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)

The level of expression of mRNAs encoding somatostatin and two isoforms of glutamic acid decarboxylase (Mr 65,000, GAD65 and 67,000, GAD67) was examined by quantitative in situ hybridization histochemistry in the striatum of adult rats after local injections of quinolinic acid. After a 2-week survival period, Nissl strains showed a profound loss of neurons in the injected striata. With a dose of 120 nmol quinolinic acid, the lesioned area was completely devoid of somatostatin mRNA-positive neurons but contained cells expressing nicotinamide adenine dinucleotide-diaphorase activity (a marker of somatostatinergic interneurons in striatum). After 60 nmol of quinolinic acid, the number of neurons expressing somatostatin mRNA in the lesioned area was similar to controls but the level of labeling per neuron was increased. In the lesioned area, labeling for GAD65 mRNA was abolished and labeling for GAD67 mRNA markedly reduced. However, scattered neurons expressing GAD67 mRNA could still be detected. The majority of surviving GABA-ergic neurons expressed immunoreactivity to parvalbumin, a marker for striatal GABA-ergic interneurons. The results show that quinolinic acid induces dose-dependent alterations in the expression of striatal somatostatin mRNA and reveal a relative sparing of GABA-ergic interneurons in the quinolinic acid-lesioned rat striatum.
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PMID:Effects of quinolinic acid on messenger RNAs encoding somatostatin and glutamic acid decarboxylases in the striatum of adult rats. 134 22

GABA (gamma-aminobutyric acid) immunocytochemistry was used on whole mounts of the frog stomach muscular layer to identify the GABAergic elements of the myenteric plexus. Between the labelled nerve fibres, five morphologically different types of neurons were revealed. The same cell types were also observed in the NADH-diaphorase-labelled control preparations. The different morphologies of the GABA-immunoreactive neurons may reflect the different peptide cotransmitter contents and/or different electrophysiological properties of these neurons.
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PMID:GABA immunocytochemistry reveals five morphologically different nerve cell types in the frog stomach. 175 93

The myenteric plexus of the domestic fowl (Gallus domesticus) small intestine was studied by means of silver staining, glyoxylic acid-induced fluorescence, the modified Koelle-Friedenwald method for the detection of acetylcholinesterase, NADH-diaphorase techniques and the unlabelled antibody method involving the use of an antiserum raised against GABA conjugated by glutaraldehyde to bovine serum albumin. The majority of the perikarya were in the ganglia, with an average density of 3370 +/- 942 nerve cells/cm2. Cholinesterase-positive and a few GABA-immunoreactive nerve cell bodies were seen in the myenteric ganglia, while fluorescent ganglion cells were not observed. In addition to AChE and GABA-positive nerve fibres, a rich fluorescent network of varicose and nonvaricose nerve fibres was detected, pointing to the presence of an extrinsic aminergic system in the domestic fowl myenteric plexus. Electron microscopic observations on nerve cells, axon profiles and varicosites with various vesicle populations were in good agreement with the histochemical findings.
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PMID:Histochemical characterization of myenteric plexus in domestic fowl small intestine. 207 64

NADPH-diaphorase histochemistry selectively stains discrete populations of retinal interneurons in diverse mammals, including two amacrine types in the rabbit retina. In this study, we have demonstrated that most of these neurons show GABA-like immunoreactivity by combining indirect immunofluorescence and diaphorase histochemistry on frozen retinal sections. The NADPH-diaphorase amacrines account for only a small proportion of the GABA-positive cells in rabbit retina, thus reinforcing the emerging consensus that GABAergic amacrines are remarkably diverse in their morphology and function.
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PMID:GABA-like immunoreactivity in NADPH-diaphorase amacrine cells of the rabbit retina. 320 39

