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)

This study has examined the development of cells in the rat retina which contain nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase. NADPH-diaphorase cells were first detected at postnatal day (P) 3, in somata located in the inner part of the cytoblast layer (CBL). At this age, NADPH-diaphorase reactivity was also seen in weakly labelled fibers in the presumptive outer plexiform layer (OPL). By P5, the somata of most labelled cells were in the inner part of the inner nuclear layer (INL), and by P11, their processes had spread extensively within the inner plexiform layer (IPL). By P25, there was a striking change in the pattern of NADPH-diaphorase reactivity. First, cells had lost reactivity from their large and extensive dendrites and second, there was a distinct reduction in the diameters of labelled somata. Thus, NADPH-diaphorase reactivity was most prominent during the period of synaptogenesis in the IPL. Labelled cells at P3 numbered 120 and were largely found at the superior margin of the retina. By P11, their total number had increased to the adult value of about 3400 and their density was highest in peripheral retina. With further development, the differential expansion of the retina appeared to lower the peripheral densities, resulting in an approximately uniform distribution by adulthood.
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PMID:Development of NADPH-diaphorase cells in the rat's retina. 281 96

A lattice of high oxidative metabolic activity occurs in the intermediate gray layer of the human, monkey, and cat superior colliculus. It is composed of a matrix of high enzyme activity that surrounds pale islands or bands of lower activity. In the human the pale bands are 300-400 micron wide while in the smaller colliculi of the monkey and cat they are 100-200 micron wide. The lattice was demonstrated by studying either cytochrome oxidase or succinate dehydrogenase. In the cat and monkey the lattice occurs at the same depth as the lattice of intense acetylcholinesterase activity, but the two lattices are not in spatial register. In the human the lattice of high oxidative metabolic activity is in the middle of the intermediate gray layer, whereas the lattice of intensely stained cholinesterase activity is at the base of this layer, but again the two lattices are not in spatial register. However, in the middle of the intermediate gray layer of the human, there are elongated islands and bands of very low acetylcholinesterase activity that coincide with the pale islands and bands of low cytochrome oxidase activity. An additional lattice of high enzyme activity occurs based on the enzyme nicotinamide dinucleotide phosphate (reduced form)-diaphorase. This lattice is prominent in the cat, occurs more faintly in the monkey, but did not appear to be present in the human. In the intermediate gray layer it had a high degree of overlap with the acetylcholinesterase lattice. The lattice of high oxidative metabolism contains loosely knit clusters of large multipolar cells containing high cytochrome oxidase activity and these cells do not occur in the pale islands. By contrast the cell bodies in the intermediate gray layer that contain either acetylcholinesterase or the diaphorase occur both between and within the patches of corresponding, high enzyme activity. It is suggested that the acetylcholinesterase and diaphorase lattices are mainly associated with afferent fibers while the lattice of high oxidative metabolism is mainly associated with intrinsic cells. The lattices occur in all mammals studied to date and appear to represent a fundamental principle in the organization of the mammalian colliculus. It is concluded that the lattices will provide a useful basis for further studies of the relationship between the many afferent and efferent modules thought to exist in this structure.
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PMID:Lattices of high histochemical activity occur in the human, monkey, and cat superior colliculus. 284 Jun 1

Exposure of cultures of cortical cells from mouse to either of the endogenous excitatory neurotoxins quinolinate or glutamate resulted in widespread neuronal destruction; but only in the cultures exposed to quinolinate, an N-methyl-D-aspartate agonist, was there a striking preservation of the subpopulation of neurons containing the enzyme nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d). Further investigation revealed that neurons containing NADPH-d were also resistant to the toxicity of N-methyl-D-aspartate itself but were selectively vulnerable to the toxicity of either kainate or quisqualate. Thus, neurons containing NADPH-d may have an unusual distribution of receptors for excitatory amino acids, with a relative lack of N-methyl-D-aspartate receptors and a relative preponderance of kainate or quisqualate receptors. Since selective sparing of neurons containing NADPH-d is a hallmark of Huntington's disease, the results support the hypothesis that the disease may be caused by excess exposure to quinolinate or some other endogenous N-methyl-D-aspartate agonist.
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PMID:Neurons containing NADPH-diaphorase are selectively resistant to quinolinate toxicity. 287 22

