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TARGETED DISRUPTION OF THE NEURONAL NITRIC-OXIDE SYNTHASE GENE
Author(s): HUANG PL, DAWSON TM, BREDT DS, SNYDER SH, FISHMAN MC
Source: CELL    Volume: 75    Issue: 7    Pages: 1273-1286    Published: DEC 31 1993  
Times Cited: 879     References: 71     
Abstract: By homologous recombination, we have generated mice that lack the neuronal nitric oxide synthase (NOS) gene. Neuronal NOS expression and NADPH-diaphorase (NDP) staining are absent in the mutant mice. Very low level residual catalytic activity suggests that other enzymes in the brain may generate nitric oxide. The neurons normally expressing NOS appear intact, and the mutant NOS mice are viable, fertile, and without evident histopathological abnormalities in the central nervous system. The most evident effect of disrupting the neuronal NOS gene is the development of grossly enlarged stomachs, with hypertrophy of the pyloric sphincter and the circular muscle layer. This phenotype resembles the human disorder infantile pyloric stenosis, in which gastric outlet obstruction is associated with the lack of NDP neurons in the pylorus.
Document Type: Article
Language: English
Reprint Address: HUANG, PL (reprint author), MASSACHUSETTS GEN HOSP, CARDIOVASC RES CTR, BOSTON, MA 02129 USA
Addresses:
1. JOHNS HOPKINS UNIV, SCH MED, DEPT NEUROSCI, BALTIMORE, MD 21205 USA
2. JOHNS HOPKINS UNIV, SCH MED, DEPT PHARMACOL & MOLEC SCI, BALTIMORE, MD 21205 USA
3. JOHNS HOPKINS UNIV, SCH MED, DEPT PSYCHIAT & BEHAV SCI, BALTIMORE, MD 21205 USA
4. JOHNS HOPKINS UNIV, SCH MED, DEPT NEUROL, BALTIMORE, MD 21205 USA
Publisher: CELL PRESS, 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138
Subject Category: Biochemistry & Molecular Biology; Cell Biology
IDS Number: MP869
ISSN: 0092-8674
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