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:1.6.99.1 (NADPH-diaphorase)
3,903 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neocortical neurons that utilise nitric oxide (NO) differ in morphology in different mammalian species. In the present study we examine these differences in the neocortex of mouse, rat, guinea-pig, rabbit, cat and monkey using histochemistry for nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) and immunocytochemistry for nitric oxide synthase (NOS), gamma amino-butyric acid (GABA), calbindin (CB), parvalbumin (PV) and calretinin (CR). NO neurons are non-pyramidal and can be divided into two distinct types, both of which react for NOS and NADPH-d. Type I neurons have a relatively large soma with heavy reaction product filling even the fine processes. They occur in all species, mainly near the border between the cortex and white matter, with fewer in the cortex, mostly in the superficial layers (II-IV). Type II cells are more numerous, smaller, and lighter in reactivity. They are in all species examined here except rodents, and in all cortical layers, but mainly layers II-IV. Most intracortical and some subcortical Type I neurons express GABA. A few intracortical Type I cells contain CB. All Type II cells express GABA and most also CB. Neither Type I nor Type II cells stain for PV or CR. We conclude that there is a tendency for a reduction of Type I cells, and increase of Type II, in mammalian neocortex with phylogeny.
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PMID:Morphological diversity of nitric oxide synthesising neurons in mammalian cerebral cortex. 917 29

The presence of nitric oxide synthase (NOS) in neuronal elements expressing the calcium-binding proteins calretinin (CR) and parvalbumin (PV) was studied in the rat main olfactory bulb. CR and PV were detected by using immunocytochemistry and the nitric oxide (NO) -synthesizing cells were identified by means of the reduced nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-diaphorase) direct histochemical method. The possible coexistence of NADPH-diaphorase and each calcium-binding protein marker was determined by sequential histochemical-immunohistochemical double-labeling of the same sections. Specific neuronal populations were positive for these three markers. A subpopulation of olfactory fibers and olfactory glomeruli were positive for either NADPH-diaphorase or CR. In the most superficial layers, groups of juxtaglomerular cells, superficial short-axon cells and Van Gehuchten cells demonstrated staining for all three markers. In the deep regions, abundant granule cells were NADPH-diaphorase- and CR-positive and a few were PV-immunoreactive. Scarce deep short-axon cells demonstrated either CR-, PV-, or NADPH-diaphorase staining. Among all these labeled elements, no neuron expressing CR or PV colocalized NADPH-diaphorase staining. The present data contribute to a more detailed classification of the chemically- and morphologically-defined neuronal types in the rodent olfactory bulb. The neurochemical differences support the existence of physiologically distinct groups within morphologically homogeneous populations. Each of these groups would be involved in different modulatory mechanisms of the olfactory information. In addition, the absence of CR and PV in neuronal groups displaying NADPH-diaphorase, which moreover are calmodulin-negative, indicate that the regulation of NOS activity in calmodulin-negative neurons of the rat olfactory bulb is not mediated by CR or PV.
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PMID:Calretinin- and parvalbumin-immunoreactive neurons in the rat main olfactory bulb do not express NADPH-diaphorase activity. 941 7

Glutamate excitocytotoxicity is implied in the cause of neuronal degeneration in the neostriatum, in which the toxicity may be mediated by different families of glutamate receptors. The precise cellular localization of alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA)-type glutamate receptor subunits (GluR1-4), one of the major family that involves in the mechanisms of glutamate excitocytotoxicity, in different populations of striatal neurons is therefore of special interest. Immunoreactivity for GluR2/3 subunits was detected in the medium-sized spiny neurons. By double labelling experiments, immunoreactivity for GluR1 and GluR4 was detected only in aspiny striatal neurons that display parvalbumin immunoreactivity, but not in the other neuron populations that display choline acetyltransferase or muscarinic m2 receptor immunoreactivity, nor neurons that display nitric oxide synthase immunoreactivity or nicotinamide adenine dinucleotide phosphate-diaphorase activity. These results indicate that GluR1 and GluR4 immunoreactivity is displayed only in the GABAergic interneurons in the neostriatum. In addition, almost all of the GluR1-immunoreactive neurons were found to display GluR4 immunoreactivity. This finding indicates for the first time that the striatal GABAergic interneurons co-express GluR1 and GluR4 subunits. The results of the present study indicate that there is a differential localization of AMPA-type glutamate receptor subunits in different populations of striatal neurons and they may have a different susceptibility to glutamate excitocytotoxicity.
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PMID:Cellular localization of GluR1, GluR2/3 and GluR4 glutamate receptor subunits in neurons of the rat neostriatum. 946 76

