| First Author | Rinaldi D | Year | 2001 |
| Journal | Behav Brain Res | Volume | 125 |
| Issue | 1-2 | Pages | 159-65 |
| PubMed ID | 11682107 | Mgi Jnum | J:72741 |
| Mgi Id | MGI:2153508 | Doi | 10.1016/s0166-4328(01)00293-5 |
| Citation | Rinaldi D, et al. (2001) Unexpected absence of correlation between the genetic mechanisms regulating beta-carboline-induced seizures and anxiety manifested in an elevated plus-maze test. Behav Brain Res 125(1-2):159-65 |
| abstractText | Among the ligands of the benzodiazepine site, one can mention the benzodiazepines as agonists and some beta-carbolines (e.g. methyl-beta-carboline-3-carboxylate, abbreviated hereafter beta-CCM) as inverse agonists. Most benzodiazepines and beta-carbolines act on processes involved in memory, anxiety, and convulsions with opposite physiological effects. Since these molecules have influences on both anxiety and convulsions, we predicted that there would exist a genetic correlation between anxiety evaluated in an elevated plus-maze and susceptibility to beta-CCM-induced seizures. Using inbred strains of mice, the genetic correlation was estimated with the Hegmann and Possidente model. An absence of genetic correlation was found, showing that the mechanisms responsible for basal anxiety measured with the elevated plus-maze test and those leading to susceptibility to beta-CCM-induced seizures do not share the same genetic pathways. |
