Estradiol's inhibitory effect on food intake is mediated, in part, by its ability to increase the activity of meal-related signals, including serotonin (5-HT), which hastens satiation. The important role that postsynaptic 5-HT 2C receptors play in mediating 5-HT's anorexigenic effect prompted us to investigate whether a regimen of acute estradiol treatment increases the anorexia associated with increased 5-HT 2C receptor activation in ovariectomized (OVX) rats. We demonstrated that intraperitoneal and intracerebroventricular (i.c.v.) administration of low doses of the 5-HT 2C receptor agonist meta-chlorophenylpiperazine (mCPP) decreased 1-h dark-phase food intake in estradiol-treated, but not oil-treated, OVX rats. During a longer feeding test, we demonstrated that i.c.v. administration of mCPP decreased 22-h food intake in oil-treated and, to a greater extent, estradiol-treated OVX rats. In a second study, we demonstrated that estradiol increased 5-HT 2C receptor protein content in the caudal brainstem, but not hypothalamus, of OVX rats. We conclude that a physiologically-relevant regimen of acute estradiol treatment increases sensitivity to mCPP's anorexigenic effect. Our demonstration that this same regimen of estradiol treatment increases 5-HT 2C receptor protein content in the caudal hindbrain of OVX rats provides a possible mechanism to explain our behavioral findings.
|Number of pages||7|
|Journal||Physiology and Behavior|
|State||Published - Jan 18 2012|
Bibliographical noteFunding Information:
This work was supported by grants from the NIH : DK-073936 and MH-063932 (LAE), T32DC-00044 (HMR) and F31 NS-062667 (JS).
- Caudal brainstem
- Food intake
ASJC Scopus subject areas
- Experimental and Cognitive Psychology
- Behavioral Neuroscience