Abstract
We investigated the role of the NMDA receptor complex in DMCM (methyl-6,7-dimethoxy-4-ethyl-β-carboline-3-carboxylate)-induced seizures in mice. The seizure threshold of DMCM was evaluated using an i.v. infusion technique. Pretreatment with the non-competitive NMDA receptor antagonist MK-801 ((+)-5-methyl-10,11-dihydro-5H-dibenzo(a,d)cycloheptan-5,10-imine maleate) or phencyclidine (PCP) significantly increased the seizure threshold for DMCM. Furthermore, the seizure threshold of DMCM was increased by intracerebroventricular (i.c.v.), but not intrathecal (i.t.), pretreatment with MK-801. Moreover, 7-chlorokynurenic acid, a glycine site antagonist, also increased the seizure threshold of DMCM, whereas ifenprodil, a non-competitive polyamine site antagonist, did not. These findings indicate that the ion-channel binding site and the glycine binding site on the NMDA receptor complex in the brain may be involved in the expression of seizures induced by DMCM.
| Original language | English |
|---|---|
| Pages (from-to) | 603-606 |
| Number of pages | 4 |
| Journal | NeuroReport |
| Volume | 8 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - Jan 1 1997 |
| Externally published | Yes |
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All Science Journal Classification (ASJC) codes
- Neuroscience(all)
Cite this
Role of the NMDA receptor complex in DMCM-induced seizure in mice. / Makoto, Tsuda; Suzuki, Tsutomu; Misawa, Miwa.
In: NeuroReport, Vol. 8, No. 3, 01.01.1997, p. 603-606.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Role of the NMDA receptor complex in DMCM-induced seizure in mice
AU - Makoto, Tsuda
AU - Suzuki, Tsutomu
AU - Misawa, Miwa
PY - 1997/1/1
Y1 - 1997/1/1
N2 - We investigated the role of the NMDA receptor complex in DMCM (methyl-6,7-dimethoxy-4-ethyl-β-carboline-3-carboxylate)-induced seizures in mice. The seizure threshold of DMCM was evaluated using an i.v. infusion technique. Pretreatment with the non-competitive NMDA receptor antagonist MK-801 ((+)-5-methyl-10,11-dihydro-5H-dibenzo(a,d)cycloheptan-5,10-imine maleate) or phencyclidine (PCP) significantly increased the seizure threshold for DMCM. Furthermore, the seizure threshold of DMCM was increased by intracerebroventricular (i.c.v.), but not intrathecal (i.t.), pretreatment with MK-801. Moreover, 7-chlorokynurenic acid, a glycine site antagonist, also increased the seizure threshold of DMCM, whereas ifenprodil, a non-competitive polyamine site antagonist, did not. These findings indicate that the ion-channel binding site and the glycine binding site on the NMDA receptor complex in the brain may be involved in the expression of seizures induced by DMCM.
AB - We investigated the role of the NMDA receptor complex in DMCM (methyl-6,7-dimethoxy-4-ethyl-β-carboline-3-carboxylate)-induced seizures in mice. The seizure threshold of DMCM was evaluated using an i.v. infusion technique. Pretreatment with the non-competitive NMDA receptor antagonist MK-801 ((+)-5-methyl-10,11-dihydro-5H-dibenzo(a,d)cycloheptan-5,10-imine maleate) or phencyclidine (PCP) significantly increased the seizure threshold for DMCM. Furthermore, the seizure threshold of DMCM was increased by intracerebroventricular (i.c.v.), but not intrathecal (i.t.), pretreatment with MK-801. Moreover, 7-chlorokynurenic acid, a glycine site antagonist, also increased the seizure threshold of DMCM, whereas ifenprodil, a non-competitive polyamine site antagonist, did not. These findings indicate that the ion-channel binding site and the glycine binding site on the NMDA receptor complex in the brain may be involved in the expression of seizures induced by DMCM.
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U2 - 10.1097/00001756-199702100-00005
DO - 10.1097/00001756-199702100-00005
M3 - Article
C2 - 9106731
AN - SCOPUS:0030936493
VL - 8
SP - 603
EP - 606
JO - NeuroReport
JF - NeuroReport
SN - 0959-4965
IS - 3
ER -