This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Fujikawa, T. Articles by Nakashima, K. Search for Related Content PubMed PubMed Citation Articles by Fujikawa, T. Articles by Nakashima, K.

Prolactin Receptor Knockdown in the Rat Paraventricular Nucleus by a Morpholino-Antisense Oligonucleotide Causes Hypocalcemia and Stress Gastric Erosion

Department of Biochemistry and Proteomics, Institute of Genomics and Regenerative Biology, Mie University Graduate School of Medicine (T.F., K.T., T.K., Y.M., M.O.), Mie 514-8507, Japan; Department of Psychiatry, University of Cincinnati Medical Center (T.F., R.R.S.), Cincinnati, Ohio 45267-0559; Department of Legal Medicine, Kyoto Prefectural University of Medicine (K.S.), Kyoto 602-8566, Japan; Department of Integrated Human Sciences, School of Dentistry, Health Sciences University of Hokkaido (A.Y.), Hokkaido 061-0293, Japan; Laboratory of Exercise Biochemistry, Institute of Health and Sport Sciences, University of Tsukuba (H.S.), Ibaraki 305-8574, Japan; and Faculty of Human Health Science, Tokai Gakuen University (K.N.), 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.

Under acute stress conditions in the rat, there is rapid and transient increase in circulating prolactin (PRL). This leads to an elevated expression of the long form of PRLR (PRLR-L) first in the hypothalamus and the choroid plexus. This increase in PRL is involved in the inhibition of stress-induced hypocalcemia and gastric erosion. In this study we used rat PRL and a PRLR morpholino-antisense oligonucleotide to elucidate the mechanism by which hypothalamic PRLR mediates the inhibition of restraint stress in water (RSW)-induced hypocalcemia and gastric erosion. We found that this effect is largely mediated by PRLRs in the paraventricular nucleus (PVN), medial preoptic nucleus, and ventromedial hypothalamus. We also show that when measured after 7 h of RSW, microinjection of the PRLR antisense oligonucleotide into these areas down-regulates RSW-enhanced expression of PRLR-L protein in the PVN and increases the plasma PRL level, but does not affect plasma levels of another hormone, GH. Furthermore, our experiments demonstrated that under nonstress conditions, knockdown of the PRLR in the PVN significantly lowers circulating Ca²⁺ levels, but does not affect gastric erosion. These results suggest that PRL acting on the PRLR-L in the PVN is one of the critical pathways for regulating circulating Ca²⁺ levels under both acute stress and nonstress conditions.

This article has been cited by other articles:

				C. T. De Souza, E. P. Araujo, L. F. Stoppiglia, J. R. Pauli, E. Ropelle, S. A. Rocco, R. M. Marin, K. G. Franchini, J. B. Carvalheira, M. J. Saad, et al. Inhibition of UCP2 expression reverses diet-induced diabetes mellitus by effects on both insulin secretion and action FASEB J, April 1, 2007; 21(4): 1153 - 1163. [Abstract] [Full Text] [PDF]