Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.8.1.4 (diaphorase)
 2,754 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nicotinamide adenine dinucleotide phosphate diaphorase reactive neurons were found in several regions of human brainstem. Three major groups were located in the medulla: a dorsomedial group in the central gray and floor of the fourth ventricle, a ventromedial group in the vicinity of the medullary raphe, and a lateral group in the lateral reticular nucleus. In the upper pons a large cluster of reactive neurons was centered in the nucleus centralis oralis extending into the locus coeruleus and dorsal tegmental region. A second cluster in the lateral parabrachial nucleus merged with this group more rostrally and continued into the midbrain tegmentum (paracoeruleus-cuneiform group). Nicotinamide adenine dinucleotide phosphate diaphorase neurons in this region often contained acetylcholinesterase activity. A second midbrain group was seen in the nucleus paranigralis. Aside from these discrete neuronal collections, scattered reactive neurons were found in the medullary reticular formation, periaqueductal gray, inferior colliculus and superior colliculus. Nicotinamide adenine dinucleotide phosphate diaphorase neurons were classified into three groups based on somal size. Parvocellular neurons (10-20 micron) were primarily found in the ventromedial medulla and lateral parabrachial nucleus. Intermediate neurons (20-25 micron) were located in the paranigralis nucleus and dorsomedial medulla. Magnocellular neurons (25-35 micron) were characteristically found in the lateral reticular nucleus and paracoeruleus-cuneiform region. Nicotinamide adenine dinucleotide phosphate diaphorase reactive neurons are present in substantial numbers in human brainstem and their distribution is complex. They represent the caudal end of a widespread network of nicotinamide adenine dinucleotide phosphate diaphorase-enriched neurons that extend rostrally from the brainstem reticular formation into the basal forebrain, striatum, and cerebral cortex.
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PMID:Morphology and distribution of nicotinamide adenine dinucleotide phosphate (reduced form) diaphorase reactive neurons in human brainstem. 317 92

Two populations of neurons in the cat cerebral white matter were detected using histochemistry for reduced nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase activity. One type was bipolar in shape with two cell processes extending in opposite directions, existed mainly in the subcortical areas and was oriented parallel to fiber bundles. The second type had 4 or 5 very long, prominent and varicose cell processes radiating in various directions. They were round or polygonal in shape and formed networks in the white matter of the frontoparietal area. NADPH-diaphorase-positive neurons were also examined by the modified Golgi-Cox silver impregnation method. With this impregnation method, the same two morphological types could be detected but the detailed morphology of these particular populations of neurons was revealed much more fully by NADPH-diaphorase enzyme histochemistry than by the silver impregnation method.
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PMID:Reduced nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase-positive neurons in cat cerebral white matter. 317 18

The cholinergic neurons located within the pedunculopontine nucleus (Ch5) of patients with Alzheimer's disease (AD; n = 15), Parkinson's disease (PD; n = 2), and neurologically normal (n = 6) subjects were visualized immunohistochemically using choline acetyltransferase, pharmacohistochemically using acetylcholinesterase, or by reduced histochemical methods using nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d). Each histochemical procedure localized a well-delineated, compact lateral group and a more diffuse medial group of neurons within the pedunculopontine nucleus. Co-localization experiments revealed that all three enzymes marked the same population of cholinergic neurons. The extent of pathological alterations associated with the cholinergic neurons within the compact lateral sector of the pedunculopontine nucleus was examined in sections that reacted for NADPH-d, counterstained with thioflavin-S. The average number of neurofibrillary tangles within this portion of the pedunculopontine nucleus was 25.4 (range 0-70) in patients with AD, 1.5 (range 1-2) in those with PD, and 1.2 (range 0-4) in aged control subjects. Of the total number of neurofibrillary tangles counted in AD cases, 72.7% were end-stage ghosts and 27.3% were tangle-bearing neurons. The pathological alteration of cholinergic neurons of the compact lateral aspect of the pedunculopontine nucleus may play a role in some of the behavioral features characteristic of AD.
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PMID:Neurofibrillary tangles in cholinergic pedunculopontine neurons in Alzheimer's disease. 320 15

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

Littermate rat pups underwent either unilateral surgical occlusion of the right external naris or sham surgery on postnatal day 1. At 10, 20 or 30 days postpartum olfactory bulbs were sectioned and stained using nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) histochemistry. Two types of staining were observed and analyzed. The reaction produced a Golgi-like filling of short-axon cells in both deep and superficial bulb areas. No differences in the number, morphology or distribution of these cells were found either across ages or treatment conditions, indicating that the cells are resistant to the effects of the deprivation paradigm. Large regional variations in glomerular and olfactory nerve layer staining density were also observed at each age, reinforcing notions of functional or structural differences between glomeruli at very early ages.
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PMID:NADPH diaphorase staining within the developing olfactory bulbs of normal and unilaterally odor-deprived rats. 322 64

The mesencephalic locomotor region (MLR) was identified physiologically by inducing controlled locomotion on a treadmill in the precollicular rat following application of low amplitude current pulses to areas of the pontomesencephalic tegmentum. The same brains were processed using either of two techniques known to label neurons of the pedunculopontine nucleus (PPN)-choline acetyltransferase (ChAT) immunocytochemistry or nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase histochemistry. Histological reconstruction of locomotion-inducing sites were localized within or adjacent to ChAT or NADPH-diaphorase labeled cell groups. Three dimensional reconstructions of the PPN were used to visualize the colocalization of low threshold locomotion-inducing stimulation sites within PPN neuronal aggregates. These findings lend further support to the suggestion that the PPN is part of the MLR. A theoretical framework is proposed to account for results derived from various lines of research on this area.
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PMID:Locomotion-inducing sites in the vicinity of the pedunculopontine nucleus. 330 44

