The effect of nicotine on central catecholamine neurons and gonadotropin secretion.

The action of nicotine was studied on dopamine (DA) and noradrenaline (NA) stores and its turnover in discrete regions of the median eminence and in the forebrain of ovariectomized female rats by measuring the decline of the catecholamine (CA) stores after tyrosine-hydroxylase inhibition using α-methyl-tyrosine methylester (H44/68). The CA stores were measured with the help of a quantitative microfluorimetric technique involving the use of a Leitz microspectrofluorimeter equipped with an MPV system. In the same group of animals measurements were made of LH, FSH and prolactin serum levels, using radioimmunoassay procedures. Nicotine treatment (4 x 2 mg/kg i.p., 30 min intervals) with the last injection made 30 min before killing significantly reduced the CA stores in the subependymal layer and the medial and lateral external zone of the rat median eminence. This treatment also significantly increased the H44/68-induced disappearance of CA stores in all th layers mentioned above. Lowering the dose of nicotine to 1 mg/kg resulted in significant increases of CA disappearance only in the medial and lateral external zone. The results of the present and previous papers indicate that the reduction of LH and prolactin secretion caused by nicotine can in part be mediated via an activation of the tuberoinfundibular DA neurons to the lateral and medial palisade zone, respectively. The hypersecretion of FSH in the ovariectomized female rat was affected by nicotine treatment only after combined treatment with H44/68. In most experiments with nicotine a reduction of the LH/FSH ratio was observed. The present study, therefore, supports the view that there may exist a differential control of LH and FSH secretion which could exist at the pituitary and/or hypothalamic level. Nicotine treatment (4 x 1-2 mg/kg, as above) selectively reduced DA turnover in the posterior half of the nuc. accumbens in the ovariectomized female rat as evaluated from the reduction of the H44/68-induced DA disappearance caused by nicotine. It is possible that the biochemical and functional changes observed may primarily involve the activation of a central 'nicotinic' acetylcholine receptor.