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)

1. Nitric oxide (NO) is highly reactive gaseous molecule to which many physiological and pathological functions have been attributed in the central (CNS) and peripheral (PNS) nervous system. The present investigation was undertaken to map the distribution pattern of the enzyme responsible for the synthesis of NO, nitric oxide synthase (NOS), and especially its neuronal isoform (nNOS) in the population of primary afferent neurons of the trigeminal ganglion (TG) and mesencephalic trigeminal nucleus (MTN) of the rabbit. 2. In order to identify neuronal structures expressing nNOS we applied histochemistry to its specific histochemical marker nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd). 3. We found noticeable amount of NADPHd-exhibiting primary afferent neurons in TG of the rabbit under physiological conditions. The intensity of the histochemical reaction was highly variable reaching the maximum in the subpopulation of small-to-medium-sized neurons. The large-sized neurons were only weakly stained or actually did not posses any NADPHd-activity. In addition, NADPHd-positive nerve fibers were detected between clusters of the ganglionic cells and in the peripheral branches of the trigeminal nerve (TN). NADPHd-exhibiting MTN neurons were noticed in the whole rostrocaudal extent of the nucleus even though some differences were found concerning the ratio of NADPHd-positive versus NADPHd-negative cell bodies. Similarly, we observed striking diversity in the intensity of NADPHd histochemical reaction in the subpopulations of small-, medium-, and large-sized MTN neurons. 4. The predominant localization of NADPHd in the subpopulation of small-to-medium-sized TG neurons which are generally considered to be nociceptive suggests that NO probably takes part in the modulation of nociceptive inputs from the head and face. Furthermore, we tentatively assume that NADPHd-exhibiting MTN neurons probably participate in transmission and modulation of the proprioceptive impulses from muscle spindles of the masticatory muscles and mechanoreceptors of the periodontal ligaments and thus provide sensory feedback of the masticatory reflex arc.
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PMID:Distribution of NADPH diaphorase-exhibiting primary afferent neurons in the trigeminal ganglion and mesencephalic trigeminal nucleus of the rabbit. 1677 44

1. Brief interruption of spinal cord blood flow resulting from transient abdominal aortic occlusion may lead to degeneration of specific spinal cord neurons and to irreversible loss of neurological function. The alteration of nitric oxide/nitric oxide synthase (NO/NOS) pool occurring after ischemic insult may play a protective or destructive role in neuronal survival of affected spinal cord segments. 2. In the present study, the spatiotemporal changes of NOS following transient ischemia were evaluated by investigating neuronal NOS immunoreactivity (nNOS-IR), reduced nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) histochemistry, and calcium-dependent NOS (cNOS) conversion of [(3)H] l-arginine to [(3)H] l-citrulline. 3. The greatest levels of these enzymes and activities were detected in the dorsal horn, which appeared to be most resistant to ischemia. In that area, the first significant increase in NADPHd staining and cNOS catalytic activity was found immediately after a 15-min ischemic insult. 4. Increases in the ventral horn were observed later (i.e., after a 24-h reperfusion period). While the most intense increase in nNOS-IR was detected in surviving motoneurons of animals with a shorter ischemic insult (13 min), the greatest increase of cNOS catalytic activity and NADPHd staining of the endothelial cells was found after stronger insult (15 min). 5. Given that the highest levels of nNOS, NADPHd, and cNOS were found in the ischemia-resistant dorsal horn, and nNOS-IR in surviving motoneurons, it is possible that NO production may play a neuroprotective role in ischemic/reperfusion injury.
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PMID:Spatiotemporal alterations of the NO/NOS neuronal pools following transient abdominal aorta occlusion: morphological and biochemical studies in the rabbit. 1678 31

