Tags

Type your tag names separated by a space and hit enter

Neuroprotective and neurodestructive functions of nitric oxide after spinal cord hemisection.
Exp Neurol. 2000 Feb; 161(2):472-80.EN

Abstract

Nitric oxide (NO) may subserve different functions in different central neurons subjected to axotomy. The difference may depend on whether the neurons basally express neuronal nitric oxide synthase (nNOS), a biosynthetic enzyme of NO. This is supported by our previous finding that suggests the differential role of NO in neurons of nucleus dorsalis (ND) and red nucleus (RN) which have different basal expression of nNOS. This study aimed to establish firmly the functions of NO, as revealed by nNOS immunoreactivity and nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) histochemistry, by the administration of endogenous NO donor, l-arginine (l-arg), and NOS inhibitor, l-N(G)-nitroarginine methyl ester (l-NAME). To relate the role of NO to glutamate receptors (GluR), the distributions of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) and N-methyl-d-aspartate receptor (NMDAR) in the two nuclei were revealed by immunohistochemical techniques. nNOS immunoreactivity was void in ND neurons, but expressed weakly in the RN normally. It was induced in ipsilateral ND neurons and upregulated on both sides of RN after spinal cord hemisection. Neuronal loss in the ipsilateral ND was augmented by l-arg, but reduced by l-NAME. In the contralateral RN, l-arg attenuated neuronal loss. NMDAR1 was present in most neurons in ND. After axotomy, some NMDAR1 immunoreactive neurons of the ipsilateral ND were induced to express NOS, whereas RN neurons showed strong staining for NMDAR1 and all the AMPA subunits. Most of the NOS-positive neurons in the RN were coexistent with GluR2 in normal rats and those subjected to axotomy. The present data demonstrated that NO exerted neurodestructive function in the non-NOS-containing ND neurons characterized by NMDAR as the predominant glutamate receptor. NO might be beneficial to the NOS-containing RN neurons. This could be attributed to the presence of GluR2. Possible diverse synthesizing pathways of NO in two different central nuclei were suggested from the observation that NOS was colocalized with NADPH-d in ND neurons, but not in RN neurons.

Authors+Show Affiliations

Department of Anatomy, Faculty of Medicine, The National University of Singapore, 10 Kent Ridge Crescent, Singapore, 119260.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

10686069

Citation

Xu, M, et al. "Neuroprotective and Neurodestructive Functions of Nitric Oxide After Spinal Cord Hemisection." Experimental Neurology, vol. 161, no. 2, 2000, pp. 472-80.
Xu M, Ng YK, Leong SK. Neuroprotective and neurodestructive functions of nitric oxide after spinal cord hemisection. Exp Neurol. 2000;161(2):472-80.
Xu, M., Ng, Y. K., & Leong, S. K. (2000). Neuroprotective and neurodestructive functions of nitric oxide after spinal cord hemisection. Experimental Neurology, 161(2), 472-80.
Xu M, Ng YK, Leong SK. Neuroprotective and Neurodestructive Functions of Nitric Oxide After Spinal Cord Hemisection. Exp Neurol. 2000;161(2):472-80. PubMed PMID: 10686069.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neuroprotective and neurodestructive functions of nitric oxide after spinal cord hemisection. AU - Xu,M, AU - Ng,Y K, AU - Leong,S K, PY - 2000/2/25/pubmed PY - 2000/4/1/medline PY - 2000/2/25/entrez SP - 472 EP - 80 JF - Experimental neurology JO - Exp Neurol VL - 161 IS - 2 N2 - Nitric oxide (NO) may subserve different functions in different central neurons subjected to axotomy. The difference may depend on whether the neurons basally express neuronal nitric oxide synthase (nNOS), a biosynthetic enzyme of NO. This is supported by our previous finding that suggests the differential role of NO in neurons of nucleus dorsalis (ND) and red nucleus (RN) which have different basal expression of nNOS. This study aimed to establish firmly the functions of NO, as revealed by nNOS immunoreactivity and nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) histochemistry, by the administration of endogenous NO donor, l-arginine (l-arg), and NOS inhibitor, l-N(G)-nitroarginine methyl ester (l-NAME). To relate the role of NO to glutamate receptors (GluR), the distributions of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) and N-methyl-d-aspartate receptor (NMDAR) in the two nuclei were revealed by immunohistochemical techniques. nNOS immunoreactivity was void in ND neurons, but expressed weakly in the RN normally. It was induced in ipsilateral ND neurons and upregulated on both sides of RN after spinal cord hemisection. Neuronal loss in the ipsilateral ND was augmented by l-arg, but reduced by l-NAME. In the contralateral RN, l-arg attenuated neuronal loss. NMDAR1 was present in most neurons in ND. After axotomy, some NMDAR1 immunoreactive neurons of the ipsilateral ND were induced to express NOS, whereas RN neurons showed strong staining for NMDAR1 and all the AMPA subunits. Most of the NOS-positive neurons in the RN were coexistent with GluR2 in normal rats and those subjected to axotomy. The present data demonstrated that NO exerted neurodestructive function in the non-NOS-containing ND neurons characterized by NMDAR as the predominant glutamate receptor. NO might be beneficial to the NOS-containing RN neurons. This could be attributed to the presence of GluR2. Possible diverse synthesizing pathways of NO in two different central nuclei were suggested from the observation that NOS was colocalized with NADPH-d in ND neurons, but not in RN neurons. SN - 0014-4886 UR - https://www.unboundmedicine.com/medline/citation/10686069/Neuroprotective_and_neurodestructive_functions_of_nitric_oxide_after_spinal_cord_hemisection_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4886(99)97278-3 DB - PRIME DP - Unbound Medicine ER -