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Corticotropin Releasing Factor Receptor Type II (CRF₂) Messenger Ribonucleic Acid Levels in the Hypothalamic Ventromedial Nucleus of the Infant Rat Are Reduced by Maternal Deprivation

Departments of Anatomy & Neurobiology (M.E.A., C.G.H., T.Z.B.) and Pediatrics (S.A.E., T.Z.B.), University of California Irvine, Irvine, California 92697-4475

Address all correspondence and requests for reprints to: Tallie Z. Baram, M.D., Ph.D., University of California Irvine, Medical Sciences I, Department of Pediatrics, ZOT 4475, Irvine, California 92717-4475.

	Abstract

Top Abstract

 
The stress neurohormone corticotropin releasing factor (CRF) activates at least two receptor types. Expression of corticotropin releasing factor receptor type II (CRF₂) has been demonstrated in the hypothalamic ventromedial nucleus (VMH) of the adult and developing rat, but the physiological functions of VMH-CRF₂ have not been elucidated. The VMH has been documented as an important participant in the regulation of food intake and its interactions with the hypothalamic-pituitary-adrenal axis and circadian rhythms. Regulation of VMH-CRF₂ may thus play a role in the interplay of physiological alterations in metabolic state with the neuroendocrine and anorexic effects of CRF. This study determined the regulation of CRF₂-mRNA expression in infant rats by the physiological consequences of maternal deprivation, i.e., fasting and stress. Using in situ hybridization, maternally deprived pups had an average 62% reduction of VMH-CRF₂-mRNA levels compared with stress-free controls. Maternal deprivation also resulted in elevated plasma corticosterone levels (3.8 ± 0.3 vs. 1.3 ± 0.1 µg/dl) and an average 5.7% body weight loss. This study demonstrates that maternal deprivation, via fasting and HPA activation, leads to a dramatic decrease of CRF₂-mRNA levels in the VMH. These results are consistent with a role for CRF₂ activation in mediating some of the complex interactions of CRF (or urocortin) with regulation of food intake in the developing rat.

Received July 8, 1997.

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