Tuyển tập các báo cáo nghiên cứu khoa học quốc tế về bệnh thú y đề tài: Increased expression of neuronal nitric oxide synthase in astrocytes and macrophages in the spinal cord of Lewis rats with autoimmune encephalomyelitis" | J. Vet. Sá. 2001 2 3 195-199 D1S0HSK9EBHIỊỊBDDHI Veterinary Science Increased expression of neuronal nitric oxide synthase in astrocytes and macrophages in the spinal cord of Lewis rats with autoimmune encephalomyelitis Taekyun Shin Department of Veterinary Medicine Cheju National University Jeju 690-756 Republic of Korea 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 mgkg significantly delayed the onset oỉ 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. Key word neuronal nitric oxide synthase autoimmune encephalomyelitis macrophages INTRODUCTION Experimental autoimmune encephalomyelitis EAE is a T cell-mediated autoimmune disease of the central nervous system CNS that is used as a model for human demyelinating diseases such as multiple sclerosis. The clinical course of EAE is characterized by weight loss ascending progressive paralysis and spontaneous recovery. These symptoms coincide with an inflammatory response that is characterized by the infiltration
