| First Author | Hanbury R | Year | 2003 |
| Journal | J Mol Neurosci | Volume | 20 |
| Issue | 2 | Pages | 93-102 |
| PubMed ID | 12794303 | Mgi Jnum | J:121246 |
| Mgi Id | MGI:3709681 | Doi | 10.1385/JMN:20:2:93 |
| Citation | Hanbury R, et al. (2003) Knockout of p75NTR does not alter the viability of striatal neurons following a metabolic or excitotoxic injury. J Mol Neurosci 20(2):93-102 |
| abstractText | Following metabolic or excitotoxic injury to the striatum, there is de novo expression of the low-affinity p75 neurotrophin receptor (p75NTR). The novel expression of this pan neurotrophin receptor in rodents occurs within the lesion core and surrounding area, creating a division between viable and nonviable tissue. The present series of experiments sought to elucidate whether the p75NTR expression seen following metabolic and excitotoxic injury alters neuronal viability within the striatum. Toward this end, we compared the extent of striatal lesion created with quinolinic acid (QA) or 3-nitropropionic acid (3-NP) in p75NTR null and wild-type mice. Using stereological techniques, we found that the lesion volume and neuronal cell counts between p75NTR null and wild-type mice were similar 1, 2, and 4 weeks post-QA or -3-NP lesion. The results indicate that the expression of p75NTR within reactive astrocytes in the mouse striatum is not a key factor in protecting neuronal cell death following metabolic and excitotoxic insults. |