Neuropeptide Y and somatostatin immunoreactive neurons and processes were examined in human striatum using both immunofluorescence and avidin biotin immunoperoxidase methods. Reduced nicotinamide adenine dinucleotide phosphate diaphorase activity was histochemically determined by the reduction of nitro blue tetrazolium. Immunofluorescence using a monoclonal anti-somatostatin antibody and a polyclonal anti-neuropeptide Y antibody, followed by diaphorase histochemistry, showed that these three neurochemical markers are co-localized in a single population of medium-sized aspiny intrinsic neurons. Cells were evenly distributed in clusters throughout the striatum, but fiber density was higher in the nucleus accumbens and ventromedial regions of the caudate and putamen. Double-stained reduced nicotinamide adenine dinucleotide phosphate diaphorase-acetylcholinesterase sections demonstrated that these neurons are located in zones of high acetylcholinesterase activity, often at the interface of these zones with regions of low enzyme activity. These biochemically distinctive neurons are uniquely situated to modulate activity between striatal compartments. Our findings provide new information about the modular organization of the striatum and extend these observations in human brain.
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PMID:Neuropeptide Y, somatostatin, and reduced nicotinamide adenine dinucleotide phosphate diaphorase in the human striatum: a combined immunocytochemical and enzyme histochemical study. 288 80

Somatostatin and neuropeptide Y are two neuropeptides that are of particular interest in Alzheimer's disease because they are reported to be depleted in cerebral cortex. In the present study we examined somatostatin, neuropeptide Y, and nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase neurons in nine cortical regions in both normal and Alzheimer's disease brains. These three neurochemical markers show a high degree of co-localization (greater than 90%) in nonpyramidal neurons that are primarily distributed in cortical layers II-III, V-VI, and, most prominently, in infracortical white matter. The highest cell density was in temporal and parietal association cortex. The major morphological abnormality in Alzheimer's disease brains was a marked pruning and distortion of fiber plexuses with an apparent reduction in fiber density. In contrast, perikaryal density was preserved except for a reduction in parietal association cortex. Approximately 10 to 15% of senile plaques in the inferior temporal gyrus contained abnormal neurites. Additional abnormal collections of neurites without plaque cores were frequently found in layers II-III and V-VI. Neuropeptide Y and somatostatin were co-localized in abnormal neurites, suggesting an origin from local intrinsic neurons in which the two peptides are co-localized. Double immunofluorescence staining for both tau protein, a major antigenic component of paired helical filaments, and either somatostatin or neuropeptide Y showed that these neurons do not contain tau-immunoreactive neurofibrillary tangles. The morphological correlate of reduced somatostatin and neuropeptide Y content in Alzheimer's disease brain therefore appears to be a distortion and reduction in fiber plexuses. In addition, it is apparent that these neurons can develop widespread morphological abnormalities in the absence of neurofibrillary tangle formation.
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PMID:Cortical somatostatin, neuropeptide Y, and NADPH diaphorase neurons: normal anatomy and alterations in Alzheimer's disease. 289 22

Excitatory amino acids have been implicated in ischemic neuronal injury. To test this hypothesis in neonatal hypoxia-ischemia, lesions of the cortex and striatum were induced in 7-day-old rats by unilaterally ligating their carotid arteries and subjecting them to hypoxic conditions for 2 hours. Brains examined 1 week later demonstrated, within the regions of ischemic damage, a striking preservation of neurons that stained histochemically for nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) activity. Concentrations of the neuropeptides somatostatin and neuropeptide Y, which colocalize in neurons containing NADPH-d, were unaffected in the areas of ischemic damage. The same pattern of injury with sparing of NADPH-d-reactive neurons was reproduced by focal microinfusion of the excitotoxin quinolinic acid, an endogenous N-methyl-d-aspartate (NMDA) agonist, into the striatum. These results support the hypothesis that neonatal hypoxic-ischemic injury is mediated through excitatory transmitters acting at the NMDA receptor and that the NADPH-d-reactive neurons in the neonate are resistant to excitotoxic damage. This pattern of cell vulnerability is unique to the developing striatum and may relate to the distinct pathological appearance of the basal ganglia that follows neonatal asphyxia.
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PMID:Selective sparing of NADPH-diaphorase neurons in neonatal hypoxia-ischemia. 290 92

