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:1.6.5.2 (NQO1)
6,196 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

NO performs a wide array of cell signaling functions. Neuronal NO synthase (nNOS) immunoreactivity and nicotinamide adenine dinucleotide phosphate diaphorase (NDP) activity, a marker of nNOS, were concentrated at adult rat neuromuscular junctions and persisted in denervated muscle indicating the localization of the enzyme to the postsynaptic surface. The concentration of nNOS at the muscle endplate suggests NO could serve as a messenger pre- and postsynapticly.
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PMID:Nitric oxide synthase is concentrated at the skeletal muscle endplate. 888 10

We investigated the pathophysiological role of nitric oxide synthesized by inducible nitric oxide synthase in the brain, by injecting lipopolysaccharide directly into the rat cerebral cortex/hippocampus. The levels of nitric oxide metabolites, nitrite and nitrate, began to increase in a dose-dependent manner with a 3-h lag, and reached approximately seven-fold the basal levels 8 h after the direct injection of lipopolysaccharide (5 microg). The lipopolysaccharide-induced increase in nitrite and nitrate levels was inhibited by treatment with the specific inducible nitric oxide synthase inhibitor aminoguanidine. The protein synthesis inhibitor cycloheximide delayed the onset of the increase in nitric oxide metabolite levels, and reduced the peak levels. Lipopolysaccharide increased Ca2+-independent, but not Ca2+-dependent, nitric oxide synthase activity in the brain. Intense nicotinamide adenine dinucleotide phosphate-diaphorase activity was observed in round cells in the vicinity of the site of injection of lipopolysaccharide 8 h after the injection. Neuronal death was observed seven days after the injection of lipopolysaccharide. Spatial memory, as assessed by performance in a water maze task and spontaneous alternation behavior in a Y-maze, was significantly impaired in rats which had had previous bilateral injections of lipopolysaccharide into the hippocampus. The lipopolysaccharide-induced neuronal death and spatial memory impairments were prevented by aminoguanidine. These results suggest that direct injection of lipopolysaccharide into the brain causes an induction of inducible nitric oxide synthase in vivo. Furthermore, it is suggested that nitric oxide produced by inducible nitric oxide synthase is responsible for the lipopolysaccharide-induced brain dysfunction.
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PMID:Brain dysfunction associated with an induction of nitric oxide synthase following an intracerebral injection of lipopolysaccharide in rats. 1005 Dec 7

Nitric oxide (NO) has been proposed to function as an inhibitory neurotransmitter in the lower urinary tract. This study investigates the distribution of NO-containing neurons and its changes following urethral obstruction in the guinea-pig. By using nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) histochemistry and NO synthase (NOS) immunohistochemistry, the highest frequency of NO-containing neurons was observed in the bladder base. Double labelling studies showed that 70.9% of NADPH-d reactive neurons co-expressed NOS immunoreactivity. Acetylcholinesterase reactivity was present in the majority of the intramural neurons with 54% of them expressed NOS immunoreactivity. NADPH-d reactivity was colocalized with vasoactive intestinal polypeptide, calcitonin gene-related peptide and substance P immunoreactivities in both neurons and fibres. Colocalization study also revealed that NADPH-d reactive neurons formed a distinct cell population from tyrosine hydroxylase positive neurons. At 12 hours after urethral obstruction, NADPH-d reactivity in the intramural ganglion cells was noticeably enhanced and this was sustained till 24 hours whence some intensely stained neurons appeared to undergo degenerative changes. Neuronal degeneration was more drastic at 48 hours so that the number of NADPH-d positive neurons was significantly reduced. The present study suggests that NO is an important neurotransmitter in the urinary bladder and that it may be involved in the relaxation activity in the bladder base during micturition. It is speculated that the increased NADPH-d reactivity in intramural ganglion cells elicited by urethral obstruction may be responsible for the cell death. It is suggested that the resulting cell loss or bladder denervation may account for the urinary dysfunction such as frequency and urgency of micturition in patients with urethral obstruction.
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PMID:Nitric oxide synthase--its distribution and alteration in the intramural ganglia of the urinary bladder in normal and urethra-obstructed guinea pigs. 1037 26

Neuronal nitric oxide synthase (nNOS) is induced in dorsal root ganglion neurons following axotomy in young rats, and is also increased in the gracile nucleus neurons of intact aged rats. The present study examined the influence of sciatic nerve axotomy on nNOS expression in the gracile nucleus in young compared to aged rats. The unilateral transection of the sciatic nerve was performed in young (4 months) and old (24 months) Fischer rats. Sections of rat medulla obtained 14 days after axotomy were immunolabelled using a polyclonal antibody directed against nNOS and stained by nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) histochemistry, a marker of nNOS activity. In young rats, unilateral axotomy produced increased NADPHd containing neurons in the rostral region and the caudal region of the ipsilateral gracile nucleus compared to the side with intact sciatic nerve. In old rats, the NADPHd containing neurons in the ipsilateral gracile nucleus were moderately increased by axotomy over the age changes seen in the contralateral side. Similar results were obtained with nNOS immunoreactivity in young rats, but more cells were seen with NADPHd staining compared to nNOS immunostaining in old rats. The results suggest that unilateral sciatic axotomy causes an increase in nNOS expression in the ipsilateral gracile nucleus of young rats, which is still seen in old rats as an increase over normal aging changes.
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PMID:Responses of nitric oxide synthase expression in the gracile nucleus to sciatic nerve injury in young and aged rats. 1065 Jan 38

