Alpha 1-adrenergic agonists act on the ventromedial hypothalamus to cause neuronal excitation and lordosis facilitation: electrophysiological and behavioral evidence.

To see if activation of central alpha 1-adrenergic receptors can cause facilitation of lordosis in rats, the behavioral effects of centrally administered alpha 1-agonists, methoxamine (MA) and phenylephrine (PhE), and related agents were studied. In ovariectomized rats treated with estrogen, infusion of MA, PhE, or a beta-agonist isoproterenol, into the lateral ventricle, or bilateral infusions of MA or PhE into the ventromedial hypothalamus (VMH) facilitated lordosis. Conversely, intra-VMH infusion of the alpha 1-antagonist prazosin (PZ) inhibited lordosis. Intra-VMH infusion of isoproterenol or an alpha 2-agonist clonidine, had no effect. Neither was the intra-VMH infusion of MA effective if: (i) the rats were not primed with estrogen; (ii) the tips of the cannulae were outside the VMH; or (iii) it was preceded by an intra-VMH infusion of the alpha 1b-antagonist, chloroethylclonidine (CEC). These results not only verify implications from recent studies that alpha 1-receptors in the hypothalamus are important for lordosis facilitation, but further show that the adrenergic facilitatory effect are: (i) mediated specifically by alpha 1b-subtype of the alpha 1-receptor, (ii) estrogen-dependent, and (iii) site-specific to VMH. To investigate neural mechanisms potentially underlying the lordosis-facilitating effect of alpha 1-activation, the actions of MA and PhE on the electrical activity of single neurons of the ventromedial nucleus of the hypothalamus (VMN) in vitro were studied.(ABSTRACT TRUNCATED AT 250 WORDS)