The effects of nicotine, cotinine and mecamylamine on central dopamine (DA) and noradrenaline (NA) pathways of normal male rat were studied and the effects of nicotine on serum prolactin, LH and FSH levels evaluated. Nicotine, cotinine and mecamylamine in a concentration of 10 -5 M had only weak - if any - effects on [ 3H]DA and [ 3H]NA uptake, retention and release in various in vitro models. Nicotine in four doses of 2 mg/kg (30 min intervals) caused a significant reduction of the catecholamine (CA) stores (microspectrofluorimetrical evaluation of CA fluorescence intensities) in the medial palisade zone (MPZ) of the median eminence but in no other brain region. Nicotine in four doses of 3 mg/kg (30 min intervals) caused a trend for NA depletion (spectrofluorimetrical determination after cation exchange chromatography) in whole brain, and in the spinal cord it could be shown with the help of spinal cord transection that the reduction of spinal cord NA levels by nicotine was nerve impulse dependent. Using the tyrosine hydroxylase inhibition model to study changes in CA turnover it could be shown that four doses of nicotine (2-3 mg/kg; 30 min intervals) increased NA turnover (spectrofluorimetrical determination after cation exchange chromatography) in whole brain and reduced DA turnover (microspectrofluorimetrical evaluation of CA fluorescence) in nuc. caudatus. Nicotine in four doses of 2 mg/kg blocked the increase in serum prolactin levels caused by the tyrosine hydroxylase inhibitor α-methyltyrosine methylester (H44/68), whereas the basal serum levels of prolactin and FSH levels were not affected. LH levels were too low to be measured in most of the animals studied. It is suggested that nicotine affects central DA and NA neurons via activation of central 'nicotinic' acetylcholine receptors which are probably not located on the DA and NA nerve terminals. It is suggested that nicotine partly lowers prolactin secretion via its effects on CA nerve terminals in MPZ, since a significantly positive intraindividual correlation was found between prolactin levels and CA levels in MPZ in the normal male rat. The hypothesis is given that nicotine increases the activity in the DA nerve terminals of the MPZ, the DA being released into the portal system to act as a prolactin inhibitory factor at the anterior pituitary level.
|Original language||English (US)|
|Number of pages||10|
|State||Published - Dec 1 1977|
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