The co-localization of calretinin (CR) and parvalbumin (PV) immunoreactivity with nicotinamide adenine dinucleotide phosphate-diaphorase (ND) activity was analyzed in the Mauthner cells of the tench. Mauthner cells were ND active, and ND staining was observed in the soma, axon cap region, and axon of these neurons. CR co-localized with ND in the axon of the Mauthner cells but not in the cell body or in the dendrites, whereas PV immunoreactivity co-localized with ND in the soma, axon and dendrites. The presence of two different calcium-binding proteins in the Mauthner cells indicates that these neurons need complex calcium-buffering systems. The co-localization of these calcium-binding proteins with ND might suggests their involvement in nitric oxide-related events.
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PMID:Co-localization of calretinin and parvalbumin with nicotinamide adenine dinucleotide phosphate-diaphorase in tench Mauthner cells. 969 30

We recently reported the existence of a new class of aspiny interneurons characterized by their immunoreactivity for the calcium-binding protein calretinin (CR) in human striatum. This group is composed of numerous medium-sized (10-20 microm) neurons with poorly branched dendrites and a smaller number of large-sized (24-42 microm) neurons with highly ramified dendrites. We further demonstrated the selective sparing of the medium-sized, but not all the large-sized, CR+ striatal neurons in Huntington's disease. In the present study, we applied a double-antigen localization method to postmortem striatal tissue obtained from normal individuals to further characterize the chemical phenotype of these two subsets of CR+ neurons. Our results reveal that in the medium-sized neurons, CR is not colocalized with any of the following current markers of striatal neurons: calbindin, parvalbumin, beta-nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d), or choline acetyltransferase (ChAT). Furthermore, quantitative estimates show that the medium-sized CR+ neurons are by far the most abundant type of interneurons in the human striatum. In contrast, CR is colocalized with ChAT in about 80% of the large-sized CR+ neurons. Thus, the medium-sized CR+ neurons appear to form a distinct class of striatal interneurons, whereas most of the large-sized CR+ neurons belong to the population of giant cholinergic neurons. This study has provided the first exhaustive characterization of the chemical phenotype of the CR + neurons in the human striatum.
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PMID:Chemical phenotype of calretinin interneurons in the human striatum. 977 32

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

To gain insight into the cellular organisation of the zona incerta, we have examined the chemoarchitectonic properties of this "uncertain zone". The brains of Sprague-Dawley rats and common cats were processed for immunocytochemistry or NADPH-diaphorase histochemistry using standard methods. For the immunocytochemistry, antibodies to y-aminobutyric acid (GABA), glutamic acid decarboxylase (GAD), parvalbumin, calbindin, tyrosine hydroxylase, somatostatin, serotonin and glutamate were used. Two general patterns of distribution in the zona incerta were seen. First, labelled cells were restricted largely to one of the cytoarchitectonically defined sectors of the zona incerta. For instance, GABA, GAD and parvalbumin-immunoreactive cells were found principally within the ventral sector, NADPH-diaphorase and glutamate-immunoreactive cells within the dorsal sector and tyrosine hydroxylase- and somatostatin-immunoreactive cells within the rostral sector. Second, labelled cells were scattered somewhat across all incertal sectors, with no clear region of concentration. This pattern included the calbindin- and serotonin-immunoreactive cell groups. These results indicate that the zona incerta is made up of many neurochemically distinct cell groups, some of which respect the well-defined cytoarchitectonic boundaries of the nucleus, whilst others do not. This rich neurochemical diversity in the zona incerta suggests that this nucleus may have differential effects on the different structures that it projects to.
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PMID:Distribution of various neurochemicals within the zona incerta: an immunocytochemical and histochemical study. 1006 92

