| First Author | Broide RS | Year | 2001 |
| Journal | Neuroreport | Volume | 12 |
| Issue | 8 | Pages | 1643-8 |
| PubMed ID | 11409732 | Mgi Jnum | J:267172 |
| Mgi Id | MGI:6259269 | Doi | 10.1097/00001756-200106130-00026 |
| Citation | Broide RS, et al. (2001) Normal apoptosis levels in mice expressing one alpha7 nicotinic receptor null and one L250T mutant allele. Neuroreport 12(8):1643-8 |
| abstractText | The alpha7 nicotinic receptor (nAChR) is a ligand-gated ion channel mediating cholinergic transmission throughout the nervous system. To further characterize the function of this receptor, we generated mice expressing the alpha7 L250T nAChR mutation and demonstrated that homozygous (T/T) L250T mice die within 24 h of birth and display extensive apoptosis and abnormal layering within their cortex. We now demonstrate that mice with one alpha7 null and one L250T allele (-/T) show little apoptosis and normal development of their cortex yet exhibit the same lethal phenotype as T/T mice. Furthermore, L250T mice show normal levels of apoptosis in other nervous system regions expressing alpha7 nAChRs. These results suggest that apoptosis is not the cause of death for L250T neonatal mice. |