Previous histochemical studies have suggested that reduced nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase exists in distinct subsets of neurons that neither belong to a single transmitter type nor embrace all the neurons using a single transmitter. As a step toward establishing the role of this enzyme, the distribution of NADPH-diaphorase-positive neurons and fibers in the cat central nervous system was mapped by using a direct histochemical method. Heavily stained NADPH-diaphorase-positive neurons with many prominent cell processes were observed in the cerebral cortex, white matter, caudate nucleus, putamen, nucleus accumbens, septal nucleus, amygdala, anterior, lateral and posterior hypothalamic areas, dorsolateral part of the periaqueductal gray, superior colliculus, central tegmental field (Berman) (pedunculopontine tegmental area), dorsal tegmental nucleus, nucleus coeruleus, mesencephalic and pontine reticular formation, gigantocellular and magnocellular tegmental fields, nucleus facialis, and motor nucleus of the vagus. Moderately stained neurons with two or three prominent cell processes were observed in the nucleus of the diagonal band of Broca, globus pallidus, and substantia innominata. Medium-size, moderately stained neurons that had round large nuclei and no visible cell processes were found in the subthalamic nucleus, pontine gray, trapezoid body, and infratrigeminal, cochlear, and vestibular nuclei. Very dense NADPH-diaphorase-positive nerve terminal fields were seen in the olfactory tubercle, cortex, caudate nucleus, putamen, dentate gyrus, and interpeduncular nucleus. Intensely stained NADPH-diaphorase-positive nerve fibers were found in the stria terminalis, marginal region of the central tegmental field, dorsal tegmental nucleus, and spinal trigeminal tract as well as around the brachium conjunctivum. Although the staining of neurons and tracts was highly selective, they did not correspond to any single known neuronal or neurotransmitter type. Positive staining occurred in discrete subsets of neurons known to be associated with a variety of peptides and classical neurotransmitters. The functional significance of high NADPH diaphorase activity is unknown.
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PMID:Distribution of reduced-nicotinamide-adenine-dinucleotide-phosphate diaphorase-positive cells and fibers in the cat central nervous system. 291 70

A new modification of the nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase reaction was used to study the distribution of a specific subset of neurons in rat striatum. These neurons are known to also contain somatostatin-like immunoreactivity (SLI). We have previously found a heterogeneous distribution of SLI in rat striatum. In the present study, we found NADPH-diaphorase neurons to be evenly distributed throughout the striatum and nucleus accumbens. There was no increase in the number of NADPH-diaphorase neurons in ventromedial striatum or nucleus accumbens where concentrations of SLI are highest. This suggests that there may be somatostatin afferents to ventromedial striatum and nucleus accumbens. In addition, the NADPH-diaphorase reaction was stable for up to 24 h in an animal model stimulating human autopsy conditions.
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PMID:Topography of nicotinamide adenine dinucleotide phosphate-diaphorase staining neurons in rat striatum. 293 30

A distinct subpopulation of striatal aspiny neurons, containing the enzyme nicotinamide adenine dinucleotide phosphate diaphorase, is preserved in the caudate nucleus in Huntington's disease. Biochemical assays confirmed a significant increase in the activity of this enzyme in both the caudate nucleus and putamen in postmortem brain tissue from patients with this disease. The resistance of these neurons suggests that the gene defect in Huntington's disease may be modifiable by the local biochemical environment. This finding may provide insight into the nature of the genetically programmed cell death that is a characteristic of the disease.
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PMID:Selective sparing of a class of striatal neurons in Huntington's disease. 293 2

We have previously found that a biochemically distinct subset of neurons, containing nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d), is selectively resistant to the degenerative process that affects the striatum in Huntington's disease (HD). We report the morphologic and histochemical characteristics of these striatal neurons and their distribution with respect to the histochemical compartments as defined by acetylcholinesterase (AChE) activity. Sections of striatum were stained histochemically for NADPH-d and AChE and immunocytochemically for somatostatin and neuropeptide Y-like immunoreactivity. The diaphorase end-product was contained within medium-sized neurons which corresponded morphologically to a category of aspiny interneurons. Combined techniques showed that NADPH-d, somatostatin, and neuropeptide Y coexisted within the same neurons in controls and patients with HD. The density of these neurons was greater in the ventral putamen and the nucleus accumbens than in the remainder of the striatum. The distinctive AChE pattern of high and low enzyme activity was altered in HD. The AChE-rich matrix zone was markedly reduced in size, while the total area of zones of low enzyme activity was not different from that found in control striatum. The relation between these AChE chemical compartments and the distribution of preserved diaphorase neurons remained intact; NADPH-d neurons were predominantly observed in the matrix zone.
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PMID:Morphologic and histochemical characteristics of a spared subset of striatal neurons in Huntington's disease. 294 77


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