Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.6.99.1 (NADPH-diaphorase)
3,903 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuronal nitric oxide synthase (NOS), an enzyme capable of synthesizing nitric oxide, appears to be identical to neuronal NADPH diaphorase. The correlation was examined between NOS immunoreactivity and NADPH diaphorase staining in neurons of the ileum and colon of the guinea-pig. There was a one-to-one correlation between NOS immunoreactivity and NADPH diaphorase staining in all neurons examined; even the relative staining intensities obtained were similar with each technique. To determine whether pharmacological methods could be employed to demonstrate that NADPH diaphorase staining was due to the presence of NOS, tissue was pre-treated with NG-nitro-L-arginine, a NOS inhibitor, or L-arginine, a natural substrate of NOS. In these experiments on unfixed tissue, it was necessary to use dimethyl thiazolyl tetrazolium instead of nitroblue tetrazolium as the substrate for the NADPH diaphorase histochemical reaction. Neither treatment caused a significant decrease in the level of NADPH diaphorase staining, implying that arginine and NADPH interact at different sites on the enzyme.
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PMID:Co-localization of nitric oxide synthase immunoreactivity and NADPH diaphorase staining in neurons of the guinea-pig intestine. 137 64

Neuronal degeneration that occurs in both ischemia and degenerative neurologic illnesses may involve excitotoxic mechanisms. In the present study, we examined whether cortical lesions with agonists acting at subtypes of glutamate receptors result in selective patterns of neuronal death. Injections of quinolinic acid, NMDA, homocysteic acid, kainic acid (KA), and alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA) were made at 2 sites in the dorsolateral frontoparietal cortex in rats. After 1 week, the cerebral cortex was either dissected for neurochemical studies, or animals were perfused for histologic evaluation. Concentrations of somatostatin (SS), neuropeptide Y (NPY), substance P (SP), cholecystokinin (CCK), and vasoactive intestinal polypeptide (VIP) were measured by radioimmunoassay, while amino acids and catecholamines were measured by high-performance liquid chromatography (HPLC) with electrochemical detection. NMDA agonists (quinolinic acid, homocysteic acid, and NMDA itself) resulted in dose-dependent reductions in glutamate and GABA, while SS, NPY, SP, CCK, and VIP were either unchanged or significantly increased in concentration. KA and AMPA at doses that resulted in comparable GABA depletions caused significant reductions in SS concentrations. Markers of cortical afferents were spared. All excitotoxins resulted in dose-dependent marked increases in uric acid concentrations. Histologic examination verified that lesions with NMDA agonists produced relative sparing of NADPH-diaphorase, SS, VIP, and CCK neurons. These results show that NMDA excitotoxin lesions result in a pattern of selective neuronal damage in the cerebral cortex that is similar to that which occurs in both ischemia and Huntington's disease.
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PMID:Neurochemical characterization of excitotoxin lesions in the cerebral cortex. 167 Jul 82

An investigation was made on the frog stomach myenteric plexus with 2 different histochemical techniques. Neuronal perikarya were stained with nicotinamide-adenine-dinucleotide-diaphorase (NADHd), while the acetyl-cholinesterase (AChE) staining showed rather the axoarchitectonic arrangement of the frog myenteric plexus. In double-labelled "whole mounts", NADHd-positive cell bodies and AChE-positive nerve processes were revealed. Some of the nerve cells and neuronal processes did not exhibit AChE activity at all. Since glyoxylic acid-induced fluorescence (GIF) was not detected in the myenteric plexus, the presence of catecholamines can be excluded. As a consequence of these observations, we suggest the presence of a non-cholinergic, non-adrenergic intrinsic neuronal system in the frog stomach myenteric plexus, containing purines or peptides as transmitters.
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PMID:Consecutive diaphorase-acetylcholinesterase histochemistry in the myenteric plexus of frog stomach. 250 Aug 25

Recordings of single unit activity in the posterior midbrain of the cat were carried out in the "fictive spontaneous locomotion" preparation. Neuronal activity was studied in relation to the onset, alternation and termination of cyclic hindlimb neurographic activity in the precollicular-postmammillary transected animal. Histochemical identification of pedunculopontine (nicotinamide adenine dinuceotide phosphate-diaphorase positive) neurons allowed the localization of recording sites in relation to this nucleus. Neurons located in the area of the cuneiform nucleus dorsal to the pedunculopontine nucleus were found to be related preferentially to cyclic (bursting) neurographic activity, while neurons in the area of the pedunculopontine were found to be related preferentially to the onset ("on") or termination ("off") of cycling episodes. Different populations of cells in the area appeared to be related to the frequency of alternation (bursting) compared with the duration of the cyclic episodes (on/off). While the area of the cuneiform-pedunculopontine nucleus has been found to be equivalent to the mesencephalic locomotor region, the same area has been found to be related to other rhythmic activities (e.g. respiratory, masticatory, sleep cycle, pressor, vesico-motor, etc.). A hypothesis is proposed to account for the weight of evidence implicating the same region in a host of distinct rhythmic activities. This hypothesis suggest that an oscillatory reverberation between cholinergic (pedunculopontine, laterodorsal tegmental nuclei) and aminergic (locus coeruleus, substantia nigra) centers is responsible for generating the various function-related "frequencies" (bursting) or "states" (on/off) of activity.
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PMID:Modulation of rhythmic function in the posterior midbrain. 321 8

