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Hindbrain Administration of Estradiol Inhibits Feeding and Activates Estrogen Receptor--Expressing Cells in the Nucleus Tractus Solitarius of Ovariectomized Rats

Vetsuisse Faculty (S.T., T.A.L.), Institute of Veterinary Physiology, University of Zurich, CH-8057 Zurich, Switzerland; Physiology and Behaviour Group (N.G., L.A.), Institute of Animal Science, ETH-Zurich, CH-8603 Schwerzenbach, Switzerland; and Department of Psychiatry (N.G.), Weill Medical College of Cornell University, New York, New York 10021

Address all correspondence and requests for reprints to: Lori Asarian, Ph.D., Institute of Animal Science, Physiology and Behaviour Group, ETH-Zürich, Schorenstrasse 16, 8603 Schwerzenbach, Switzerland. E-mail: lasarian{at}ethz.ch.

17β-Estradiol (E2), acting via estrogen receptor (ER)-, inhibits feeding in animals. One mechanism apparently involves an increase in the satiating potency of cholecystokinin (CCK) released from the small intestine by ingested food. For example, the satiating potency of intraduodenal lipid infusions is increased by E2 in ovariectomized rats; this increased satiation is dependent on CCK, and it is accompanied by increases in the numbers of ER-positive cells that express c-Fos in a subregion of the caudal nucleus tractus solitarius (cNTS) that receives abdominal vagal afferent projections. To test whether direct administration of E2 to this area of the hindbrain is sufficient to inhibit food intake, we first implanted 0.2 µg estradiol benzoate (EB) in cholesterol or cholesterol alone either sc or onto the surface of the hindbrain over the cNTS. Food intake was significantly reduced after hindbrain EB implants but not after sc EB implants. Next we verified that equimolar hindbrain implants of E2 and EB had similar feeding-inhibitory effects and determined that only small amounts of E2 reached brain areas outside the dorsal caudal hindbrain after hindbrain implants of ³H-labeled E2. Neither plasma estradiol concentration nor plasma inflammatory cytokine concentration was increased by either hindbrain or sc EB implants. Finally, hindbrain EB implants, but not sc implants, increased c-Fos in ER-positive cells in the cNTS after ip injection of 4 µg/kg CCK-8. We conclude that E2, acting via ER in cNTS neurons, including neurons stimulated by ip CCK, is sufficient to inhibit feeding.

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