| First Author | Drexel M | Year | 2018 |
| Journal | Epilepsia | Volume | 59 |
| Issue | 11 | Pages | e166-e171 |
| PubMed ID | 30298565 | Mgi Jnum | J:295488 |
| Mgi Id | MGI:6454094 | Doi | 10.1111/epi.14573 |
| Citation | Drexel M, et al. (2018) Effects of galanin receptor 2 and receptor 3 knockout in mouse models of acute seizures. Epilepsia 59(11):e166-e171 |
| abstractText | There exists solid evidence that endogenous galanin and galanin agonists exert anticonvulsive actions mediated both by galanin 1 receptor (GAL1-R) and galanin 2 receptor (GAL2-R). We have now investigated whether depletion of the recently identified third galanin receptor, GAL3-R, and that of GAL2-R, alters the threshold to the systemically applied gamma-aminobutyric acid (GABA) antagonist pentylenetetrazole (PTZ) or to intrahippocampally administered kainic acid (KA). In neither model, GAL3-KO mice differed in their latency to the first seizure, mean seizure duration, total number of seizures, or time spent in seizures compared to wild-type controls. In addition, consistent with previous data, the response to PTZ was not altered in GAL2-KO mice. In contrast, intrahippocampal KA resulted in a significantly increased number of seizures and time spent in seizures in GAL2-KO mice, although the latency to the first seizure and the duration of individual seizures was not altered. These results are consistent with the previous data showing that GAL2-R knockdown does not affect the number of perforant path stimulations required for initiating status epilepticus but significantly increases the seizure severity during the ongoing status. In conclusion, our data support a specific role of GAL2-R but not of GAL3-R in mediating the anticonvulsive actions of endogenous galanin. |
