aimed to the left CeA and the left VTA were submitted to the elevated plus-maze (EPM). The nicotine injection (1 μg/rat) into the CeA decreased the percentage of open arm time and open arm entries, but not locomotor activity, indicating an anxiogenic-like response. Intra-VTA injection of a dopamine D1 receptor antagonist, SCH23390 (0.25 μg/rat), and a dopamine D2/3 receptor antagonist, sulpiride (0.7 μg/rat), inhibited the anxiogenic-like response caused by intra-CeA injection of nicotine. These results suggest that the relationship between the VTA and the CeA may be involved in nicotine-induced anxiogenic-like behavior via dopamine D(1) and D(2)/(3) receptors. An understanding of these cellular processes will be crucial for the development of new intervention to combat nicotine effect.
authors.affiliation: Department of Neuroscience, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran. zarinmr@ams.ac.ir
authors.forename: Mohammad Reza
authors.initials: MR
authors.lastname: Zarrindast
authors.forename: Nafiseh
authors.initials: N
authors.lastname: Eslahi
authors.forename: Ameneh
authors.initials: A
authors.lastname: Rezayof
authors.forename: Parvin
authors.initials: P
authors.lastname: Rostami
authors.forename: Maryam
authors.initials: M
authors.lastname: Zahmatkesh
mesh_terms: D000679:Amygdala / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D000818:Animals; D001007:Anxiety / Q000139:chemically induced / Q000517:prevention & control* / Q000523:psychology; D001552:Benzazepines / Q000008:administration & dosage; D018492:Dopamine Antagonists / Q000008:administration & dosage; D007276:Injections, Intraventricular; D008297:Male; D009538:Nicotine / Q000008:administration & dosage / Q000037:antagonists & inhibitors* / Q000633:toxicity*; D051381:Rats; D017208:Rats, Wistar; D011954:Receptors, Dopamine / Q000096:biosynthesis* / Q000502:physiology; D017447:Receptors, Dopamine D1 / Q000096:biosynthesis / Q000378:metabolism / Q000502:physiology; D017448:Receptors, Dopamine D2 / Q000096:biosynthesis / Q000378:metabolism / Q000502:physiology; D050637:Receptors, Dopamine D3 / Q000096:biosynthesis / Q000502:physiology; D013469:Sulpiride / Q000008:administration & dosage; D017557:Ventral Tegmental Area / Q000187:drug effects / Q000502:physiology*
chemical_list: D001552:Benzazepines; D018492:Dopamine Antagonists; D011954:Receptors, Dopamine; D017447:Receptors, Dopamine D1; D017448:Receptors, Dopamine D2; D050637:Receptors, Dopamine D3; C534628:SCH 23390; D009538:Nicotine; D013469:Sulpiride