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Weill Medical College of Cornell University and E.W. Bourne Behavioral Laboratory, New York Presbyterian Hospital, Westchester Division, White Plains New York 10509
The ovarian hormone estradiol reduces
meal size and food intake in female rats, at least in part by
increasing the satiating potency of CCK. Here we used c-Fos
immunohistochemistry to determine whether estradiol increases
CCK-induced neuronal activation in several brain regions implicated in
the control of feeding. Because the adiposity signals leptin and
insulin appear to control feeding in part by increasing the satiating
potency of CCK, we also examined whether increased adiposity after
ovariectomy influences estradiol's effects on CCK-induced c-Fos
expression. Ovariectomized rats were injected subcutaneously with 10 µg 17
-estradiol benzoate (estradiol) or vehicle once each on
Monday and Tuesday for 1 wk (experiment 1) or for 5 wk
(experiment 2). Two days after the final injection of
estradiol or vehicle, rats were injected intraperitoneally with 4 µg/kg CCK in 1 ml/kg 0.9 M NaCl or with vehicle alone. Rats were
perfused 60 min later, and brain tissue was collected and processed for
c-Fos immunoreactivity. CCK induced c-Fos expression in the nucleus of
the solitary tract (NTS), area postrema (AP), paraventricular nucleus
of the hypothalamus (PVN), and central nucleus of the amygdala (CeA) in
vehicle- and estradiol-treated ovariectomized rats. Estradiol treatment
further increased this response in the caudal, subpostremal, and
intermediate NTS, the PVN, and the CeA, but not in the rostral NTS or
AP. This action of estradiol was very similar in rats tested before
(experiment 1) and after (experiment 2)
significant body weight gain, suggesting that adiposity does not
modulate CCK-induced c-Fos expression or interact with estradiol's
ability to modulate CCK-induced c-Fos expression. These findings
suggest that estradiol inhibits meal size and food intake by increasing
the central processing of the vagal CCK satiation signal.
ingestive behavior; feeding; satiation; nucleus of the solitary tract; area postrema; paraventricular nucleus of the hypothalamus; amygdala; female rats
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