The arrangement of the enteric nerve plexuses, and the distributions and projections of chemically specified neurons in the proximal colon of the guinea-pig were studied. The neural plexuses were examined using immunoreactivity to neuron specific enolase, and individual subpopulations were studied using antibodies raised against vasoactive intestinal peptide (VIP), substance P (SP), enkephalin, neuropeptide Y (NPY), gastrin releasing peptide (GRP), galanin, somatostatin, calbindin and calretinin. Nitric oxide producing neurons were studied using NADPH diaphorase histochemistry. The myenteric and submucous plexuses were not uniform around the entire circumference; at the mesenteric aspect of the colon there was almost no longitudinal muscle and the circular muscle was unusually thick and cord-like. In this region there was no tertiary plexus of fibres, and the ganglia of the myenteric and submucous plexuses were elongated in the direction of the circular muscle. Neuronal pathways within the antimesenteric aspect of the colon were investigated using nerve lesioning procedures. VIP, GRP, galanin, calbindin and NADPH diaphorase containing neurons lay in anally projecting pathways within the myenteric plexus, while enkephalin and somatostatin appeared in orally projecting nerve pathways. Few NPY immunoreactive nerve cells were found in the myenteric plexus of the proximal colon. The longitudinal muscle was innervated with VIP, SP, enkephalin and NADPH diaphorase containing fibres. The circular muscle was innervated by axons containing all substances investigated except NPY. Galanin, NPY, somatostatin and VIP fibres, all particularly dense in the mucosa, largely arose from nerve cell bodies in the submucous plexus. The results of the present study indicate that chemically specified neuronal populations in the proximal colon of the guinea-pig are more similar to the distal colon than the ileum, but that neuro-chemical and anatomical differences exist between the proximal and distal colon.
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PMID:Immunohistochemical analysis of neurons and their projections in the proximal colon of the guinea-pig. 751 May 7

Pancreatic ganglia are innervated by neurons in the gut and are formed by precursor cells that migrate into the pancreas from the bowel. The innervation of the pancreas, therefore, may be considered an extension of the enteric nervous system. NADPH-diaphorase is present in a subset of enteric neurons. We investigated the presence of NADPH-diaphorase in the enteropancreatic innervation, the contribution of extrinsic nerves to the NADPH-diaphorase-containing fibers of the gut and pancreas, and the coincident expression of NADPH-diaphorase NADPH-diaphorase in intrinsic neurons of these organs with neuropeptides. The possible role of nitric oxide in the neural regulation of pancreatic secretion was studied in isolated pancreatic lobules. Neuronal perikarya with NADPH-diaphorase activity were found in both Dogiel type I and type II neurons of the myenteric plexus of the stomach and duodenum. All galanin (GAL)-immunoreactive neurons and a small subset of vasoactive intestinal polypeptide (VIP)- and neuropeptide Y (NPY)-immunoreactive neurons contained NADPH-diaphorase activity. NADPH-diaphorase activity was also found in a subset of VIP and NPY-immunoreactive pancreatic neurons. Retrograde tracing with FluoroGold established that NADPH-diaphorase-containing neurons in the bowel project to the pancreas. NADPH-diaphorase-containing fibers were also found to be provided to both organs by neurons in dorsal root ganglia. Secretion of amylase was evoked by L-arginine. This effect was prevented by N(G)-nitro-L-arginine (L-NNA), which also inhibited VIP-stimulated secretion of amylase; however, L-NNA had no effect on amylase secretion stimulated by carbachol. These results provide support for the hypothesis that nitric oxide plays a role in the neural regulation of pancreatic secretion.
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PMID:NADPH diaphorase (nitric oxide synthase)-containing nerves in the enteropancreatic innervation: sources, co-stored neuropeptides, and pancreatic function. 751 4

Neuronal nitric oxide synthase (NOS), visualized immunohistochemically or with NADPH diaphorase histochemistry, is transiently expressed in discrete areas of the developing rat nervous system. In the brain transient NOS expression occurs in the cerebral cortical plate. At E15-E19, the majority of cells in the plate stain, with their processes extending through the corpus striatum to the thalamus. This staining decreases after birth and vanishes by the 15th postnatal day. Neurons in olfactory epithelium also express NOS from E15 till early postnatal life. In embryonic sensory ganglia virtually all neuronal cells are NOS positive, whereas by early adulthood only 1% express NOS. By contrast to these areas of transient NOS expression, in other neuronal sites NOS staining appears after cell bodies cease dividing and cells extend processes, and the staining persists in adult life. The transient expression of neuronal NOS may reflect a role in developmental processes such as programmed cell death.
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PMID:Transient nitric oxide synthase neurons in embryonic cerebral cortical plate, sensory ganglia, and olfactory epithelium. 752 Feb 52

