Abstract
We studied the effects of an acute dose of (−)-nicotine (1 mg/kg) on Fos-like immunostaining (IS) in rat brain areas. Nicotine increased Fos IS significantly in the medial terminal nucleus of accessory optic tract (MT), and tended to increase it in the interpeduncular nucleus (IP), as well as in the stress-related areas, the paraventricular hypothalamic nucleus (PVN) and the supraoptic nucleus (SON). Previously nicotine was reported to increase Fos IS also in another stress-related area, the central nucleus of amygdala (ACe). This led us to study the interaction of nicotine with diazepam (10 mg/kg). Diazepam alone increased Fos IS in PVN and in SON as well as in ACe. In diazepam- and nicotine-treated rats Fos IS was increased in PVN and SON as well as in MT and IP. In MT and IP of diazepam and nicotine-treated rats Fos IS was similar to that induced by nicotine alone, and in PVN and SON of these rats Fos IS was similar to that induced by diazepam alone. Nicotine tended to antagonise the diazepam-induced elevation of Fos IS in ACe. Taken together, diazepam induced Fos IS in all stress-related areas studied (PVN, SON, ACe), but not in central visual structures, where nicotine induces Fos IS (MT, IP). No significant interactions on Fos expression were found between acute effects of diazepam and nicotine suggesting that these drugs activate different sets of neurons within the stress-related brain areas.
Published Version
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