By observing the ultrastructural intracellular Ca²⁺ distribution with Ca²⁺-oxalate-pyroantimonate method, we examined whether the protective mechanism of the nitric oxide (NO) synthase inhibitor, N^ω-nitro-l-arginine (LNNA), involves change of the intracellular Ca²⁺ movement in delayed neuronal death (DND) in gerbil hippocampal CA1 neurons following 5-min forebrain ischemia. In the group intraventricularly administered 5.0 mg/ml LNNA, 15 min after reperfusion the intracellular Ca²⁺ deposits and the mitochondrial Ca²⁺ uptake index increased to levels similar to those in the control group administered only artificial cerebro-spinal fluid, but by 180 min after reperfusion they had returned to the preischemic level. By 15 min after reperfusion Ca²⁺ deposits in the endoplasmic reticulum (ER) had almost disappeared in both groups, but at 180 min of reperfusion, the ER in only the LNNA group showed Ca²⁺ deposits. It is suggested that the neuronal toxicity of NO involves the dysfunction of the intracellular Ca²⁺ transport system including the mitochondria and ER.