This study investigated the morphology and quantitative distribution of neurons containing NADPH diaphorase activity in the ventral lateral geniculate nucleus of the rat. The pattern of diaphorase staining revealed a strongly reactive lateral subdivision and a weakly staining medial subdivision. A characteristic feature of the diaphorase staining in the lateral part was its "stripe-like" appearance. These "diaphorase stripes" resulted from regions of strong somatic and neuropil diaphorase activity lying between unstained fibre bundles coursing dorsoventrally through the nucleus. Two distinct populations of diaphorase reactive cell types were present--class A and class B neurons. The ratio of class A to class B diaphorase neurons was approximately 14:1 (A:B). Diaphorase reactive neurons made up 73% of the total neuron population in the lateral subdivision, and 31% in the medial subdivision. A third population of cells was found exclusively in the optic tract--class C neurons. Quantitative analyses in the coronal and sagittal planes indicated that the principal processes of both class A and class B neurons were oriented preferentially--either parallel with, or perpendicular to the outlying optic tract. Diaphorase enzyme histochemistry in combination with GABA immunocytochemistry demonstrated the co-localization of GABA immunoreactivity in the majority of class B neurons, whereas class A and class C neurons were GABA immunonegative. Furthermore a large population of GABA-immunoreactive neurons was present that were not stained for diaphorase activity. From this and previous studies, it can be concluded that a high proportion of the diaphorase reaction class A neurons are geniculotectal projection cells, while diaphorase reaction class B neurons represent a numerically small subpopulation of "local-circuit" inhibitory neurons. Since diaphorase activity co-localizes with nitric oxide synthase, the results indicate the likely involvement of nitric oxide in the neuronal operations of both subpopulations of geniculotectal projection neurons and "local-circuit" GABAergic neurons in the rat's ventral lateral geniculate nucleus.
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PMID:An oriented framework of neuronal processes in the ventral lateral geniculate nucleus of the rat demonstrated by NADPH diaphorase histochemistry and GABA immunocytochemistry. 752 Oct 23

The rationale for this study was to provide a comprehensive light microscopical description of the morphology of diaphorase-reactive neurons and neuropil elements in the dorsal lateral geniculate nucleus (dLGN) of the rat. An additional objective was to quantitatively assess whether a subpopulation of the diaphorase-reactive neurons, previously shown to be GABA-immunoreactive, constitute a distinct type of local-circuit neuron in the rat dLGN. Diaphorase activity was localised in a population of predominantly bipolar fusiform neurons. These cells were weak to moderately stained and possessed the morphological features of intrinsic inhibitory neurons, previously called class B neurons in the rat dLGN. Quantitative estimates indicated that the diaphorase-reactive neurons constituted approximately 10% of the total neuron composition of the dLGN. The majority (about 83%) of the diaphorase-reactive cells were located in the lateral half of the nucleus. In addition, a dense plexus of diaphorase-reactive varicose fibres was found throughout the dLGN lying between the oriented fibre bundles coursing dorsoventrally through the LGN. Diaphorase-reactive punctae were found to be closely associated with the somata and proximal dendritic segments of nonreactive neurons and also with the stained proximal dendritic segments of diaphorase-reactive dLGN neurons. The source of the diaphorase-reactive fibres in the dLGN was unknown. Evidence suggests, however, that they are of extrinsic origin. The GABA-immunoreactive nature of the diaphorase neurons in the dLGN was demonstrated by colocalising GABA immunoreactivity within the somata of diaphorase-reactive cells. The majority (> 90%) of diaphorase-reactive dLGN neurons were GABA-immunopositive. Also present was a distinct population of GABA-immunopositive neurons that were not diaphorase-reactive. In this study, cells that were solely GABA-immunopositive have been called class B1 neurons, while cells that were both diaphorase-reactive and GABA-immunoreactive have been called class B2 neurons. Size-frequency distributions of somatic profile areas established that the two populations of GABA-immunoreactive neuron were significantly different. Class B1 neurons constituted 57%, with class B2 cells representing 43% of all GABA-immunostained neurons in the rat dLGN. The characteristic morphological features, neurochemical identity and frequency of the diaphorase-reactive neurons in the rat dLGN indicate that they represent a subpopulation of inhibitory interneurons with the ability to affect intrinsic dLGN operations and thalamocortical interactions using the neuromodulator nitric oxide.
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PMID:Two types of interneuron in the dorsal lateral geniculate nucleus of the rat: a combined NADPH diaphorase histochemical and GABA immunocytochemical study. 788 43

