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Research Article Free access | 10.1172/JCI118080

Expression and localization of the cystic fibrosis transmembrane conductance regulator mRNA and its protein in rat brain.

A E Mulberg, L P Resta, E B Wiedner, S M Altschuler, D M Jefferson, and D L Broussard

Division of Gastroenterology and Nutrition, Children's Hospital of Philadelphia, Pennsylvania 19104, USA.

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Division of Gastroenterology and Nutrition, Children's Hospital of Philadelphia, Pennsylvania 19104, USA.

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Division of Gastroenterology and Nutrition, Children's Hospital of Philadelphia, Pennsylvania 19104, USA.

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Division of Gastroenterology and Nutrition, Children's Hospital of Philadelphia, Pennsylvania 19104, USA.

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Division of Gastroenterology and Nutrition, Children's Hospital of Philadelphia, Pennsylvania 19104, USA.

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Division of Gastroenterology and Nutrition, Children's Hospital of Philadelphia, Pennsylvania 19104, USA.

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Published July 1, 1995 - More info

Published in Volume 96, Issue 1 on July 1, 1995
J Clin Invest. 1995;96(1):646–652. https://doi.org/10.1172/JCI118080.
© 1995 The American Society for Clinical Investigation
Published July 1, 1995 - Version history
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Abstract

In previous studies we have characterized the expression of the cystic fibrosis transmembrane conductance regulator (CFTR) protein in clathrin-coated vesicles derived from bovine brain and in neurons of rat brain. In this study we have further characterized the expression of the CFTR protein mRNA and protein in rat brain with reverse transcriptase polymerase chain reaction amplification (RT-PCR), in situ hybridization, and immunocytochemistry. The expression of CFTR mRNA and protein in discrete areas of brain, including the hypothalamus, thalamus, and amygdaloid nuclei, which are involved in regulation of appetite and resting energy expenditure, is identical. The presence of CFTR in neurons localized to these regions of brain controlling homeostasis and energy expenditure may elucidate the pathogenesis of other nonpulmonary and gastrointestinal manifestations which commonly are observed in children with cystic fibrosis. Dysregulation of normal neuropeptide vesicle trafficking by mutant CFTR in brain may serve as a pathogenic mechanism for disruption of homeostasis.

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