Immunocytochemical localization of endothelial nitric oxide synthase (e-NOS) and inducible nitric oxide synthase (i-NOS) in rat neurohypophysis after transient cerebral ischemia.
The expression pattern of endothelial and inducible forms of nitric oxide synthase (e-NOS, i-NOS) in rat neurohypophysis after transient ischemia was investigated using post-embedding immunogold method. We demonstrate that ischemia induced an early (10 min) expression of e-NOS not only in endothelium but also in the mast cells. Expression of i-NOS was almost exclusively confined to glial cells (pituicytes) and perivascular macrophages of experimental animals, and peaked at 24 h after ischemia. This evidence indicates that NO plays a significant role in mechanisms of cerebral ischemia. Taking into account the known beneficial role of e-NOS in ischemia it is likely that mast cells protect against post-ischemic brain damage by producing vasodilatation via nitric oxide. In contrast, cerebral macrophages and pituicytes may mediate neuronal and endothelial damage in late period after ischemia in rat neurohypophysis.
Gajkowska
B
B
Laboratory of the Ultrastructure of the Nervous System, Medical Research Centre, Polish Academy of Sciences, Warszawa, Poland.
Viron
A
A
Cholewiński
M
M
D000818:Animals; D001921:Brain / Q000098:blood supply* / Q000201:enzymology*; D002536:Cerebral Arteries / Q000201:enzymology*; D004727:Endothelium / Q000201:enzymology; D004790:Enzyme Induction; D007150:Immunohistochemistry; D002546:Ischemic Attack, Transient / Q000201:enzymology*; D008297:Male; D008407:Mast Cells / Q000201:enzymology / Q000648:ultrastructure; D019001:Nitric Oxide Synthase / Q000096:biosynthesis*; D010904:Pituitary Gland, Posterior / Q000201:enzymology* / Q000648:ultrastructure; D051381:Rats; D017208:Rats, Wistar; D013268:Stimulation, Chemical; D014664:Vasodilation / Q000502:physiology
D019001:Nitric Oxide Synthase