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)

To characterize the specificity of a novel cholinergic immunotoxin (conjugate of the monoclonal antibody 192IgG against the low-affinity nerve growth factor receptor with the cytotoxic protein saporin), coronal sections through the basal forebrain of adult rats, that received a single intracerebro-ventricular injection of 4 micrograms of 192IgG-saporin conjugate, were subjected to histochemical and immunocytochemical procedures to evaluate cholinergic (choline acetyltransferase (ChAT)-immunoreactive, acetylcholinesterase-positive, NADPH-diaphorase-positive) and GABAergic structures (parvalbumin-immunoreactive, labeling of perineuronal nets with Wisteria floribunda agglutinin) as well as microglia (visualized with Griffonia simplicifolia agglutinin) and astrocytes (immunostaining for glial fibrillary acidic protein). Seven days following injection of the immunotoxin, ChAT-immunoreactive cells nearly completely disappeared throughout the magnocellular basal forebrain complex, including globus pallidus, as compared to vehicle-injected controls. However, there was no significant difference in the number of ChAT-positive cells in the adjacent ventral pallidum and in the caudate-putamen of immunolesioned and control animals. NADPH-diaphorase-containing cells, including a significant subpopulation of cholinergic cells, also strikingly decreased in number by more than 90% in the magnocellular basal forebrain complex following immunolesion, and only a few noncholinergic diaphorase-positive cells survived in the medial septum, vertical and horizontal diagonal band, and nucleus basalis of Meynert. In contrast, the number of parvalbumin-containing GABAergic projection neurons in the septum-diagonal band of Broca complex and nucleus basalis of Meynert from immunolesioned rats was not different from that of vehicle-injected control animals. Immunolesioning also did not result in any change in either number or shape of cells surrounded by perineuronal nets, which are frequently associated with parvalbumin-containing GABAergic neurons. Seven days following injection of the immunotoxin, a very strong activation of microglia with an identical distribution pattern was observed in all experimental animals. Large numbers of activated microglia were found in all magnocellular basal forebrain nuclei, corresponding to the distribution of degenerating cholinergic cells. Additionally, immunolesioning also resulted in a dramatic activation of microglia in the lateral septal nuclei, which are known to be almost free of cholinergic cells, but not of penetrating cholinergic dendrites in adjacent zones, and in the ventral pallidum, where there was no observed loss of cholinergic cells. There was no significant increase in microglia activation in striatum and cortical areas, and no astrocytic response in any of the basal forebrain nuclei at this particular time point of survival. These results suggest that 192IgG-saporin specifically destroys basal forebrain cholinergic neurons and does not suppress their neuronal activity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:192IgG-saporin immunotoxin-induced loss of cholinergic cells differentially activates microglia in rat basal forebrain nuclei. 756 26

Control of sympathetic preganglionic neurons appears to be mediated, in part, through polysynaptic pathways using spinal interneurons. To identify spinal interneurons antecedent to adrenal sympathetic preganglionic neurons, we injected herpes simplex virus type 1 into the adrenal gland of hamsters as this virus is an effective trans-synaptic tracer of neural pathways. After a three day survival period, immunocytochemistry was used to visualize virus-infected spinal cord cells. Infected sympathetic preganglionic neurons with somata that were either kite-shaped, elliptical or fusiform and that had extensive dendrite arbors were identified as well as a group of smaller round cells with finer processes. For comparison, in additional hamsters, labelling with the retrograde tracer Fluoro-Gold and histochemical reactions for the enzyme nicotinamide adenine dinucleotide phosphate-diaphorase were used to identify sympathetic preganglionic neurons. Sympathetic preganglionic neurons identified with Fluoro-Gold or herpes virus were present mostly in the nucleus intermediolateralis, pars intermediolateralis and nucleus intermediolateralis, pars funicularis of the spinal cord. The smaller herpes virus-infected cells were found mostly medial to the preganglionic neurons in lamina VII and also dorsally in lamina V of the spinal cord. Assessing immunoreactivity for glial fibrillary acidic protein demonstrated that the smaller herpes virus-infected cells were not reactive astrocytes. Furthermore, these cells were immunoreactive for two neuronal markers, neuron-specific enolase and for microtubule-associated protein 2. These findings suggest that these smaller round cells with finer processes are distinct from sympathetic preganglionic neurons and astrocytes and may be interneurons antecedent to the sympathetic preganglionic neurons.
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PMID:Identification of spinal interneurons antecedent to adrenal sympathetic preganglionic neurons using trans-synaptic transport of herpes simplex virus type 1. 760 86

