MAJZOUB, JOSEPH A., ENRIQUE J. CARRAZANA, JANE S. SHULMAN, KAREN J. BAKER, AND RODICA L. EMANUEL. Defective of expression . Am. J. Physiol. 252 (Endocrol. Metab. 15): E637-E642, 1987.-The rat has severe diabetes sipidus due to an autosomal recessive trait resultg the ability to synthesize detectable amounts of hypothalamic . To determe whether this abnormality is due to a regulatory defect the ratâs , we studied changes the hypothalamic content of mRNA normal Long-Evans and homozygous subjected to osmotic stress and correlated these changes with systemic responses to water deprivation. We report that the rat does have a marked defect the of expression consistg of an ability to crease hypothalamic mRNA content response to severe osmotic stress. diabetes sipidus; Rattus norvegicus neuropeptide; messenger ribonucleic acid; METHODS RAT carries as a recessive trait the ability to synthesize detectable amounts of its magnocellular hypothalamic neurons (30). Homozygous have severe diabetes sipidus, which is corrected by replacement therapy (6). tic studies suggest that a sgle autosomal is responsible for the observed phenotype (25). Recently the DNA sequence of a obtaed from a rat has been reported (28). This lacks a sgle guanose residue the second exon of the prote-codg region, givg
AJP - Endocrinology and Metabolism – The American Physiological Society
Published: May 1, 1987
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