Abstract
G A A b st ra ct s 10d, EAAT2 activator) normalized the VMR to CRD in VH rats. On the other hand, microinfusion of ACC with dihydrokainate (20 mM for 10 d, EAAT2 blocker) in normal rats resulted in enhanced VMR responses similar to those observed in VH rats. In conclusion, we showed that downregulation of EAAT2 in ACC occurs in the VH state. This appears to be negatively regulated by the ET system. Delayed clearance of extracellular glutamate as a result of reduced expression of EAAT2 plays a critical role in the pathogenesis of visceral hypersensitivity. Agents that modulate glutamate reuptake system may provide new therapeutic options to the treatment of visceral hypersensitivity disorders.
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