We examined alterations in Na(+)-K(+)-Cl(-) cotransporter 1 (NKCC1) immunoreactivity following ischemia. Twelve hours after ischemia, NKCC1 immunoreactivity in the CA1 region and in the hilar region was significantly diminished. Twenty-four hours after ischemia, NKCC1 immunoreactivity was intensified in these hippocampal regions as well as CA2-3. Two days after ischemia, NKCC1 immunoreactivity in the CA1 and the hilar neurons had disappeared, although in the CA2-3 and the granule cell layer NKCC1 immunoreactivities had recovered to the sham level. This finding suggests that NKCC1 may play an important role in the ischemic neuronal injury induced by excitotoxicity as well as neuronal edema.