The presence of Cajal-Retzius cells in the adult human prefrontal and visual cortices has been demonstrated with calcium binding protein immunocytochemistry and NADPH-diaphorase histochemistry. These cells expressed parvalbumin, calbindin and calretinin calcium binding proteins and displayed NADPH-diaphorase enzyme activity. The three basic morphological profiles-horizontal, pyriform and multipolar-were observed. The morphologies of labelled cells resembled those of neurons observed in Golgi studies of the human cerebral cortex. The presence of calcium binding proteins and NADPH-diaphorase in these cells suggests a possible inhibitory role as GABAergic neurons. The persistence of Cajal-Retzius cells in the adult cerebral cortex supports the idea that they undergo developmental dilution rather than postnatal degeneration.
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PMID:Persistence of Cajal-Retzius cells in the adult human cerebral cortex. An immunohistochemical study. 1021 10

The neurochemical classification of GABAergic cells in the lizard hippocampus resulted in a further division into four major, non-overlapping subtypes. Each GABAergic cell subtype displays specific targets on the principal hippocampal neurons. The synaptic targets of the GABA/neuropeptide subtype are the distal apical dendrites of principal neurons. Calretinin- and parvalbumin-containing GABAergic cells synapse on the cell body and proximal dendrites of principal cells. Calbindin is expressed in a distinct group of interneurons, the synapses of which are directed to the dendrites of principal neurons. Finally, another subtype displays NADPH-diaphorase activity, but its synaptic target has not been established.
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PMID:GABAergic cell types in the lizard hippocampus. 1034 35

Huntington disease is characterized by the selective loss of striatal neurons, particularly of medium-sized spiny glutamate decarboxylase67 staining/GABAergic projection neurons which co-contain the calcium binding protein calbindin. Lesioning of the adult rat striatum by intrastriatal injection of the N-methyl-D-aspartate receptor agonist quinolinic acid (100 nmol) results in a pattern of striatal neuropathology seven days later that resembles that seen in the Huntington brain. Using this animal model of human Huntington's disease we investigated the effect of daily intrastriatal infusion of the nerve cell survival molecule ActivinA (single bolus dose of 0.73 microg daily for seven days) on the quinolinic acid-induced degeneration of various striatal neuronal phenotypes. By seven days, unilateral intrastriatal infusion of quinolinic acid produced a partial but significant loss (P < 0.01) in the number of striatal neurons immunoreactive for glutamate decarboxylase (to 51.0+/-5.8% of unlesioned levels), calbindin (to 58.7+/-5.1%), choline acetyltransferase (to 68.6+/-6.1%), NADPH-diaphorase (to 47.4+/-5.4%), parvalbumin (to 58.8+/-4.1%) and calretinin (to 60.6+/-8.6%) in adult rats that were administered intrastriatal phosphate-buffered saline for seven days following quinolinic acid. In contrast, in rats that received intrastriatal recombinant human ActivinA once daily for seven days following quinolinic acid, phenotypic degeneration was significantly attenuated in several populations of striatal neurons. Treatment with ActivinA had the most potent protective effect on the striatal cholinergic interneuron population almost completely preventing the lesion induced decline in choline acetyltransferase expression (to 95.1+/-5.8% of unlesioned levels, P < 0.01). ActivinA also conferred a significant protective effect on parvalbumin (to 87.5+/-7.7%, P < 0.01) and NADPH-diaphorase (to 77.5+/-7.5%, P < 0.01) interneuron populations but failed to prevent the phenotypic degeneration of calretinin neurons (to 56.6+/-5.5%). Glutamate decarboxylase67 and calbindin-staining nerve cells represent largely overlapping populations and both identify striatal GABAergic projection neurons. We found that ActivinA significantly attenuated the loss in the numbers of neurons staining for calbindin (to 79.7+/-6.6%, P < 0.05) but not glutamate decarboxylase67 (to 61.1+/-5.9%) at seven days following quinolinic acid lesioning. Taken together these results suggest that exogenous administration of ActivinA can rescue both striatal interneurons (labelled with choline acetyltransferase, parvalbumin, NADPH-diaphorase) and striatal projection neurons (labelled by calbindin) from excitotoxic lesioning with quinolinic acid. Longer-term studies will be required to determine whether these surviving calbindin-expressing projection neurons recover their ability to express the glutamate decarboxylase67/GABAergic phenotype. These results therefore suggest that treatment with ActivinA may help to prevent the degeneration of vulnerable striatal neuronal populations in Huntington's disease.
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PMID:Administration of recombinant human Activin-A has powerful neurotrophic effects on select striatal phenotypes in the quinolinic acid lesion model of Huntington's disease. 1039 42


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