| | |  | | | | Record from Web of Science® | | | | | | |
| MICE LACKING NERVE GROWTH-FACTOR DISPLAY PERINATAL LOSS OF SENSORY AND SYMPATHETIC NEURONS YET DEVELOP BASAL FOREBRAIN CHOLINERGIC NEURONS |
|
|
| Author(s): CROWLEY C, SPENCER SD, NISHIMURA MC, CHEN KS, PITTSMEEK S, ARMANINI MP, LING LH, MCMAHON SB, SHELTON DL, LEVINSON AD, PHILLIPS HS |
| Source: CELL Volume: 76 Issue: 6 Pages: 1001-1011 Published: MAR 25 1994 |
| Times Cited: 620 References: 41 |
| Abstract: Homologous recombination was utilized to generate mice with a deletion in the coding sequence of the nerve growth factor (NGF) gene. Animals homozygous for NGF disruption failed to respond to noxious mechanical stimuli, and histological analysis revealed profound cell loss in both sensory and sympathetic ganglia. Within dorsal root ganglia, effects of the mutation appeared to be restricted to small and medium peptidergic neurons. These observations confirm the critical dependence of sensory and sympathetic neurons on NGF and demonstrate that other neurotrophins are not able to compensate for the loss of NGF action on these cells. Examination of the central nervous system revealed that, in marked contrast with neurons of sensory and sympathetic ganglia, basal forebrain cholinergic neurons differentiate and continue to express phenotypic markers for the life span of the null mutant mice. Thus, differentiation and initial survival of central NGF-responsive neurons can occur in the absence of NGF. |
| Document Type: Article |
| Language: English |
| Reprint Address: CROWLEY, C (reprint author), GENENTECH INC, DEPT CELL GENET, 460 POINT SAN BRUNO BLVD, S SAN FRANCISCO, CA 94080 USA |
Addresses:
1. UNITED MED & DENT SCH, DEPT PHYSIOL, LONDON SE1 7EH, ENGLAND
2. GENENTECH INC, DEPT ENDOCRINE RES, S SAN FRANCISCO, CA 94080 USA
3. GENENTECH INC, DEPT NEUROSCI, S SAN FRANCISCO, CA 94080 USA |
| Publisher: CELL PRESS, 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 |
| Subject Category: Biochemistry & Molecular Biology; Cell Biology |
| IDS Number: ND246 |
| ISSN: 0092-8674 |
|
| | | | | | | | | Record from Web of Science® | | | | | | | | | |