Barrios V, González-Parra S, Arilla E
Department of Biochemistry, University of Alcalá, Madrid, Spain.
Life Sci. 1992;51(25):1991-8. doi: 10.1016/0024-3205(92)90116-7.
Within 4 minutes a single, intravenous injection of nicotine (0.3 mg/Kg) induced increases in somatostatin-like immunoreactivity concentrations in the rat hypothalamus but not in the striatum. These changes were associated with a significant increase in the specific binding of somatostatin to putative receptor sites in hypothalamic membranes, while no significant changes were found in striatum. The enhancement of somatostatin binding resulted from a rapid increase in the number of available receptors rather than a change in receptor affinity. This effect appears to be mediated by nicotinic cholinergic receptors, because pretreatment with a centrally active nicotinic receptor antagonist, mecamylamine (5.0 mg/Kg i.v.), prevented the nicotine-induced changes in somatostatin content and binding in the hypothalamus. Mecamylamine alone had no observable effect on the hypothalamic somatostatinergic system. These results suggest that the rat hypothalamic somatostatinergic system can be regulated by nicotine-like acetylcholine receptors.
在4分钟内，单次静脉注射尼古丁（0.3毫克/千克）可使大鼠下丘脑内生长抑素样免疫反应浓度升高，但纹状体内则无此变化。这些变化与生长抑素与下丘脑膜上假定受体位点的特异性结合显著增加有关，而纹状体内未发现显著变化。生长抑素结合的增强是由于可用受体数量迅速增加，而非受体亲和力改变。这种效应似乎由烟碱型胆碱能受体介导，因为用中枢活性烟碱受体拮抗剂美加明（5.0毫克/千克静脉注射）预处理可防止尼古丁诱导的下丘脑内生长抑素含量及结合的变化。单独使用美加明对下丘脑生长抑素能系统无明显影响。这些结果表明，大鼠下丘脑生长抑素能系统可由类似尼古丁的乙酰胆碱受体调节。