The companion paper (Gabbott and Bacon [1996] J. Comp. Neurol.) describes the morphology of calretinin (CR)-, parvalbumin (PV)-, calbindin (CB)-, and GABA-immunoreactive neurons, and NADPH diaphorase-reactive cells, in the medial prefrontal cortex (mPFC; areas 24a, 24b, 24c, 25 and 32) of the adult monkey. Since these local circuit neurons play crucial functional roles, the aim of this study was to provide supportive quantitative data defining their areal and laminar distribution in mPFC. The numerical densities of neurons (Nv, number of cells per mm3) in each area and layer were calculated stereologically. The mean total neuronal NV estimates across mPFC was 55,727 +/- 3,319 per mm3 (mean +/- S.D.; n = 3); values ranged from 50,489 +/- 8,374 per mm3 (area 24a) to 59,938 +/- 7,214 per mm3 (area 24c). Interareal differences were not significant. Cortical depth measurements and neuronal NV estimates for each area allowed the absolute number of neurons in a column of cortex under 1 mm2 of surface to be calculated; values varied between 86,457 +/- 15,063 (area 24a) and 128,464 +/- 24,050 (area 24c). Using immunolabelled Nissl-stained sections of mPFC, CR+ neurons constituted 11.2%, PV+ neurons 5.9%, and CB+ neurons 5.0% of the total neuron population. GABA+ neurons represented an overall 24.9% (23.5-27.3%) of neurons in the mPFC. Differences between areas were not significant. The cortical depth distribution histograms of CR+, PV+, CB+, and GABA+ cell populations in each area were derived and the percentage of a given cell population in each layer subsequently calculated. Peaks in the cortical depth distributions of CR+ and CB+ neurons occurred in layer 2 and upper layer 3, respectively; the peak distribution of PV+ neurons occurred between lower layer 3 and upper layer 5. The depth distribution of GABA+ cells reflected the combined distributions of CR+, PV+ and CR+ neurons. In all areas, the majority (74.4-84.0%) of the GABA cell population was located in layers 2/3. The depth distributions for each cell type were similar between areas. Diaphorase-reactive neurons accounted for 0.25% (0.2-0.32%) of all cortical neurons in mPFC and were distributed in two horizontal strata, in midlayer 3 and in mid/upper layer 6. A large population of diaphorase-reactive cells was present in the white matter. The absolute numbers of CR+, PV+, CB+ and GABA+ neurons within individual layers in a column of cortex under 1 mm2 and 50 x 50 microns of cortical surface have been derived. The data presented provide the basis for a quantitative definition of cortical circuits in monkey mPFC.
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PMID:Local circuit neurons in the medial prefrontal cortex (areas 24a,b,c, 25 and 32) in the monkey: II. Quantitative areal and laminar distributions. 882 50

Huntington's disease is a genetic disorder that results from degeneration of striatal neurons, particularly those containing GABA (gamma-aminobutyric acid). There is no effective treatment for preventing or slowing this neuronal degeneration. Ciliary neurotrophic factor (CNTF) is a trophic factor for striatal neurons and therefore a potential therapeutic agent for Huntington's disease. Here we evaluate CNTF as a neuroprotective agent in a nonhuman primate model of Huntington's disease. We gave cynomolgus monkeys intrastriatal implants of polymer-encapsulated baby hamster kidney fibroblasts that had been genetically modified to secrete human CNTF. One week later, monkeys received unilateral injections of quinolinic acid into the previously implanted striatum to reproduce the neuropathology seen in Huntington's disease. Human CNTF was found to exert a neuroprotective effect on several populations of striatal cells, including GABAergic, cholinergic and diaphorase-positive neurons which were all destined to die following administration of quinolinic acid. Human CNTF also prevented the retrograde atrophy of layer V neurons in motor cortex and exerted a significant protective effect on the GABAergic innervation of the two important target fields of the striatal output neurons (the globus pallidus and pars reticulata of the substantia nigra). Our results show that human CNTF has a trophic influence on degenerating striatal neurons as well as on critical non-striatal regions such as the cerebral cortex, supporting the idea that human CNTF may help to prevent the degeneration of vulnerable striatal populations and cortical-striatal basal ganglia circuits in Huntington's disease.
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PMID:Protective effect of encapsulated cells producing neurotrophic factor CNTF in a monkey model of Huntington's disease. 912 55