The subventricular zone (SVZ) of the lateral ventricle remains mitotically active in the adult mammalian central nervous system (CNS). Recent studies have suggested that this region may contain neuronal precursors (neural stem cells) in adult rodents. A variety of neuronal and glial markers as well as three extracellular matrix (ECM) markers were examined with the hope of understanding factors that may affect the growth and migration of neurons from this region throughout development and in the adult. This study has characterized the subventricular zone of late embryonic, postnatal, and adult mice using several neuronal markers [TuJ1, nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d), neuron-specific enolase (NSE)], glial markers [RC-2, vimentin, glial fibrillary acidic protein (GFAP), galactocerebroside (Gal-C)], ECM markers [tenascin-C (TN-C), chondroitin sulfate, a chondroitin sulfate proteoglycan termed dermatan sulfate-dependent proteoglycan-1 (DSD-1-PG)], stem-cell marker (nestin), and proliferation-specific marker [bromodeoxyuridine (BrdU)]. TuJ1+ and nestin+ cells (neurons and stem cells, respectively) persist in the region into adulthood, although the numbers of these cells become more sparse as the animal develops, and they appear to be immature compared to the cells in surrounding forebrain structures (e.g., not expressing NSE and having few, if any, processes). Likewise, NADPH-d+ cells are found in and around the SVZ during early postnatal development but become more sparse in the proliferative zone through maturity, and, by adulthood, only a few labeled cells can be found at the border between the SVZ and surrounding forebrain structures (e.g., the striatum), and even smaller numbers of positive cells can be found within the adult SVZ proper. BrdU labeling also seems to decrease significantly after the first postnatal week, but it still persists in the SVZ of adult animals. The disappearance of RC-2+ (radial) glia during postnatal development and the persistence of glial-derived ECM molecules such as tenascin and chondroitin sulfate proteoglycans (as well as other "boundary" molecules) in the adult SVZ may be associated with a persistence of immaturity, cell death, and a lack of cell emigration from the SVZ in the adult.
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PMID:Cell and molecular analysis of the developing and adult mouse subventricular zone of the cerebral hemispheres. 854 61

Spinal cord injury results in abnormal sympathetic control of the cardiovascular system, perhaps because of reactions of sympathetic preganglionic neurons to loss of their supraspinal afferent inputs. We investigated morphological changes in sympathetic preganglionic neurons in rats one week after midthoracic spinal cord hemisection or complete transection and one month after complete transection. Morphological changes in adrenal sympathetic preganglionic neurons retrogradely-labelled by cholera toxin were examined as well as changes in other thoracic preganglionic neurons identified by their expression of reduced nicotinamide adenine dinucleotide phosphate-diaphorase. Reactive astrogliosis around these neurons was determined by assessing changes in immunoreactivity to glial fibrillary acidic protein. Changes in immunoreactivity to the synaptic vesicular protein synaptophysin were also evaluated in these areas. One week after transection, a comparison of sympathetic preganglionic neurons rostral and caudal to the lesion revealed significant loss of dendrites and decreased cell size caudal to the injury. Reactive astrocytes surrounded sympathetic preganglionic neurons as far as six segments below the transection. Constitutive expression of synaptophysin was observed rostral to the cord hemisection and synaptophysin expression was increased caudal to the lesion by seven days after the injury. One month after transection, the dendritic arbor of preganglionic neurons was re-established and the intensity of the reactive gliosis around the preganglionic neurons was diminished throughout the thoracic cord. These findings demonstrate that sympathetic preganglionic neurons undergo significant atrophy within a week after deafferentation and that this reaction is reversed within one month. Reactive astrogliosis could contribute to plastic changes in the neuropil that affect the sympathetic neurons, and the enhanced expression of synaptophysin in the gray matter caudal to a cord injury is consistent with fibre outgrowth leading to new synapse formation. Such re-organization could be one of the mechanisms for disorders in blood pressure control that occur after spinal cord injury.
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PMID:Morphological changes in sympathetic preganglionic neurons after spinal cord injury in rats. 884 26