This study describes calbindin-D28k (CB), neuronal nitric oxide synthase (nNOS), and nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) expression in the lateral nucleus of the sheep amygdaloid complex. Double immunofluorescence protocol was used in order to determine whether there is colocalization of CB and nNOS. The CB-immunoreactive (IR) neuronal population was composed especially of non-pyramidal neurons, but a few pyramidal cells were also present. The non-pyramidal neurons showed a multipolar and, occasionally, a fusiform morphology. The comparison between single-labeled CB-IR non-pyramidal neurons and cells belonging to CB-IR neuronal population showed they were identical for morphology, mean size, and distribution. The single-labeled CB-IR non-pyramidal neurons were only the 17.8% of the total non-pyramidal neurons counted. The nNOS-IR neuronal population was represented by non-pyramidal multipolar and fusiform neurons. Single-labeled nNOS-IR non-pyramidal neurons had the same morphology, mean area, and distribution as cells belonging to nNOS-IR neuronal population. Single-labeled nNOS-IR non-pyramidal neurons were more numerous than single-labeled CB-IR, and represented the 73.7% of total non-pyramidal neurons counted. NADPH-d-positive cells had the same morphology and distribution as the nNOS-IR neurons. Double immunolabeling (CB/nNOS) was found mostly in non-pyramidal multipolar neurons and only in a few non-pyramidal fusiform cells. These neurons had a mean perikaryal area significantly higher and significantly smaller than that of single-labeled nNOS and single-labeled CB-IR non-pyramidal neurons, respectively. CB and nNOS coexist only in a minority of non-pyramidal neurons (8.5%). The 32.4% of all CB-IR non-pyramidal neurons were nNOS-positive; only 10.4% of nNOS-IR non-pyramidal neurons were CB-positive. These results indicate that CB and nNOS are expressed by selective neurons and that the majority of nNOS-IR non-pyramidal neurons are lacking in CB.
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PMID:Distribution of calbindin-D28k, neuronal nitric oxide synthase, and nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) in the lateral nucleus of the sheep amygdaloid complex. 1704 87

In the course of a morphological investigation of age-related changes in the rat spinal cord, using nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry, we found abundant NADPH-d positive bodies, which were characteristically expressed in the aged lumbosacral spinal cord. Together with a normally stained fiber network and a few neurons, the dense, spheroidal NADPH-d positive bodies occurred in portions of the sacral dorsal spinal cords, such as the dorsal commissural nucleus, intermediolateral nuclei, and superficial dorsal horn, and were scattered throughout the dorsal white column. These NADPH-d positive bodies were occasionally observed in a fibrous structure. Two morphologically distinctive subsets of NADPH-d positive bodies were noted in the spinal cord of rats aged 8 to 36 months: 1) highly-dense spheroidal shapes with sharp edges; 2) moderately-dense spheroidal or multiangular shapes with a central "core" and a peripheral "halo". The quantitative analysis, particularly the stereological measurement, confirmed a gradual increase in the incidence and size of NADPH-d positive bodies with increasing age. With nNOS immunohistochemistry, no corresponding structures to NADPH-d positive bodies were detected in aged rats; thus NADPH-d activity is not always specific to the NO-containing neural structures. The major distribution of the NADPH-d positive bodies in the aged lumbosacral spinal cord indicates some anomalous changes in the neurite, which might account for a disturbance in the aging pathway of the autonomic and sensory nerve in the pelvic visceral organs.
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PMID:Age-related NADPH-diaphorase positive bodies in the lumbosacral spinal cord of aged rats. 1737 86

Neocortical gamma-aminobutyric acid (GABA)ergic neurons have been previously described as largely involved in local intracortical circuitry. However, our recent findings in the murine model described select neocortical GABAergic neurons that project to both neighboring and more distant neocortical regions. Here, we investigated whether such GABAergic projection neurons are also found in the cat neocortex. Wheat germ agglutinin-conjugated horseradish peroxidase (WGA-HRP) was injected into the visual, auditory, or somatosensory cortex, in order to label efferent cortical neurons retrogradely and to label axons and terminals orthogradely. Staining for nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d), an enzyme involved in nitric oxide synthesis, was employed, and co-localization with WGA-HRP was determined by means of both polarizing and brightfield microscopy. We concluded that neurons double-labeled with WGA-HRP and NADPH-d in a distant region from the WGA-HRP-injection site are GABAergic neurons with long-range projection axons. All double-labeled neurons were found in cortical layers VIa and VIb and in the white matter. Neurons with intense NADPH-d reactivity (type I) were determined to be neuronal nitric oxide synthase (nNOS) positive in all cases. However, weakly NADPH-d-reactive neurons (type II) lacked nNOS immunoreactivity. Moreover, nNOS often co-localized with GABA, neuropeptide-Y, and somatostatin in the cat neocortex. In summary, the GABAergic neurons described here projected in a manner similar to that previously described for neocortical principal neurons, although some unique GABAergic long-range projections were also demonstrated.
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PMID:Long-range GABAergic projection neurons in the cat neocortex. 1750 78