The spectral properties of ten redox indicator dyes were evaluated with the aim of finding the optimal choice for coupling to enzymatic reactions with high sensitivity for the production of the reduced form. Eight of the dyes were selected for coupling into a reaction cycle formed by yeast alcohol dehydrogenase with substrates ethanol and nicotinamide adenine dinucleotide (NAD+) and diaphorase with substrates reduced nicotinamide adenine dinucleotide (NADH, produced by the prior reaction) and the oxidized form of the respective dye. Two of the dyes exhibited decreased absorption on reduction, whereas all (eight) tetrazolium dyes increased in their absorption substantially upon reduction. Bis-tetrazolium dyes had a significantly higher molar extinction coefficient (up to 23,000 M-1.cm-1) than mono-tetrazolium dyes (down to 8000 M-1.cm-1). Kinetically, most dyes could be reduced with NADH (and diaphorase), but the rate of reduction varied considerably among the dyes with nitroblue tetrazolium (NBT) and tetranitroblue tetrazolium (TNBT) being the fastest. Therefore, NBT and TNBT seem to be the most suitable for fast response.
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PMID:Coupling of redox indicator dyes into an enzymatic reaction cycle. 337 38

Quantitative concentration-toxicity relationships were determined for the injury of cultured murine cortical neurons by several excitatory amino acid (EAA) agonists. All tested agonists produced concentration-dependent neuronal injury at concentrations between 1 and 1000 microM. With 5 min exposure, glutamate, aspartate, N-methyl-D-aspartate (NMDA), L-homocysteate (HCA), and quisqualate all had similar potencies, destroying half of the neuronal population (LD50) at concentrations of 50-200 microM, and similar efficacies, with 88-92% neuronal loss produced by exposure to high agonist concentrations. Quinolinate and kainate were substantially weaker toxins, producing only 20-30% neuronal loss after 5 min exposure to 3 mM concentrations; with prolonged (24 hr) exposure, 85-95% neuronal loss could be attained. The comparative EAA vulnerability of a specific cortical neuronal subpopulation containing high concentrations of the enzyme, reduced nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d), was also examined. Glutamate had no differential toxicity on these cells, damaging them at all concentrations in proportion to the general population; however, other, more selective, agonists produced strikingly differential injuries. These NADPH-d-containing [NADPH-d(+)]neurons were selectively resistant to damage by low concentrations of the NMDA agonists quinolinate, HCA, aspartate, or NMDA itself. By contrast, NADPH-d(+)neurons were selectively destroyed by concentrations of quisqualate or kainate too low to produce much general neuronal injury. The differential susceptibility of these neurons was not absolute, as high concentrations of all tested agonists produced nonselective neuronal injury. In light of recent evidence that forebrain NADPH-d(+)neurons are selectively spared in Huntington's disease, the present study continues to support the hypothesis that neuronal loss in Huntington's disease might result from excessive NMDA-receptor stimulation by any selective NMDA agonist. Furthermore, the demonstration that the differential susceptibility of NADPH-d(+)neurons is agonist concentration-dependent, rather than absolute, could provide a basis for explaining some existing conflicting experimental data.
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PMID:Vulnerability of cultured cortical neurons to damage by excitotoxins: differential susceptibility of neurons containing NADPH-diaphorase. 338 92

Recent studies have suggested that large amounts of free zinc may be coreleased during excitatory synaptic transmission at glutamatergic synapses, and may act postsynaptically to decrease actions mediated by N-methyl-D-aspartate (NMDA) receptors, while often increasing neuroexcitation mediated by quisqualate receptors. The present study examined the ability of zinc to alter excitatory amino acid (EAA) neurotoxicity. Murine cortical cell cultures were exposed to EAAs for 5 min in defined solutions, and neuronal cell injury was examined the following day both morphologically and by lactate dehydrogenase assay. Inclusion of 30-500 microM zinc in the exposure solution produced a zinc concentration-dependent, noncompetitive attenuation of NMDA-induced neuronal injury, with an ED50 of about 80 microM. In contrast, zinc produced the same concentration-dependent potentiation of quisqualate neurotoxicity; and with 500 microM zinc, a small potentiation of kainate neurotoxicity was suggested. The effect of zinc on the neurotoxicity of the broad-spectrum agonist glutamate was consistent with these effects on specific agonists, as well as with a previous study showing that glutamate neurotoxicity normally depends predominantly on NMDA-receptor activation. Zinc produced a concentration-dependent reduction in glutamate-induced neuronal injury in a fashion similar to that seen with NMDA, but less effectively. In addition, despite this overall protective effect, zinc paradoxically increased the glutamate-induced destruction of nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d)-containing neurons, a subpopulation that was shown in the preceding paper (Koh and Choi, 1988) to exhibit resistance to NMDA receptor-mediated neurotoxicity, and vulnerability to non-NMDA receptor-mediated neurotoxicity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Zinc alters excitatory amino acid neurotoxicity on cortical neurons. 338 93

The ultrastructure of reduced nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase-positive neurons in cat cerebral cortex, amygdala and caudate nucleus was investigated by electron microscopy using a modified method applicable to aldehyde-fixed tissues. These NADPH diaphorase-positive neurons were morphologically similar to neurons immunohistochemically positive for somatostatin. They had large amounts of electron-dense formazan reaction products scattered through the whole cytoplasm but not in the mitochondria or nucleus. Similar electron-dense reaction products were visible in the dendrites of these neurons. The results indicate that NADPH diaphorase histochemistry is a useful method for the ultrastructural examination of particular groups of neurons.
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PMID:Ultrastructure of reduced nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase-positive neurons in the cat cerebral cortex, amygdala and caudate nucleus. 340 36


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