Kalash J, Romita V, Billiar R B
Department of Obstetrics-Gynecology, McGill University Faculty of Medicine, Montreal, Canada.
Neuroendocrinology. 1989 May;49(5):462-70. doi: 10.1159/000125153.
The injection of purified alpha-bungarotoxin (alpha-BTX), an antagonist of the muscle nicotinic cholinergic receptors, into the third ventricle (3rd V) of ovariectomized rats decreased the frequency of pulses of luteinizing hormone (LH) but had no significant effect on the amplitude or nadir of LH secretion. Approximately 24 h after the 3rd V injection of alpha-BTX, the pulsatile secretion rate of LH was increased and thus the alpha-BTX effect was reversible. The 3rd V injection of the two nicotinic cholinergic agents, cytisine (10 micrograms) and dihydro-beta-erythroidine, also decreased the frequency of pulses of LH. Cytisine and dihydro-beta-erythroidine inhibited the binding of (125I)alpha-BTX to rat hypothalamic synaptosomes (P2B) and also to frozen coronal sections of the hypothalamus as studied by film autoradiography. Injection of a lower dose of cytisine (1 micrograms) had no effect on LH secretion, but when administered with alpha-BTX into the 3rd V, cytisine significantly reduced the alpha-BTX-induced decreased LH secretion. The injection of cytisine with (125I)alpha-BTX into the 3rd V also decreased in vivo labeling of the (125I)alpha-BTX-binding sites in the hypothalamus of ovariectomized rats. The results suggest that alpha-BTX can inhibit the pulsatile secretion of LH in ovariectomized rats and this inhibition may be mediated by specific subclass of a CNS (central nervous system) nicotinic acetylcholine receptor.
将纯化的α-银环蛇毒素（α-BTX）（一种肌肉烟碱型胆碱能受体拮抗剂）注入去卵巢大鼠的第三脑室（3rd V），可降低促黄体生成素（LH）脉冲频率，但对LH分泌的幅度或最低点无显著影响。在第三脑室注射α-BTX后约24小时，LH的脉冲分泌率增加，因此α-BTX的作用是可逆的。第三脑室注射两种烟碱型胆碱能药物，金雀花碱（10微克）和二氢β-刺桐啶，也降低了LH的脉冲频率。金雀花碱和二氢β-刺桐啶抑制（125I）α-BTX与大鼠下丘脑突触体（P2B）以及通过放射自显影片研究的下丘脑冰冻冠状切片的结合。注射较低剂量的金雀花碱（1微克）对LH分泌无影响，但当与α-BTX一起注入第三脑室时，金雀花碱可显著减轻α-BTX诱导的LH分泌减少。将金雀花碱与（125I）α-BTX一起注入第三脑室也降低了去卵巢大鼠下丘脑（125I）α-BTX结合位点的体内标记。结果表明，α-BTX可抑制去卵巢大鼠LH的脉冲分泌，这种抑制作用可能由中枢神经系统（CNS）烟碱型乙酰胆碱受体的特定亚类介导。
