Neuronal nitric oxide synthase expression in resected epileptic dysplastic neocortex

2009 ◽  
Vol 110 (2) ◽  
pp. 343-349 ◽  
Author(s):  
Jorge A. González-Martínez ◽  
Gabriel Möddel ◽  
Zhong Ying ◽  
Richard A. Prayson ◽  
William E. Bingaman ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Neuronal Nitric Oxide Synthase ◽  
Cresyl Violet ◽  
Control Group ◽  
Mesial Temporal Sclerosis ◽  
Type I ◽  
Type Ii ◽  
Cresyl Violet Staining ◽  
Oxide Synthase

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.

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
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Neuronal Nitric Oxide Synthase ◽  
Type I ◽  
Oxide Synthase

scholarly journals Role of Type I (Neuronal) Nitric Oxide Synthase in Pulmonary Vascular Tone in the Ovine Fetus ♦ 348

1998 ◽  
Vol 43 ◽  
pp. 62-62 ◽  
Author(s):  
Robyn L Rairigh ◽  
Laurent Storme ◽  
Timothy D Le Cras ◽  
Marilee P Horan ◽  
Steven H Abman
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Vascular Tone ◽  
Neuronal Nitric Oxide Synthase ◽  
Type I ◽  
Ovine Fetus ◽  
Oxide Synthase

scholarly journals Endurance training does not alter the level of neuronal nitric oxide synthase in human skeletal muscle

2000 ◽  
Vol 89 (3) ◽  
pp. 1033-1038 ◽  
Author(s):  
U. Frandsen ◽  
L. Höffner ◽  
A. Betak ◽  
B. Saltin ◽  
J. Bangsbo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endurance Training ◽  
Vastus Lateralis ◽  
Neuronal Nitric Oxide Synthase ◽  
Vastus Lateralis Muscle ◽  
Type I ◽  
Oxide Synthase ◽  
Male Subjects ◽  
Muscle Biopsies

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.

scholarly journals Distribution of Nitric Oxide Synthase in the Human Cerebral Blood Vessels and Brain Tissues

1994 ◽  
Vol 14 (6) ◽  
pp. 930-938 ◽  
Author(s):  
Hidekazu Tomimoto ◽  
Masaki Nishimura ◽  
Toshihiko Suenaga ◽  
Sinichi Nakamura ◽  
Ichiro Akiguchi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Cerebral Cortex ◽  
Nitric Oxide Synthase ◽  
Blood Vessels ◽  
Nadph Diaphorase ◽  
Type I ◽  
Type Ii ◽  
Cerebral Blood Vessels ◽  
Oxide Synthase

The distribution of nitric oxide synthase was investigated in human cerebral blood vessels and brain tissues. NADPH-diaphorase histochemistry, which is a marker for nitric oxide synthase in neurons and endothelial cells, revealed periadventitial nerve fibers in the arteries of the circle of Willis and their cortical branches, as well as the common carotid and subclavian arteries. The fibers were mostly nonvaricose in the periadventitial nerve trunk and were varicose within the adventitia. Patchy reaction products were distributed in the perinuclear region of each endothelial cell. Smooth muscle cells in the tunica media were weakly stained. Staining was particularly intense in regions with atherosclerotic changes, which consist of macrophage infiltration and proliferation of fibroblasts. In the neural parenchyma, two types of NADPH-diaphorase reactive neurons were differentiated. Type I neurons were intensely stained, medium-sized, and bipolar or multipolar. They were distributed in the cerebral cortex and white matter, mostly in the subcortical white matter. Type II neurons were lightly stained, small oval neurons with fine processes and were distributed in the cerebral cortex. Endothelial cells were intensely reactive for NADPH-diaphorase in the arteries, arterioles, and capillaries but weakly in veins. Immuno-histochemistry for neural nitric oxide synthase labeled perivascular nerves in the larger arteries and those in the neural parenchyma. Both type I and type II neurons were labeled. Nitric oxide synthase in endothelial cells and the nerve encircling blood vessels further suggests a dual control of cerebral circulation by nitric oxide in human brain.

Reduction of penile nitric oxide synthase in diabetic BB/WORdp (type I) and BBZ/WORdp (type II) rats with erectile dysfunction.

Endocrinology ◽  
1995 ◽  
Vol 136 (12) ◽  
pp. 5709-5717 ◽  
Author(s):  
D Vernet ◽  
L Cai ◽  
H Garban ◽  
M L Babbitt ◽  
F T Murray ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Erectile Dysfunction ◽  
Nitric Oxide Synthase ◽  
Type I ◽  
Type Ii ◽  
Oxide Synthase

scholarly journals [3H]L-NG-Nitroarginine Binding after Transient Focal Ischemia and NMDA-Induced Excitotoxicity in Type I and Type III Nitric Oxide Synthase Null Mice

1997 ◽  
Vol 17 (5) ◽  
pp. 515-526 ◽  
Author(s):  
H. Hara ◽  
C. Ayata ◽  
P. L. Huang ◽  
C. Waeber ◽  
G. Ayata ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Focal Ischemia ◽  
Type I ◽  
Type Ii ◽  
Wild Type ◽  
Type Iii ◽  
In The Wild ◽  
Transient Focal Ischemia ◽  
Oxide Synthase

We investigated the density and distribution of nitric oxide synthase (NOS) binding by quantitative autoradiography using [3H]L- NG-nitroarginine ([3H]L-NNA) after transient focal ischemia or intrastriatal injection of N-methyl-D-aspartate (NMDA) in wild-type (SV-129 and C57black/6) and type I (neuronal) and type III (endothelial) NOS-deficient mice. The middle cerebral artery (MCA) was occluded by an intraluminal filament for 3 h followed by 10 min to 7 days of reperfusion. Specific [3H]L-NNA binding, observed in the wild-type and type III mutant mouse at baseline, increased by 50–250% in the MCA territory during ischemia and the first 3 h of reperfusion. The density of binding sites ( Bmax), but not the dissociation constant ( Kd), increased significantly during the ischemic period as did type I NOS mRNA as detected by quantitative reverse transcription polymerase chain reaction. [3H]L-NNA binding after intrastriatal NMDA injection also increased by 20–230%. In the type I NOS-deficient mouse, [3H]L-NNA binding was low and only a very small increase was observed after ischemia or excitotoxicity. Under conditions of this study, [3H]L-NNA did not bind to type II NOS as there was no difference in the distribution or density of [3H]L-NNA binding in the rat spleen obtained after lipopolysaccharide treatment despite induction of NOS type II catalytic activity. Our data suggest that an ischemic/excitotoxic insult up-regulates type I NOS gene expression and [3H]L-NNA binding and that this up-regulation may play a pivotal role in the pathogenesis of ischemic/excitotoxic diseases.

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