ELECTROCONVULSIVE SHOCK INCREASES INTERSTITIAL CONCENTRATIONS OF URIC-ACID IN THE RAT-BRAIN

This study examined the effects of electroconvulsive shock (ECS) on st riatal interstitial concentrations of the purine metabolite uric acid (UA) using microdialysis in freely moving rats. UA increased to about 200% of baseline following ECS. Intense seizure activity induced by th e convulsant agent flurothyl also resulted in a two-fold increase of U A concentrations suggesting that the ECS-induced UA increase is relate d to the seizure activity per se. Local administration of tetrodotoxin or perfusion with a Ca2+-free solution failed to affect the basal or the ECS-induced increase in UA concentrations. These data indicate tha t both the basal and the stimulated interstitial concentrations of uri c acid are not dependent upon neuronal activity and exocytotic release . The UA response to ECS appears to be refractory to a second ECS deli vered 2 but not 24 h after the first. Intrastriatal infusion of allopu rinol (1 mM), an inhibitor of UA synthesis, decreased basal UA concent rations to 26% but did not influence the ECS-induced UA increase. Syst emic injection of allopurinol (20 mg/kg, i.p.) decreased basal UA conc entrations to 25% and prevented the ECS-induced UA elevation. ECS also increased serum concentrations of UA to almost 200% of baseline. Allo purinol (20 mg/kg, i.p.) markedly decreased serum UA concentrations to non-detectable levels and completely abolished the ECS-induced increa se. The estimated concentration difference between blood and brain int erstitial UA strongly suggests that ECS-induced increase in brain inte rstitial UA concentrations is of peripheral origin possibly due to dis ruption of the blood brain barrier during seizure activity.