Some behavioral symptoms and neuropathological features of schizophrenia, like alterations of local GABAergic interneurons, could be emulated in an animal model of psychosis based on prolonged low-dose exposure to N-methyl-D-aspartate (NMDA) receptor antagonists, e.g. MK-801. Employing this model, we examined distinct subpopulations of GABAergic interneurons within the hippocampus and prefrontal cortex. Compared to saline control, animals receiving MK-801 exhibited a decreased density of hippocampal parvalbumin-positive interneurons. A co-administration of the antipsychotic drug haloperidol ameliorated this effect of MK-801 on PV(+) interneurons in the hippocampus, but led to a marked reduction of PV immunoreactivity in the prefrontal cortex, when comparing with saline, MK-801 or haloperidol treatment alone. Neither calretinin immunoreactivity nor nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase staining, representing neuronal nitric oxide synthase activity mostly detectable in interneurons, was altered by either treatment. With special reference to the hippocampus, these data show that a prolonged application of low-dose NMDA receptor antagonist could, in part, mimic some neuropathologic findings in human schizophrenia, thus strengthening the idea that (sub-) chronic NMDA receptor antagonism in animals is a viable approach in mimicking aspects of schizophrenia. Moreover, this study provides further evidence for regional differences in the response of GABAergic interneurons to NMDA receptor antagonism and antipsychotic treatment.
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PMID:Alterations of hippocampal and prefrontal GABAergic interneurons in an animal model of psychosis induced by NMDA receptor antagonism. 1760 3

Excessive production of nitric oxide (NO) might have detrimental effects on the hypoxia-related neuropathology. This study aimed to test if mild hypoxic preconditioning (MHPC) would attenuate the pathological changes in the brainstem motoneurons having a different functional component after peripheral nerve crush injury (PNCI). Prior to PNCI treatment, young adult rats were caged in the mild hypoxic altitude chamber with 79Torr of the partial oxygen concentration ( pO(2)) (i.e., 0.5atm at 5500m in height) for 4 weeks to adapt the environmental changes. After that, all the animals having successfully crushed both the hypoglossal and vagus nerves (left-side) were allowed to survive for 3, 7, 14, 30 and 60 successive days in normoxic condition. Nicotinamine adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry and neuronal nitric oxide synthase (nNOS) immunohistochemistry revealed that MHPC reduces NADPH-d/nNOS expression in the hypoglossal nucleus (HN) and the dorsal motor nucleus of the vagus (DMN) at different time points after PNCI. The morphological findings were further ascertained by Western blot analysis of nNOS and nitrite assay for NO production. Both the morphological and quantitative results peaked at 7 days in HN, whereas for those in DMN were progressively increased up to 60 days following PNCI. The staining intensity of NADPH-d/nNOS(+) neurons, expression of nNOS protein, NO production levels as well as the neuronal loss in HN and DMN of MHPC rats following PNCI were attenuated, especially for those having a longer survival period over 14 days. The MHPC treatment might induce minute amounts of NO to alter the state of milieu of the experimental animals to protect against the PNCI.
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PMID:Mild hypoxic preconditioning attenuates injury-induced NADPH-d/nNOS expression in brainstem motor neurons of adult rats. 1794 75

