Electrophysiological actions of XXXX on @entity1024 receptor-mediated responses in @entity35 hippocampus in vitro.

@entity1024 @entity1025 @entity1249 @entity73273 @entity1372 @entity13981 @entity1023 @entity143 @entity3174 @entity140 @entity35 @entity3390
1. The effects of the anticonvulsant, @entity3174 , have been examined on @entity1024 ( @entity143 ) receptor-mediated population spikes in the @entity1249 region of the @entity35 hippocampus in vitro. 2. The 'conventional' ( @entity140 receptor-mediated) @entity1249 population spike, evoked by electrical stimulation of the Schaffer collateral/commissural pathway, was abolished by 5 min treatment with 5 x 10(-6) M @entity1023 ( @entity1023 ), after which superfusion with a nominally @entity1025 -free Krebs solution (containing 5 x 10(-6) M CNQX) led to the appearance of an epileptiform population spike which was fully developed by 30-40 min. 3. The epileptiform population spike was abolished by the non-competitive @entity143 antagonist, @entity3390 (1 x 10(-6) M, 20-30 min) and inhibited by the competitive @entity143 receptor antagonist, @entity73273 (IC50 for reducing the amplitude of the first spike in the train = 8.3 x 10(-7) M), demonstrating that the response was mediated by activation of @entity143 receptors and validating its use as an assay for antagonists acting at the @entity143 receptor/channel complex. 4. @entity3174 (0.1, 0.3 and 1 x 10(-4) M applied cumulatively for 30 min at each concentration) failed to inhibit the @entity143 receptor-mediated epileptiform population response (n = 7 slices). 5. @entity3174 (3 x 10-6 M to 1 x 10-4M) attenuated the effects of the @entity1372 channel activator, @entity13981 (2 x 10-6 M), on the CAl population spike amplitude (recorded in normal Krebs solution),indicating that the previously observed lack of effect of @entity3174 on the @entity143 receptor-mediated response was not due to impaired access of @entity3174 to the biophase.6. These data support the conclusion that antagonism of @entity143 receptor-mediated events is not a pharmacological property of @entity3174 and that such an action is therefore unlikely to contribute to the anticonvulsant activity of this drug.
