Time course of nitric oxide synthase activity in neuronal, glial, and endothelial cells of rat striatum following focal cerebral ischemia

Cell Mol Neurobiol. 1995 Jun;15(3):341-9. doi: 10.1007/BF02089944.


1. The time course of nitric oxide synthase (NOS) activity in neuronal, endothelial, and glial cells in the rat striatum after middle cerebral artery (MCA) occlusion and reperfusion was examined using a histochemical NADPH-diaphorase staining method. 2. In sham-operated rats, neuronal cells of the striatum exhibited strong NADPH-diaphorase activities. When rats were subjected to MCA occlusion for 1 hr, neuronal damage, including neurons with positive NADPH-diaphorase activities, appeared in the striatum at 3 hr after and extended to all areas of the striatum 3-4 days after reperfusion. 3. NADPH-diaphorase activities in the endothelial cells increased in the damaged part of striatum from 3 hr after, peaked at 1-2 days after MCA occlusion/reperfusion, then gradually decreased. 4. In parallel with the development of neuronal damage, some astrocytes and a high proportion of microglia/macrophages located in the perisite and in the center of the damaged striatum, respectively, exhibited a moderate to high level of NADPH-diaphorase activities. Most of these activities disappeared at 4 days after MCA occlusion. 5. These findings provided evidence that an inappropriate activation of NOS in endothelial cells and microglia/macrophages, in response to MCA occlusion/reperfusion, is closely associated with initiation and progression of ischemic neuronal injury in the striatum.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Astrocytes / pathology
  • Cerebral Arteries
  • Corpus Striatum / blood supply*
  • Corpus Striatum / enzymology*
  • Corpus Striatum / pathology
  • Endothelium, Vascular / enzymology*
  • Endothelium, Vascular / pathology
  • Glial Fibrillary Acidic Protein / analysis
  • Immunohistochemistry
  • Ischemic Attack, Transient / enzymology*
  • Ischemic Attack, Transient / pathology
  • Kinetics
  • Male
  • NADPH Dehydrogenase / metabolism
  • Neuroglia / enzymology*
  • Neuroglia / pathology
  • Neurons / enzymology*
  • Neurons / pathology
  • Nitric Oxide Synthase / metabolism*
  • Rats
  • Rats, Wistar
  • Reperfusion
  • Time Factors


  • Glial Fibrillary Acidic Protein
  • Nitric Oxide Synthase
  • NADPH Dehydrogenase