The cellular damage over time and the alterations of neuronal subtypes was characterized in the striatum after 90-min
middle cerebral artery occlusion and reperfusion in rats. We investigated the immunohistochemical alterations of
choline acetyltransferase (ChAT)-positive (
cholinergic-positive),
gamma-aminobutyric acid (
GABA)ergic
parvalbumin (PV)-positive, GABAergic nNOS (
neuronal nitric oxide synthase)-positive interneurons, neuronal nuclei (NeuN)-positive spiny projection neurons,
glial fibrillary acidic protein (GFAP)-positive strocytes and microglial response factor-1 (MRF-1)-positive microglia in the striatum after focal
cerebral ischemia in rats. In the present study, transient focal
cerebral ischemia in rats caused severe damage against interneurons as well as spiny projection neurons in the striatum. In contrast, a significant increase in the number of GFAP-immunopositive astrocytes was observed in the ipsilateral striatum 15 days after focal
cerebral ischemia. Furthermore, a significant increase of MRF-1 immunoreactivity was observed in microglia of the ipsilateral striatum 7 days and 15 days after focal
cerebral ischemia. Among three types of
cholinergic interneurons, GABAergic PV-positive interneurons and GABAergic nNOS-positive interneurons, the severe damage of
cholinergic and GABAergic PV-positive interneurons was more pronounced than that of GABAergic nNOS-positive interneurons after transient focal
cerebral ischemia in rats. Furthermore, the present results suggest that GABAergic nNOS-positive interneurons in the striatum after focal
cerebral ischemia undergo cellular death in a delayed manner.