Rat hippocampal slices were subjected to hypoxia and/or hypoglycemia for 10 min, and free fatty acids released in CA1 and CA3 regions were separately analyzed. Fatty acid accumulation in CA1 was not so significant under hypoglycemia, but very prominent under hypoxia. Free fatty acid levels in CA3 were much less than those in CA1 even under hypoxia plus hypoglycemia. This observation seems to be consistent with the selective vulnerability of CA1 neurons seen in in vivo ischemia. The decreasing order of accumulation of free fatty acid species in CA1 was C16:0>C18:0>C18:1>C20:4>C22:6. The increment fold as compared to control level was decreasing as follows: C22:6, 28 times; C20:4, 13 times, C18:1, 10 times; C18:0=C 16:0, 3 times. The present experimental conditions using hippocampal slices provided a good in vitro model to prove the selective hypoxic damages of the CA1 subfield in terms of free fatty acid release in association with the membrane degradation.