| First Author | Chapman AG | Year | 1996 |
| Journal | Epilepsy Res | Volume | 26 |
| Issue | 1 | Pages | 25-35 |
| PubMed ID | 8985683 | Mgi Jnum | J:37962 |
| Mgi Id | MGI:85355 | Doi | 10.1016/s0920-1211(96)00036-8 |
| Citation | Chapman AG, et al. (1996) Anticonvulsant effect of reduced NMDA receptor expression in audiogenic DBA/2 mice. Epilepsy Res 26(1):25-35 |
| abstractText | Pretreatment of DBA/2 mice (n = 14-15 per group) with an 18-mer antisense probe to the NMDA-receptor submit NR1 (2 x 1 micrograms, or 2 x 83 pmol, NR1 antisense probe intracerebroventricularly, -29 and -7 h before testing for seizure response) resulted in almost complete suppression of sound-induced clonic seizures. A saline-treated group gave a 100% seizures response, while the group treated with NR1 antisense probe gave a 7% seizure response to the sound stimulus. The group treated with NR1 nonsense-probe showed no anticonvulsant protection (93% seizure response). The anticonvulsant protection observed following NR1 antisense administration was of relatively short duration, with seizure response gradually returning to control levels 12 to 24 h following the termination of antisense administration. When NR1 receptor levels were assessed by receptor autoradiography ([3H]-MK 801 and -CGP 39653 binding) in the same groups of mice, significant (20%) reductions in NR1 levels were observed in the retrosplenial cortex and the overall cortex. The seizure-induced expression of c-fos and NGFI-A in thalamus, hypothalamus, inferior colliculus and medical geniculate seen in vehicle- and NR1 nonsense-treated mice was completely blocked by NR1 antisense pretreatment. |
