DELAYED TREATMENT WITH 1,3-BUTANEDIOL REDUCES LOSS OF CA1 NEURONS IN THE HIPPOCAMPUS OF RATS FOLLOWING BRIEF FOREBRAIN ISCHEMIA

This study examined the effect of 1,3-butanediol on the selective loss of CA1 pyramidal neurons following a short period of near-complete fo rebrain ischemia. Injection of 55 mmol 1,3-butanediol/kg body weight a t 24 h of recirculation and again at 36 h following 10 min of forebrai n ischemia markedly reduced damage to CA1 neurons examined at 72 h of recirculation compared with that in saline-treated rats. Comparable tr eatment with ethanol did not cause significant protection. Neuronal lo ss was also not reduced by 1,3-butanediol treatment when the ischemic period was extended to 15 min or by single treatments at 24 h or 36 h following 10 min of ischemia. However, a single treatment 5 min after reversal of 10 min of ischemia was effective in ameliorating cell loss . The difference in effectiveness of 1,3-butanediol following 10 min a nd 15 min of ischemia is consistent with a number of previous studies, indicating that the processes leading to loss of CA1 neurons are modi fied when the ischemic period is extended. Previous findings that 1,3- butanediol reduced damage in other ischemia-susceptible neuronal subpo pulations but not in CA1 neurons most likely reflected the longer peri od of ischemia which was used. The results of the present investigatio n demonstrate that administration of 1,3-butanediol offers a novel app roach for interfering with post-ischemic loss of CA1 neurons following a brief ischemic period which is effective even when initiated after prolonged recirculation periods.