Abstract:
: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)
journal_name
Brain Resjournal_title
Brain researchauthors
Kow LM,Weesner GD,Pfaff DWdoi
10.1016/0006-8993(92)91581-xsubject
Has Abstractpub_date
1992-08-21 00:00:00pages
237-45issue
2eissn
0006-8993issn
1872-6240pii
0006-8993(92)91581-Xjournal_volume
588pub_type
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