Ischemic brain injury in neonates can result in the degeneration of cortical and subcortical areas of brain and is associated with neurologic deficits. One approach to restoring function in conditions of ischemic brain injury is the use of neural transplants to repair damaged connections. This approach has been shown to reestablish neural circuitry and to ameliorate associated motor deficits in models of neonatal sensorimotor cortex damage. In this study, we utilized the Rice et al. rodent model of neonatal ischemic-hypoxic (IH) brain injury to assess whether transplantation of fetal neocortical tissue can promote functional recovery in tests of sensorimotor and locomotor ability throughout development and as adults. We show that animals that received neocortical grafts 3 days following the IH injury performed significantly better as adults on two measures of motor ability, the Rota-Rod treadmill and apomorphine-induced rotations, than did control animals that received sham transplants after the IH injury. Transplants were identifiable in 72% of the animals 10-12 weeks after implantation. Histochemical studies revealed that while the transplanted tissue did not establish normal cortical cytoarchitecture, cells and fibers within the grafts stained for nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d), choline acetyl transferase (ChAT), cholecystokinin (CCK), and glial fibrillary acidic protein (GFAP). These results suggest that transplantation of fetal neocortical tissue following IH injury in the neonatal period is associated with amelioration of motor deficits and that the grafted tissue demonstrated a neurochemical phenotype that resembled normal neocortex. This approach warrants continued investigation in light of potential therapeutic uses.
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PMID:Transplantation of fetal neocortex ameliorates sensorimotor and locomotor deficits following neonatal ischemic-hypoxic brain injury in rats. 934 72

In the central nervous system (CNS), nitric oxide (NO) is thought to be involved in a variety of functions including synaptic plasticity, long term potentiation, and neurotoxicity. The aim of the present study was to investigate the expression of nitric oxide synthase (NOS) in the mouse CNS, following surgical injury to the hippocampus. NOS expression was assessed by histochemical detection of nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-diaphorase) activity and immunohistochemistry of the inducible NOS (iNOS). Two days after injury to the CA1 hippocampal field, NADPH-diaphorase activity was detected in pyramidal and granular neurons and also in glial cells in the hippocampus, in contrast to the non-injured one where NADPH-diaphorase staining was observed only in a few interneurons. NADPH-diaphorase histochemistry combined with immunolabelling for GFAP and F4/80 demonstrated that these glial cells were astrocytes and microglia. This pattern of NOS expression is induced specifically after a hippocampal injury since lesion to the prefrontal or cerebellar cortex leads to NOS activity only in monocytes/macrophages like cells. Despite the large expression of NOS detected by NADPH-diaphorase histochemistry after lesioning the hippocampus, immunostaining for iNOS was confined to microglia. The fact that induction of high levels of NOS activity are detected in glial cells after a lesion to the hippocampus could be accounted for by the sensitivity of this structure to a high release of glutamate.
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PMID:Specific pattern of nitric oxide synthase expression in glial cells after hippocampal injury. 951 65

Neuronal degeneration followed by glial activation (microglia and astrocytes) and nitric oxide synthase (NOS) expression in the hippocampus was investigated at 3 months after domoic acid (DA) administration and compared with DA treated rats at 5 days time interval which was reported earlier. Massive degeneration with complete absence of neurons in the hippocampal CA1 and CA3 regions and hypertrophied microglial cells showing intense immunoreaction with the antibody OX-42 was observed at 3 months after DA administration. Sparsely distributed OX-42 positive microglial cells were observed in the hippocampus of control rats at 3 months after saline treatment No apparent changes could be observed in the immunoreactivity of GFAP at 3 months after saline and DA administration. Neuronal nitric oxide synthase immunoreactive neurons were completely absent in the hippocampus at 3 months after DA administration. In contrast, nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) histochemical analysis revealed absence of NADPH-d reactivity in the neurons, but positive reactivity in the microglial cells of CA1-CA3 regions in the hippocampus after DA treatment. Double immunofluorescense revealed co-expression of inducible nitric oxide synthase with immunoreactive OX-42 positive microglial cells in the hippocampal subfields at 3 months after DA administration. The microglia-produced NO appears to be a secondary phenomenon in the prolonged inflammatory process following DA-induced neuronal degeneration.
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PMID:Induction of inducible nitric oxide synthase expression in activated microglia following domoic acid (DA)-induced neurotoxicity in the rat hippocampus. 1256 38