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.
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PMID:Neuroprotective and neurodestructive functions of nitric oxide after spinal cord hemisection. 1068 69

This study had as its purpose to assess the effects of acute diabetes induced by streptozotocin (35 mg/kg body weight) on the number and size of the myenteric neurons of the duodenum of adult rats considering equally the antimesenteric and intermediate regions of the intestinal circumference. Experimental period extended for a week. Neuronal counts were carried out on the same number of fields of both regions of the duodenal circumference and measurements of neuronal and nuclear areas on equal numbers of cells. Number and size of the myenteric neurons stained with Giemsa were not significantly different between groups. On the other hand, the proportion of NADH-positive neurons increased from 18.54% on the controls to 39.33% on the diabetics. The authors discuss that this increased reactivity probably results from a greater NADH/NAD+ ratio, described in many tissues of diabetic animals, which has consequences on the modulation of the enzymes that use these cofactors and whose activity is detected by the NADH-diaphorase technique.
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PMID:Number and size of myenteric neurons of the duodenum of adult rats with acute diabetes. 1075 7

This is the first detailed description of the nitrergic nervous system in a fluke. In this study, the authors analysed the distribution of the nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) reactivity in neuronal and nonneuronal tissues of the adult fluke Fasciola hepatica and compared this with the distribution of the musculature using tetramethylrhodamine isothiocyanate-phalloidin. To assess the correlation between the number of muscle cells in different parts of the fluke and the NADPH-d-stained cells, the nuclei were stained with Hoechst 333 42, which is specific for chromatin. The spatial relation between the NADPH-d-positive nerves and the 5-hydroxytryptamine (serotonin; 5-HT)-immunoreactive (-IR) and GYIRFamide-IR nervous elements was also examined. The methods complement each other. NADPH-d-positive staining occurs in both in neuronal tissue and nonneuronal tissue. Large, NADPH-d-stained neurones were localised in the nervous system. The oral and ventral suckers are innervated with many large NADPH-d-stained neurones. In addition, the NADPH-d staining reaction follows closely the muscle fibres in both the suckers, in the body, and in the ducts of the reproductive organs. The presence of NADPH-d activity along muscle fibres in F. hepatica and in other flatworms supports a possible myoinhibitory role for nitric oxide. Neuronal nitric oxide synthase in flatworms may form a novel drug target, which would facilitate the development of a novel anthelminthic.
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PMID:Comparative study of the spatial relationship between nicotinamide adenine dinucleotide phosphate-diaphorase activity, serotonin immunoreactivity, and GYIRFamide immunoreactivity and the musculature of the adult liver fluke, Fasciola hepatica (Digenea, fasciolidae). 1108 90

Brain-derived neurotrophic factor (BDNF) is neuroprotective for motoneurons undergoing degeneration, including those in natural motor neuron disease (MND) in wobbler mice. To assess the role of BDNF in this model of MND, endogenous BDNF immunoreactivity was analyzed by semiquantitative video-image analysis. Affected cervical spinal cord motoneurons had significantly greater BDNF immunoreactivity compared to motoneurons of healthy littermates (P = 0.01) and affected lumbar spinal cord motoneurons (P = 0.008 at age 4 weeks; P = 0.005 at age 8 weeks). Neuronal nitric oxide synthase (n-NOS) immunocytochemistry revealed increased immunoreactivity in the affected cervical spinal cord motoneurons. Exogenous BDNF treatment partially inhibited the increased NOS activity, as quantitatively measured by nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) histochemistry. The mean number of NADPH-d(+) motoneurons in the cervical anterior horn decreased from 3.5 +/- 1.2 to 1.5 +/- 1.2 (P = 0.002). The increase in endogenous BDNF immunoreactivity in the affected spinal cord may be compensatory in diseased motoneurons, yet it appears to still be inadequate because exogenous BDNF treatment is required to suppress increased NOS activity in degenerating motoneurons. Our study indicates that BDNF is important in halting nitric oxide (NO)-mediated motor neuron degeneration, which has potential implications for the treatment of neurodegenerative disorders.
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PMID:Role of brain-derived neurotrophic factor in wobbler mouse motor neuron disease. 1126 18


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