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Growth Hormone Increases Connexin-43 Expression in the Cerebral Cortex and Hypothalamus¹

Institute of Clinical Neuroscience (N.D.Å., L.Ros., L.Rön., P.S.E.) and Research Center for Endocrinology and Metabolism, Department of Internal Medicine (B.C., O.G.P.I.), Sahlgrenska University Hospital, Göteborg University, and Department of Physiology and Pharmacology (J.O.), Göteborg University, SE-413 45 Göteborg, Sweden

Address all correspondence and requests for reprints to: Dr. Peter S. Eriksson, Institute of Clinical Neuroscience, Sahlgrenska University Hospital, Göteborg University, SE-413 45 Göteborg, Sweden. E-mail: per{at}neuro.gu.se

Several studies indicate that systemic GH influences various brain functions. Connexin-43 forms gap junctions that mediate intercellular communication and establish the astroglial syncytium. We investigated the effects of peripheral administration of bovine GH (bGH) and recombinant human insulin-like growth factor I (rhIGF-I) on the expression of connexin-43 in the rat brain. Hypophysectomized female Sprague Dawley rats were substituted with cortisol (400 µg/kg·day) and L-T₄ (10 µg/kg·day) and treated with either bGH (1 mg/kg·day) or rhIGF-I (0.85 mg/kg·day) for 19 days. The abundance of connexin-43 messenger RNA (mRNA) and protein in the brainstem, cerebral cortex, hippocampus, and hypothalamus was quantified by means of ribonuclease protection assays and Western blots. Treatment with bGH increased the amounts of connexin-43 mRNA and protein in the cerebral cortex and hypothalamus. No changes were found in the brainstem or hippocampus. Infusion of rhIGF-I did not affect connexin-43 mRNA or protein levels in any of the brain regions studied. These results show that administration of bGH increases the abundance of cx43 in specific brain regions, suggesting that GH may influence gap junction formation and thereby intercellular communication in the brain.

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