The cytoarchitecture of the optic tectum of the Japanese quail, Coturnix coturnix japonica, was studied using the Golgi-Kopsch method, parvalbumin, calbindin and GABA immunohistochemistry and nicotinamide adenine dinucleotide phosphate-diaphorase histochemistry. Our results reveal a large number of different types of interneurons in the quail tectum opticum, only part of which are described in the chick or pigeon. Application of parvalbumin and calbindin immunohistochemistry and nicotinamide adenine dinucleotide phosphate-diaphorase histochemistry reveals the following lamination pattern: The stratum opticum, stratum griseum centrale and stratum album centrale remain unstained, while the laminae of the stratum griseum et fibrosum superficiale exhibit a roughly complementary staining pattern of calbindin (laminae c, d, e, f, g, i) and parvalbumin (laminae a, h, i). Nicotinamide adenine dinucleotide phosphate-diaphorase histochemistry yields a dense band in lamina i. The Golgi material reveals the following cell types in the stratum griseum et fibrosum superficiale: marginal cells in the stratum opticum and in lamina h and i, horizontal cells in laminae a and c, large and small radial cells in laminae b, d, h and i, multiform cells in lamina b, bitufted cells in lamina d and e, large pear-shaped cells in lamina g, wide-field cells in lamina j, and stellate cells in lamina j and in the stratum griseum centrale. We consider horizontal cells, bitufted cells, multiform cells and small radial cells to be GABAergic interneurons of the stratum griseum et fibrosum superficiale which seem to be more numerous than in the pigeon tectum opticum. Golgi impregnation and injection of Phaseolus vulgaris leucoagglutinin into the pretectal nucleus lentiformis yielded regularly distributed clusters of telodendra of pretectal axons in lamina d of the stratum griseum et fibrosum superficiale, which are identical in shape and position with axon plexus revealed by Golgi staining.
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PMID:Cytoarchitecture of the tectum opticum in the Japanese quail. 988 78

Recent evidence suggests an important role for NO in cholinergic models of epilepsy. Nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd), a marker of NO containing neurons, was shown to intensely colocalize with GABA in double-labeling studies performed in the hippocampal formation (exception made for the pyramidal cell layer) (Valtschanoff et al., J Comp Neurol 1993:331:111-121). In this sense, it further characterizes an extremely important cell category due to the relevant involvement of inhibitory systems in the mechanisms of genesis and propagation of seizures. Here, we assessed the histochemistry for NADPHd in the hippocampal complex of chronic pilocarpine-epileptic animals. NADPHd-positive cells were lost in almost every hippocampal subfield in pilocarpine-treated rats. The central portion of the polymorphic layer of the dentate gyrus (hilus) presented one of the highest losses of NADPHd-positive cells (55-79%) in the hippocampus. A significant loss of NADPHd-positive cells was seen in strata oriens, pyramidale, and radiatum CA1, CA2, and CA3 subfields. NADPHd staining in the subicular pyramidal cell layer was not different from that observed in controls. A significant loss of NADPHd-stained cells was observed in entorhinal cortex layers II and III in the epileptic group. For entorhinal cortex layers V and VI, however, results varied from an almost complete tissue destruction to an overexpression of NADPHd-positive cells, as well as an increase in neuropil staining. In summary, loss of NADPHd staining was not uniform throughout the hippocampal formation. There has been a growing support for the notion that GABAergic neurons in the hippocampal formation are not equally sensitive to insults. Our results suggest that, as a marker for a subpopulation of GABAergic neurons, NADPHd helps in further refining the characterization of the different neuronal populations sensitive to epileptic activity.
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PMID:Loss of NADPH diaphorase-positive neurons in the hippocampal formation of chronic pilocarpine-epileptic rats. 1040 44


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