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Prolactin Prevents Acute Stress-Induced Hypocalcemia and Ulcerogenesis by Acting in the Brain of Rat

Department of Biochemistry, Faculty of Medicine, Mie University (T.F., N.N., M.O.), Tsu, Mie 514-8507, Japan; Department of Exercise Biochemistry, Institute of Health and Sports Science, Tsukuba University (H.S.), Tsukuba, Ibaraki 305-8574, Japan; Department of Psychiatry, University of Cincinnati Medical Center (T.F., K.L.K.T., R.R.S.), Cincinnati, Ohio 45267-0559; Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, The Rockefeller University (B.S.M.), New York, New York 10021-6399; Department of Clinical Nutrition, Faculty of Health and Hygiene, Suzuka University of Medical Science (I.S.), Suzuka, Mie 510-0293, Japan; and Faculty of Human Health Science, Tokai Gakuen University (K.N.), Tenpaku, Nagoya, Aichi 468-8514, Japan

Address all correspondence and requests for reprints to: Dr. Takahiko Fujikawa, Department of Biochemistry, Mie University School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan. E-mail: t-fuji{at}doc.medic.mie-u.ac.jp.

Stress causes hypocalcemia and ulcerogenesis in rats. In rats under stressful conditions, a rapid and transient increase in circulating prolactin (PRL) is observed, and this enhanced PRL induces PRL receptors (PRLR) in the choroid plexus of rat brain. In this study we used restraint stress in water to elucidate the mechanism by which PRLR in the rat brain mediate the protective effect of PRL against stress-induced hypocalcemia and ulcerogenesis. We show that rat PRL acts through the long form of PRLR in the hypothalamus. This is followed by an increase in the long form of PRLR mRNA expression in the choroid plexus of the brain, which provides protection against restraint stress in water-induced hypocalcemia and gastric erosions. We also show that PRL induces the expression of PRLR protein and corticotropin-releasing factor mRNA in the paraventricular nucleus. These results suggest that the PRL levels increase in response to stress, and it moves from the circulation to the cerebrospinal fluid to act on the central nervous system and thereby plays an important role in helping to protect against acute stress-induced hypocalcemia and gastric erosions.

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				T. Fujikawa, K. Tamura, T. Kawase, Y. Mori, R. R. Sakai, K. Sakuma, A. Yamaguch, M. Ogata, H. Soya, and K. Nakashima Prolactin Receptor Knockdown in the Rat Paraventricular Nucleus by a Morpholino-Antisense Oligonucleotide Causes Hypocalcemia and Stress Gastric Erosion Endocrinology, August 1, 2005; 146(8): 3471 - 3480. [Abstract] [Full Text] [PDF]