scholarly journals Huntingtin-associated protein (HAP1): discrete neuronal localizations in the brain resemble those of neuronal nitric oxide synthase.

1996 ◽  
Vol 93 (10) ◽  
pp. 4839-4844 ◽  
Author(s):  
X. J. Li ◽  
A. H. Sharp ◽  
S. H. Li ◽  
T. M. Dawson ◽  
S. H. Snyder ◽  
...  
2015 ◽  
Vol 70 (5) ◽  
pp. 608-613 ◽  
Author(s):  
V. M. Chertok ◽  
A. E. Kotsyuba ◽  
M. S. Startseva

Objective: To conduct a comparative study of the structural organization of internuclear interneurons involved in the metabolism of nitrogen monoxide, hydrogen sulphide and carbon monoxide in the caudal brain stem humans.Methods: The cross-sectional study was performed. We used histochemical and immunohistochemical methods to study the internuclear interneurons expressing neuronal nitric oxide synthase, cystathionine β-synthase and heme oxygenase-2 which are located between the giant and small cell reticular nuclei (cell group 1), small cell reticular nucleus and the nucleus of the solitary tract (cell group 2) or is surrounded by reticular lateral nucleus (cell group 3).Results: The work was carried out on the corpses of 6 men 18–44 years old who died from causes unrelated to the damage of the central nervous system. We revealed the differences between internuclear organization and intranuclear interneurons and local structural features of internuclear interneurons that are more clearly visible between the cell group 1 including a relatively large number of large neurons and cell groups 2 and 3 (р 0,001). In the latter two groups small cells with high concentrations of the neuronal nitric oxide synthase and heme oxygenase-2 dominated.Conclusion: Despite the fact that the number of internuclear interneurons significantly is less than the number of intranuclear cells, they have structural prerequisites to control integration processes in the brain. Internuclear interneurons produce gasotransmitters and classical mediators of nerve impulse, form a local chain of interneurons between vasomotor nuclei, share many links with the above and the lower parts of the brain.


Author(s):  
Nymphaea Arora ◽  
Vikash Prashar ◽  
Tania Arora ◽  
Randeep Sidhu ◽  
Anshul Mishra ◽  
...  

Introduction: Nitric oxide (NO) is a diatomic free radical gaseous molecule that is formed from L-arginine through NOS (Nitric oxide synthase) catalyzed reaction. NO controls vascular tone (hence blood pressure), insulin secretion, airway tone, and peristalsis and is involved in angiogenesis (growth of new blood vessels) and in the development of the nervous system. In the CNS, NO is an important messenger molecule, which is involved in various major functions in the brain. NOS has been classified into three isoforms which include nNOS (neuronal NOS), eNOS (endothelial NOS), and iNOS (inducible NOS). NOS1 is localized on chromosome 12, consisting of 1434 amino acids and 161 KDa molecular weight. nNOS is involved in synaptic transmission, regulating the tone of smooth muscles, penile erection. We studied NOS1 gene and protein network analysis through in silico techniques as human nNOS sequence was fetched from GenBank, and its homologous sequences were retrieved through BLAST search. Moreover, the results of this study exploit the role of NOS1 in various pathways, which provide ways to regulate it in various neurodegenerative diseases. Background: Previous research has revealed the role of Nitric Oxide (NO) formed from L-arginine through NOS (Nitric Oxide Synthase) as a physiological inter/intracellular messenger in the central as well as the peripheral nervous system. The diverse functions of NOS include insulin secretion, airway tone, vascular tone regulation, and in the brain, it is involved in differentiation, development, synaptic plasticity, and neurosecretion. Objective: The objective of this study is to unravel the role of neuronal Nitric Oxide Synthase (nNOS) in different pathways and its involvement as a therapeutic target in various neurodegenerative disorders, which can surely provide ways to regulate its activity in different aspects. Materials and Methods: In this study, we employed various bioinformatics tools and databases, initiating the study by fetching the neuronal Nitric Oxide Synthase (nNOS) sequence(GenBank) to find its homologous sequences(BLAST) and then exploring its physical properties and post-translational modifications, enhancing the research by network analysis(STRING), leading to its functional enrichment(Panther). Results : The results positively support the hypothesis of its role in various pathways related to neurodegeneration., Its interacting partners are the probable therapeutic targets of various neurodegenerative diseases focusing on specifically multi-target analysis. Conclusion: This study considered the evolutionary trend of physical, chemical, and biological properties of NOS1 through different phyla. The neuronal Nitric Oxide Synthase (nNOS), being one of the three isoforms of NOS (Nitric Oxide Synthase), is found to be involved in more pathways than just forming Nitric Oxide. This research provides the base for further neurological research.


2012 ◽  
Vol 295 (3) ◽  
pp. 504-514 ◽  
Author(s):  
Shucai Ling ◽  
Jing Zhou ◽  
John A. Rudd ◽  
Zhiying Hu ◽  
Marong Fang

1995 ◽  
Vol 15 (5) ◽  
pp. 766-773 ◽  
Author(s):  
Paul A. T. Kelly ◽  
Isobel M. Ritchie ◽  
Gordon W. Arbuthnott

The novel nitric oxide synthase inhibitor 7-nitroindazole (7-NI) is relatively specific for the neuronal isoform of the enzyme and in this study we have used this compound to investigate the physiological role of perivascular nitric oxide-containing nerves in the cerebrovascular bed. Following injection of 7-NI (25 or 50 mg/kg, i.p.), cerebral blood flow and glucose utilization were measured in the conscious rat using the fully quantitative [14C]iodoantipyrine and 2-[14C]deoxyglucose techniques, respectively. Neither dose of the drug produced any change in arterial blood pressure, confirming a lack of effect upon the endothelial isoform of the enzyme, although there was a pronounced decrease in heart rate (−28% by 10 min postinjection). Throughout the brain 25 mg/kg 7-NI i.p. resulted in decreases in blood flow of between −20% in the hippocampus and −58% in the substantia nigra. Increasing the dose to 50 mg/kg resulted in a further generalized decrease, to almost −60% in parts of the thalamus and hippocampus, but in every animal this higher dose of 7-NI also produced randomly distributed areas of relative hyperaemia, which were most commonly found in those areas where the most intense hypoperfusion was otherwise in evidence. Despite these changes in blood flow, in all but a very few areas of the brain no significant decrease in glucose use was measured at either of the two doses of 7-NI. Thus despite the greater specificity of 7-NI for neuronal nitric oxide synthase, the cerebrovascular effects of the drug in vivo are very similar to that reported for the arginine analogues. However, these data do suggest that nitric oxide-releasing neurones in the brain may have an important role to play in the regulation of cerebral blood flow.


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