Doublecortin-immunoreactive (DCX+) cells were detected across the allo- and neo-cortical regions in the adult guinea pig cerebrum, localized to layer II specifically at its border with layer I. The density of labeled cells declined with age, whereas no apparent apoptotic activity was detectable over the cortex including layer II. DCX+ cells varied in somal size, labeling intensity, nuclear appearance, and complexity of processes. These cells were often arranged in clusters with cells of similar morphology sometimes packed tightly together. They exhibited complete colocalization with polysialylated neural cell adhesion molecule (PSA-NCAM) and neuron-specific type III beta-tubulin (TuJ1). Medium to large-sized DCX+ cells had well-developed neuritic processes, and expressed neuron-specific nuclear protein (NeuN). Large mature-looking cells with weak DCX reactivity invariably displayed heavy NeuN reactivity, implicating a transitional stage of these labeled cells. These "transitional" cells also consistently exhibited weak reactivity for gamma-aminobutyric acid (GABA), glutamate decarboxylase (GAD67), beta-nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) and neuronal nitric oxide synthase (nNOS), suggestive of them being young GABAergic/nitrinergic interneurons. Our data indicate that DCX+ cells exist widely in the adult guinea pig cerebral cortex, with a predominant localization in upper layer II. The morphological variation and differential expression of neuronal markers in these cells implicate that they might be developing neurons, and that they are probably differentiating into GABAergic interneurons. This population of cells might be involved in interneuron plasticity in the adult mammalian cerebral cortex.
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PMID:Doublecortin-expressing cells are present in layer II across the adult guinea pig cerebral cortex: partial colocalization with mature interneuron markers. 1837 31

Acupuncture-related effects on autonomic function have been explored via biological and neurophysiologic studies. The hypothalamus, known to regulate the autonomic nervous system, is likely affected by acupuncture treatment that modulates sympathetic functions. The aim of this study was to investigate the effect of electroacupuncture at the Jogsamni point (ST36, an acupoint known to modulate autonomic function) on expression of neuronal nitric oxide synthase (nNOS) in the hypothalamus of spontaneously hypertensive rat. Nitric oxide, which is produced by nNOS activity, plays an important role in the regulation of many physiologic processes, including sympathetic activities, in the hypothalamus and other parts of the brain. nNOS expression was assessed by immunohistochemistry of nNOS and histochemistry of nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d). The staining intensities of nNOS-positive neurons and NADPH-d-positive neurons were quantitatively assessed using microdensitometry to measure changes in optical density. The results show that electroacupuncture at ST36 reduced the expression and activity of nNOS in the hypothalamus of spontaneously hypertensitive rats. These findings suggest that the electroacupuncture at ST36 results in modulation of the activity of nNOS in the hypothalamus of spontaneously hypertensive rat.
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PMID:Electroacupuncture decreases nitric oxide synthesis in the hypothalamus of spontaneously hypertensive rats. 1883 24

Perinatal asphyxia (PA) is able to induce sequelae such as spinal spasticity. Previously, we demonstrated hypothermia as a neuroprotective treatment against cell degeneration triggered by increased nitric oxide (NO) release. Because spinal motoneurons are implicated in spasticity, our aim was to analyze the involvement of NO system at cervical and lumbar motoneurons after PA as well as the application of hypothermia as treatment. PA was performed by immersion of both uterine horns containing full-term fetuses in a water bath at 37 degrees C for 19 or 20 min (PA19 or PA20) or at 15 degrees C for 20 min (hypothermia during PA-HYP). Some randomly chosen PA20 rats were immediately exposed for 5 min over grain ice (hypothermia after PA-HPA). Full-term vaginally delivered rats were used as control (CTL). We analyzed NO synthase (NOS) activity, expression and localization by nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) reactivity, inducible and neuronal NOS (iNOS and nNOS) by immunohistochemistry, and protein nitrotyrosilation state. We observed an increased NOS activity at cervical spinal cord of 60-day-old PA20 rats, with increased NADPH-d, iNOS, and nitrotyrosine expression in cervical motoneurons and increased NADPH-d in neurons of layer X. Lumbar neurons were not altered. Hypothermia was able to maintain CTL values. Also, we observed decreased forelimb motor potency in the PA20 group, which could be attributed to changes at cervical motoneurons. This study shows that PA can induce spasticity produced by alterations in the NO system of the cervical spinal cord. Moreover, this situation can be prevented by perinatal hypothermia.
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PMID:Nitric oxide system alteration at spinal cord as a result of perinatal asphyxia is involved in behavioral disabilities: hypothermia as preventive treatment. 1900 88


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