The role of XXXX in @entity302 and other CNS disorders.

@entity1 @entity410 @entity2227 @entity1024 @entity1625 @entity2806 @entity63 @entity535 @entity75 @entity1372 @entity492 @entity143 @entity302 @entity35 @entity2812 @entity130
@entity2227 is the principal excitatory neurotransmitter in the brain and, as such, it inevitably plays a role in the initiation and spread of @entity410 activity. It also plays a critical role in epileptogenesis. The process of "kindling" limbic @entity410 in rodents by repeated electrical stimulation is dependent on activation of @entity1024 ( @entity143 ) receptors. The function of these receptors is enhanced in the hippocampus of kindled @entity35 and in the cerebral cortex of @entity1 with @entity1625 . Microdialysis studies show an increase in the extracellular concentration of @entity2227 and @entity492 before or during @entity410 onset, suggesting that either enhanced @entity535 release or impaired uptake contributes to @entity410 initiation. @entity2227 antagonists selective for @entity143 or non- @entity143 receptors are potent anticonvulsants when given systemically in a wide variety of animal models of @entity302 . They are of limited efficacy against kindled @entity410 in @entity35 and (on the basis of preliminary evidence) in @entity1 with drug-refractory complex partial @entity410 . Cognitive side effects appear to be a significant problem with competitive, as well as noncompetitive, @entity143 antagonists. @entity2227 receptor antagonists provide significant protection against @entity75 following global or focal @entity2806 or acute @entity130 in rodent models. Anticonvulsant compounds of the @entity2812 type, which act on @entity1372 channels and reduce @entity63 -induced @entity2227 release, are cerebroprotective in rodent @entity63 models and are free from the cognitive side effects of @entity143 -receptor antagonists.
