Increased expression of neuronal nitric oxide synthase in astrocytes and macrophages in the spinal cord of Lewis rats with autoimmune encephalomyelitis.
- Author:
Taekyun SHIN
1
Author Information
1. Department of Veterinary Medicine, Cheju National University, Jeju 690-756, Republic of Korea. shint@cheju.cheju.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- MeSH:
Animals;
Astrocytes/*enzymology;
Blotting, Western;
Encephalomyelitis, Autoimmune, Experimental/drug therapy/*enzymology;
Enzyme Inhibitors/therapeutic use;
Immunohistochemistry;
Indazoles/therapeutic use;
Macrophages/*enzymology;
Male;
Nitric Oxide Synthase/antagonists&inhibitors/*metabolism;
Rats;
Rats, Inbred Lew;
Spinal Cord/cytology/*enzymology
- From:Journal of Veterinary Science
2001;2(3):195-199
- CountryRepublic of Korea
- Language:English
-
Abstract:
Neuronal nitric oxide synthase (nNOS) is constitutively expressed in neurons of the central nervous system, where it plays a physiological role in neurotransmission. In this study, we examined the functional role of nNOS in experimental autoimmune encephalomyelitis(EAE). The effects of the specific nNOS inhibitor 7-nitroindazole on normal and EAE rats were studied by immunohistochemistry and Western blot analysis. We found that nNOS is constitutively expressed in the spinal cords of normal rats, whilst in the spinal cords of EAE rats, nNOS expression slightly increased, concomitant with the infiltration of T cells and macrophages. Immunohistochemical studies showed that nNOS expression in macrophages and astrocytes increased at the peak stage of EAE and declined thereafter. Treatment with 7-nitroindazole (30 mg/kg) significantly delayed the onset of EAE paralysis, but had no effect on either the incidence or the severity of the paralysis. These findings suggest that nNOs inhibition has a limited role in the induction of rat EAE, and that constitutive nNOS in the spinal cord functions as a novel neurotransmitter, rather than a pro-inflammatory agent.
