Noradrenergic innervation to the VMN or MPN is not necessary for lordosis.

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.