Neonatal agonism of ERα masculinizes serotonergic (5-HT) projections to the female rat ventromedial nucleus of the hypothalamus (VMN) but does not impair lordosis

Serotonin (5-HT) is known to play a role in the suppression of the lordosis response in males. We have previously shown that there is a sex difference in the density of 5-HT immunoreactive (5-HT-ir) fibers in the ventrolateral division of the adult ventromedial nucleus of the hypothalamus (VMNvl) an...

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Published inBehavioural brain research Vol. 196; no. 2; pp. 317 - 322
Main Authors Patisaul, Heather B., Adewale, Heather B., Mickens, Jillian A.
Format Journal Article
LanguageEnglish
Published Shannon Elsevier B.V 23.01.2009
Elsevier
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Summary:Serotonin (5-HT) is known to play a role in the suppression of the lordosis response in males. We have previously shown that there is a sex difference in the density of 5-HT immunoreactive (5-HT-ir) fibers in the ventrolateral division of the adult ventromedial nucleus of the hypothalamus (VMNvl) and that neonatal administration of estradiol (E2) increases 5-HT-ir in the female VMNvl to male-typical levels. Here we demonstrate that postnatal administration of the ERα agonist 1,3,5-tris(4-Hydroxyphenyl)-4-propyl-1H-pyrazole (PPT), but not the ERβ agonist diarylpropionitrile (DPN), also masculinizes 5-HT-ir in the female VMNvl, suggesting a mechanistic role for ERα in this process. Sexual receptivity, as ascertained by the lordosis quotient, was unaffected by either PPT or DPN treatment but nearly abolished by estradiol benzoate (EB), a synthetic estrogen with high affinity for both ERα and ERβ. Collectively, these observations show that postnatal estrogens increase the density of 5-HT projections to the VMNvl via an ERα dependent mechanism, but that this increased inhibitory input is not sufficient to suppress the lordosis response.
ISSN:0166-4328
1872-7549
DOI:10.1016/j.bbr.2008.09.026