This study investigated the expression of nitric oxide (NO)-synthesizing enzymes and the glial reaction in the rat hippocampal formation following sleep deprivation for 5 days. Nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) reactivity was markedly reduced in the hippocampal CA1, CA2 and CA3 sectors as well as in the dentate gyrus, suggesting a suppression of NO production in these areas. Microglial cells were hypertrophic and showed an up-regulation of complement type 3 receptors as determined by antibody OX-42. However, expression of major histocompatibility complex class I and II antigens, and antigen of monocyte/macrophage lineage marked by OX-18, OX-6 and ED1, respectively, was undetected. Astrocytes also displayed hypertrophied processes with enhanced glial fibrillary acidic protein (GFAP) immunoreactivity. Western blots of hippocampal tissues corroborated the above-mentioned morphological findings in that expression of NO-synthase (NOS) was decreased while that of OX-42 and GFAP was increased in the sleep-deprived rats. Since NO is thought to be involved in memory consolidation processes in the hippocampus during sleep, the inhibition of NADPH-d and NOS reactivities may account for the memory decline after long-term sleep deprivation. The concomitant reactions in microglia and astrocytes suggest the involvement of these cells in the deleterious effect of prolonged sleep deprivation.
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PMID:Sleep deprivation inhibits expression of NADPH-d and NOS while activating microglia and astroglia in the rat hippocampus. 1276 54

Hypercholesterolemia has been suggested as a risk factor for Alzheimer's disease (AD). A genetic risk factor for AD is the E4 allele of apolipoprotein E (apoE). ApoE is the major lipoprotein transporter in the brain, and is mainly produced by glial cells. The present study is focussed on analysing the effects of high cholesterol (HC) diet, duration 9 months, on glial activation in the brain, both in wild type (WT) mice and in mice with a null mutation in the apoE gene (knock-out, KO) mice. The activation of astrocytes and microglia was analysed after immunohistochemical labelling of glial fibrillary acidic protein (GFAP), and F4/80, respectively. In addition, the expression of the antioxidant enzyme NAD(P)H:quinone oxidoreductase (NQO1) was analysed. There was a marked stimulation of astrocyte and microglial activation as well as induced expression of NQO1 in the hippocampus and cerebral cortex upon HC diet. Furthermore, there was significant astrocyte activation in the apoE KO mice, as compared to the WT mice, on ND. The long time exposure to HC diet combined with apoE deficiency resulted in a synergistic effect on the expression of NQO1 in the brain.
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PMID:Effects of high cholesterol diet on gliosis in apolipoprotein E knockout mice. Implications for Alzheimer's disease and stroke. 1545 Jun 74

Retinal ischemia/reperfusion (IR) injury causes profound tissue damage, especially retinal ganglion cell death. The aims of the study were twofold: (1) to investigate the benefits of epigallocatechin-3-gallate (EGCG), the major catechin found in tea, after IR challenge, and (2) to elucidate the mechanism of EGCG inhibition of nitric oxide synthase (NOS) expression. Wistar female rats were divided into four groups: normal control, EGCG with sham operation, retinal IR, and EGCG with IR groups. EGCG (50mg/kg) was administered by intraperitoneal injection 30 min before the experiment. IR injury to a rat's retina was induced by raising intraocular pressure to 150 mmHg for 60 min. With EGCG pretreatment, retinal ganglion cell death from IR was reduced by approximately 10% 3 days afterward. EGCG significantly downregulated IR-induced glial fibrillary acidic protein expression. EGCG treatment also reduced TUNEL-positive cells after IR in the inner retina as well as IR-induced lipid peroxidation. Histological analyses showed fewer neuronal NOS and nicotinamide adenine dinucleotide phosphate diaphorase-positive cells in the retina after IR with EGCG administration. Therefore, EGCG is effective in protecting retinal ganglion cells from IR challenge by ameliorating retinal nitrosactive stress and by regulating cell death through apoptotic pathways.
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PMID:Epigallocatechin-3-gallate reduces retinal ischemia/reperfusion injury by attenuating neuronal nitric oxide synthase expression and activity. 1828 30


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