Induction and variants of neuronal nitric oxide synthase type I during synaptogenesis

1995 ◽  
Vol 9 (9) ◽  
pp. 799-806 ◽  
Author(s):  
Patricia Ogilvie ◽  
Karl Schilling ◽  
Melvin L. Bllllngslev ◽  
Harald H. H. W. Schmidt
1998 ◽  
Vol 43 ◽  
pp. 62-62 ◽  
Author(s):  
Robyn L Rairigh ◽  
Laurent Storme ◽  
Timothy D Le Cras ◽  
Marilee P Horan ◽  
Steven H Abman

2000 ◽  
Vol 89 (3) ◽  
pp. 1033-1038 ◽  
Author(s):  
U. Frandsen ◽  
L. Höffner ◽  
A. Betak ◽  
B. Saltin ◽  
J. Bangsbo ◽  
...  

The effect of endurance training on neuronal nitric oxide synthase (nNOS) content and distribution in muscle was investigated. Seven male subjects performed 6 wk of one-legged knee-extensor endurance training ( protocol A). Muscle biopsies, obtained from vastus lateralis muscle in the untrained and the trained leg, were analyzed for nNOS protein and activity as well as immunohistochemical distribution of nNOS and endothelial nitric oxide synthase (eNOS). Muscle biopsies were also obtained from another seven male subjects before and after 6 wk of training by endurance running (p rotocol B) and analyzed for nNOS protein. No difference was found in the amount of nNOS protein in the untrained and the trained muscle either with protocol Aor protocol B ( P > 0.05). In protocol A, the activity of nNOS was 4.76 ± 0.56 pmol · mg protein−1 · min−1 in the control leg, and the level was not different in the trained leg ( P> 0.05). nNOS was present in the sarcolemma and cytosol of type I and type II muscle fibers, and the qualitative distribution was similar in untrained and trained muscle. The number of eNOS immunoreactive structures and the number of capillaries per muscle fiber were higher ( P < 0.05) after training than before. The present findings demonstrate that, in contrast to findings on animals, nNOS levels remain unaltered with endurance training in humans. Evidence is also provided that endurance training may increase the amount of eNOS, in parallel with an increase in capillaries in human muscle.


2009 ◽  
Vol 110 (2) ◽  
pp. 343-349 ◽  
Author(s):  
Jorge A. González-Martínez ◽  
Gabriel Möddel ◽  
Zhong Ying ◽  
Richard A. Prayson ◽  
William E. Bingaman ◽  
...  

Object Nitric oxide has been associated with epileptogenesis. Previous studies have shown increased expression of N-methyl-d-aspartate (NMDA) subunit NR2B receptors in epileptic dysplastic human neocortex. The expression of neuronal nitric oxide synthase (nNOS), and its relation to this subunit NR2B in epileptic dysplastic tissue has never been addressed. Methods Ten patients with medically intractable epilepsy caused by focal cortical dysplasia (CD), and 2 patients with mesial temporal sclerosis (control group) underwent pre- and/or intraoperative invasive monitoring evaluations. Cortical samples from epileptogenic and nonepileptogenic areas were collected from each patient intraoperatively. Samples were processed for cresyl violet staining, immunocytochemical tests with nNOS, NeuN, and NR2B, and immunofluorescence analyses to evaluate colocalized immunoreactivity between nNOS and NR2B. Results . All samples obtained in the patients with epilepsy revealed CD in various degrees. In the nonepileptic sample group, cresyl violet staining revealed normal cortical architecture in 9 samples, but a mild degree of CD in 3. The density and intensity of nNOS-stained neurons was remarkably increased in the epileptic tissue compared with nonepileptic samples (p < 0.05). Two types of nNOS-stained neurons were identified: Type I, expressing strong nNOS immunoreactivity in larger neurons; and Type II, expressing weak nNOS immunoreactivity in slightly smaller neurons. Different from Type I neurons, Type II nNOS-stained neurons revealed immunoreactivity colocalized with NR2B antibody. Conclusions The overexpression of nNOS in the epileptic samples and the immunoreactivity colocalization between nNOS and NR2B may suggest a possible role of nNOS and NO in the pathophysiological mechanisms related to in situ epileptogenicity.


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