This study examined the effect of
1,3-butanediol on the selective loss of CA1 pyramidal neurons following a short period of near-complete forebrain
ischemia. Injection of 55 mmol 1,3-butanediol/kg
body weight at 24 h of recirculation and again at 36 h following 10 min of forebrain
ischemia markedly reduced damage to CA1 neurons examined at 72 h of recirculation compared with that in saline-treated rats. Comparable treatment with
ethanol did not cause significant protection. Neuronal loss 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 and 15 min of
ischemia is consistent with a number of previous studies, indicating that the processes leading to loss of CA1 neurons are modified when the ischemic period is extended. Previous findings that
1,3-butanediol reduced damage in other
ischemia-susceptible neuronal subpopulations but not in CA1 neurons most likely reflected the longer period of
ischemia which was used. The results of the present investigation demonstrate that administration of
1,3-butanediol offers a novel approach for interfering with post-ischemic loss of CA1 neurons following a brief ischemic period which is effective even when initiated after prolonged recirculation periods.