Davis B L, Manzanares J, Lookingland K J, Moore K E, Clemens L G
Department of Zoology, Michigan State University, East Lansing 48824.
Pharmacol Biochem Behav. 1991 Jul;39(3):737-42. doi: 10.1016/0091-3057(91)90156-v.
The purpose of the present study was to determine the importance of noradrenergic neurons terminating in the ventromedial nucleus (VMN) and medial preoptic nucleus (MPN) of the hypothalamus for lordosis behavior in ovariectomized, estrogen/progesterone-treated female rats. Seven days following bilateral injections of the noradrenergic neurotoxin 5-amino-2,4-dihydroxy-alpha-methylphenylethylamine (5-ADMP) into the ventral noradrenergic bundle (VNAB), norepinephrine (NE) concentrations (ng/mg protein) were reduced to 30-35% of control in the VMN and MPN. 5-ADMP-induced lesions of the VNAB also reduced lordosis quotients in these animals, and this effect was reversed by intracerebral ventricular administration of the alpha 1-adrenergic receptor agonist phenylephrine. These results indicate that neurotoxin-induced disruption of noradrenergic neurons in the VNAB is associated with a deficit in sexual receptivity in female rats. To determine if the reduction in sexual receptivity following 5-ADMP-induced lesions of the VNAB resulted from loss of noradrenergic neuronal projections specifically to the VMN or MPN, lordosis quotients were determined in ovariectomized, estrogen/progesterone-treated rats in which noradrenergic terminals in these hypothalamic nuclei were selectively lesioned. Injection of 5-ADMP directly into either the VMN or MPN reduced NE concentrations to 17% of control in these hypothalamic nuclei, but failed to alter lordosis. Furthermore, injection of phenylephrine into either the VMN or MPN of VNAB-lesioned rats failed to reinstate lordosis to the levels comparable to sham-lesioned controls. Taken together, these results indicate that noradrenergic neurons terminating in either the VMN or MPN are not essential for gonadal steroid induction of sexual receptivity in ovariectomized female rats.
本研究的目的是确定去甲肾上腺素能神经元在下丘脑腹内侧核（VMN）和内侧视前核（MPN）的终末对于卵巢切除、雌激素/孕酮处理的雌性大鼠的脊柱前凸行为的重要性。在双侧将去甲肾上腺素能神经毒素5-氨基-2,4-二羟基-α-甲基苯乙胺（5-ADMP）注射到腹侧去甲肾上腺素能束（VNAB）7天后，VMN和MPN中的去甲肾上腺素（NE）浓度（ng/mg蛋白）降至对照的30-35%。VNAB的5-ADMP诱导损伤也降低了这些动物的脊柱前凸商数，而脑室内给予α1-肾上腺素能受体激动剂苯肾上腺素可逆转这一效应。这些结果表明，神经毒素诱导的VNAB中去甲肾上腺素能神经元的破坏与雌性大鼠性接受能力的缺陷有关。为了确定5-ADMP诱导的VNAB损伤后性接受能力的降低是否是由于去甲肾上腺素能神经元向VMN或MPN的特异性投射丧失所致，在卵巢切除、雌激素/孕酮处理的大鼠中测定了脊柱前凸商数，这些大鼠下丘脑核中的去甲肾上腺素能终末被选择性损伤。将5-ADMP直接注射到VMN或MPN中可使这些下丘脑核中的NE浓度降至对照的17%，但未改变脊柱前凸。此外，将苯肾上腺素注射到VNAB损伤大鼠的VMN或MPN中未能使脊柱前凸恢复到与假损伤对照相当的水平。综上所述，这些结果表明，终末在VMN或MPN中的去甲肾上腺素能神经元对于卵巢切除雌性大鼠性腺类固醇诱导的性接受能力并非必不可少。