Nitric oxide is known to function as a neurotransmitter in the central nervous system. It is also known to be involved in the central nervous system excitatory amino acid neurotransmission cascade. Activation of excitatory amino acid receptors causes an influx of calcium, which activates nitric oxide synthase. The resulting increase in intracellular nitric oxide activates soluble guanylate cyclase, leading to a rise in cyclic guanosine monophosphate. The excitatory amino acids glutamate and aspartate are found in the vestibular system and have been postulated to function as vestibular system neurotransmitters. Although nitric oxide has been investigated as a neurotransmitter in other tissues, no published studies have examined the role of nitric oxide in the vestibular system. Neuronal NADPH-diaphorase has been characterized as a nitric oxide synthase. This enzyme catalyzes the conversion of L-arginine to L-citrulline, producing nitric oxide during the reaction. We used a histochemical stain characterized by Hope et al. (Proc Natl Acad Sci 1991;88:2811) as specific for neuronal nitric oxide synthase to localize the enzyme in the rat vestibular system. An immunocytochemical stain was used to examine rat inner ear tissue for the presence of the enzyme's end product, L-citrulline, thereby demonstrating nitric oxide synthase activity. Staining of vestibular ganglion sections showed nitric oxide synthase presence and activity in ganglion cells and nerve fibers. These results indicate the presence of active nitric oxide synthase in these tissues and suggest modulation of vestibular neurotransmission by nitric oxide.
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PMID:Nitric oxide in the rat vestibular system. 752 6

Neuronal nitric oxide synthase (nNOS) has been suggested to be involved in cardiovascular homeostasis. We studied the regulation of nNOS expression, determining nNOS mRNA expression levels in various tissues in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). We also investigated the effects of antihypertensive treatment with the angiotensin II antagonist hydralazine or reserpine on nNOS mRNA expression. The expression levels of nNOS mRNA and nNOS protein were determined by Northern and Western blot analysis, respectively. NADPH-diaphorase histochemistry was used to identify cells in the adrenal medulla that expressed nNOS. No significant differences in expression levels in SHR and WKY were observed in the cerebellum and brain stem. nNOS mRNA expression levels in the decapsular portion of the adrenal gland were developmentally modulated and in a 24-week-old WKY were 2.5 times higher than in an age-matched SHR. This reduced expression of nNOS mRNA in the decapsular portion of the adrenal gland of SHR seemed to be a result of hypertension in the SHR, because administration of either an angiotensin II antagonist (TCV-116) or hydralazine upregulated nNOS mRNA expression in both SHR and WKY. Marked augmentation of nNOS mRNA expression in the decapsular portion of the adrenal gland by reserpine treatment suggested an intimate relation between nNOS in the decapsular portion of the adrenal gland and the sympathoadrenal system. Reserpine treatment also increased the expression of nNOS protein; however, reserpine treatment did not affect the distribution pattern of nNOS-positive cells (NADPH-diaphorase-positive cells) in the adrenal medulla.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of neuronal nitric oxide synthase in rat adrenal medulla. 753 41

Neuronal nitric oxide (NO), thought to be a neuroactive substance of high potency, is produced by the enzyme nitric oxide synthase (NOS) which has been demonstrated to additionally exhibit a so-called NADPH-diaphorase (NADPH-d) activity. Since physiological results pointed to the involvement of NO in circadian regulation, and morphological descriptions are not available, we sought to study the distribution of NO-producing cells in the hypothalamic suprachiasmatic nucleus (SCN) in Djungarian hamsters (Phodopus sungorus) by means of histochemistry and immunohistochemistry (IHC). In the SCN, NADPH-d stained perikarya of varying intensity and number were found predominantly in the ventrolateral subdivision. Diaphorase staining combined with the IHC demonstration of NOS revealed a complete overlapping of both. The combination of NADPH-d staining with the demonstration of the retinohypothalamic tract using the anterograde neuronal transport of cholera toxin B (CTB) following intraocular injection showed CTB terminals accumulating at NADPH-d cell bodies mainly in the ventrolateral region of the SCN. These data provide morphological evidence for the involvement of nitric oxide in the mediation of photic stimulation of the circadian oscillator located in the SCN.
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PMID:Nitric oxide-synthesizing neurons in the hamster suprachiasmatic nucleus: a combined NOS- and NADPH- staining and retinohypothalamic tract tracing study. 753 35


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