5-HT2C receptors inhibit and 5-HT1A receptors activate the generation of spike-wave discharges in a genetic @entity35 model of XXXX .

@entity15015 @entity905 @entity837 @entity21483 @entity2048 @entity750 @entity10098 @entity35
The present study was conducted to investigate the role of @entity750 (2C) and @entity750 (1A) receptors in the generation of spike-wave discharges (SWD) in the genetic @entity2048 model @entity35 Albino Glaxo @entity35 from Rijswijk, Netherlands (WAG/Rij @entity35 ). We have determined the effects of the @entity750 (2C) receptor preferring agonist @entity15015 (m-CPP), the selective @entity750 (2C) receptor antagonist @entity21483 , the selective @entity750 (1A) receptor antagonist @entity10098 , two selective @entity750 re-uptake inhibitors (SSRI, @entity905 and @entity837 ) and their combinations in this model. The @entity750 (2C) agonist @entity15015 caused marked, dose-dependent decreases in the cumulative duration and number of SWD administered either intraperitoneally (0.9 and 2.5 mg/kg) or intracerebroventricularly (0.05 and 0.1 mg/kg). Treatment with @entity21483 (0.2 mg/kg, ip) alone failed to cause any significant change in SWD compared to vehicle. Pretreatment with @entity21483 (0.2 mg/kg, ip) eliminated the effects of m-CPP on SWD. @entity905 (5.0 mg/kg, ip) alone caused moderate increase in SWD. After pretreatment with @entity21483 , the effect of @entity905 was significantly enhanced. The combination of @entity21483 and @entity837 (2.5 mg/kg, ip) caused a similar effect, namely an increase in SWD. In contrast, pretreatment with @entity10098 significantly attenuated the effect of @entity905 . In conclusion, these results indicate that the increase in endogenous @entity750 produces a dual effect on SWD; the inhibition of epileptiform activity is mediated by @entity750 (2C), the activation by @entity750 (1A) receptors.
