| First Author | Nanobashvili A | Year | 2000 |
| Journal | Proc Natl Acad Sci U S A | Volume | 97 |
| Issue | 22 | Pages | 12312-7 |
| PubMed ID | 11050250 | Mgi Jnum | J:65427 |
| Mgi Id | MGI:1926567 | Doi | 10.1073/pnas.97.22.12312 |
| Citation | Nanobashvili A, et al. (2000) Development and persistence of kindling epilepsy are impaired in mice lacking glial cell line-derived neurotrophic factor family receptor alpha 2. Proc Natl Acad Sci U S A 97(22):12312-7 |
| abstractText | Seizure activity regulates gene expression for glial cell line-derived neurotrophic factor (GDNF) and neurturin (NRTN), and their receptor components, the transmembrane c-Ret tyrosine kinase and the glycosylphosphatidylinositol-anchored GDNF family receptor (GFR) alpha1 and alpha2 in limbic structures. We demonstrate here that epileptogenesis, as assessed in the hippocampal kindling model, is markedly suppressed in mice lacking GFRalpha2. Moreover, at 6 to 8 wk after having reached the epileptic state, the hyperexcitability is lower in GFRalpha2 knock-out mice as compared with wild-type mice. These results provide evidence that signaling through GFRalpha2 is involved in mechanisms regulating the development and persistence of kindling epilepsy. Our data suggest that GDNF and NRTN may modulate seizure susceptibility by altering the function of hilar neuropeptide Y-containing interneurons and entorhinal cortical afferents at dentate granule cell synapses. |
