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:1.6.99.3 (diaphorase)
5,903 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

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

The heterogeneous anatomy of both the dorsal striatum at the level of the head of the caudate nucleus and of the substantia nigra of cats was analyzed immunohistochemically using two calcium-binding proteins, namely, calbindin D-28k and parvalbumin. The striatal histochemical markers nicotinamide-adenine dinucleotide phosphate diaphorase and acetylcholinesterase were revealed in sections adjacent to those used for the immunohistochemical procedure. The distribution of both the calbindin D-28k and the parvalbumin immunoreactivities is heterogeneous in dorsal, ventral, lateral, and medial areas of the head of the caudate nucleus and is in register with the striosome/matrix pattern displayed by the histochemical markers. These calcium-binding proteins preferentially are located in the matrix compartment of the rostral caudate nucleus. Moreover, in some areas of the rostral two-thirds of the substantia nigra, calbindin D-28k and parvalbumin immunoreactivities appear to follow a complementary pattern that is quite different from the mesencephalic distribution of these two calcium-binding proteins.
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PMID:Immunohistochemical distribution of calbindin D-28k and parvalbumin in the head of the caudate nucleus and substantia nigra of the cat. 793 72

As part of a research program on the evolution of somatosensory systems in vertebrates, the dorsal column nucleus (DCN) was studied with (immuno)histochemical and tract-tracing techniques in anurans (the large green frog, Rana perezi, and the clawed toad, Xenopus laevis). The anuran DCN contains some nicotinamide adenine dinucleotide phosphate diaphorase-positive neurons, very little calbindin D-28k, and a distinct parvalbumin-positive cell population. The anuran DCN is innervated by primary and non-primary spinal afferents, by primary afferents from cranial nerves V, VII, IX, and X, by serotonin-immunoreactive fibers, and by peptidergic fibers. Non-primary DCN afferents from the spinal cord appear to arise throughout the spinal cord, but particularly from the ipsilateral dorsal gray. The present study focused on the efferent connections of the DCN, in particular the targets of the medial lemniscus. The medial lemniscus could be traced throughout the brainstem and into the diencephalon. Along its course, the medial lemniscus gives off collaterals to various parts of the reticular formation, to the octavolateral area, and to the granular layer of the cerebellum. At mesencephalic levels, the medial lemniscus innervates the lateral part of the torus semicircularis as well as various tegmental nuclei. A striking difference between the two species studied is that while in R. perezi medial lemniscal fibers do not reach the tectum mesencephali, in X. laevis, intermediate and deep tectal layers are innervated. Beyond the midbrain, both dorsal and ventral thalamic areas are innervated by the medial lemniscus. The present study shows that the anuran "lemniscal pathway" is basically similar to that of amniotes.
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PMID:Anuran dorsal column nucleus: organization, immunohistochemical characterization, and fiber connections in Rana perezi and Xenopus laevis. 864 70

The rat nucleus accumbens contains medium-sized, spiny projection neurons and intrinsic, local circuit neurons, or interneurons. Sub-classes of interneurons, revealed by calretinin (CR) or parvalbumin (PV) immunoreactivity or reduced nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase histochemistry, were compared in the nucleus accumbens core, shell and rostral pole. CR, PV and NADPH-diaphorase-containing neurons are shown to form three non-co-localising populations in these three areas. No significant differences in neuronal population densities were found between the subterritories. NADPH-diaphorase-containing neurons could be further separated morphologically into three sub-groups, but CR- and PV-immunoreactive neurons form homogeneous populations. Ultrastructurally, NADPH-diaphorase-, CR- and PV-containing neurons in the nucleus accumbens all possess nuclear indentations. These are deeper and fewer in neurons immunoreactive for PV than in CR- and NADPH-diaphorase-containing neurons. CR-immunoreactive boutons form asymmetrical and symmetrical synaptic specialisations on spines, dendrites and somata, while PV-immunoreactive boutons make only symmetrical synaptic specialisations. Both CR- and PV-immunoreactive boutons form symmetrical synaptic specialisations with medium-sized spiny neurons and contact other CR- and PV-immunoreactive somata, respectively. A novel non-carcinogenic substrate for the peroxidase reaction (Vector Slate Grey, SG) was found to be characteristically electron-dense and may be distinguishable from the diaminobenzidine reaction product. We conclude that the three markers used in this study are localised in distinct populations of nucleus accumbens interneurons. Our studies of their synaptic connections contribute to an increased understanding of the intrinsic circuitry of this area.
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PMID:A light and electron microscopic study of NADPH-diaphorase-, calretinin- and parvalbumin-containing neurons in the rat nucleus accumbens. 870 62

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

The assessment of immediate-early gene induction has proven to be a useful method for delineating the neural systems that subserve antipsychotic drug actions. In order to differentiate the sites and mechanisms of action of typical and atypical antipsychotic drugs, we examined the effects of antipsychotic drugs on Fos protein expression in the medial prefrontal cortex. The atypical antipsychotic drug clozapine selectively increased the number of neurons that expressed Fos-like immunoreactivity in the prefrontal cortex, targeting the deep layers of the infralimbic and prelimbic cortices. Pyramidal cells were the major cell type in which Fos was expressed. A small number of calbindin-like immunoreactive, but not parvalbumin- or reduced nicotinamide adenine dinucleotide phosphate diaphorase-containing, interneurons also expressed Fos after clozapine challenge. Immunoblot studies revealed that clozapine induced Fos protein in the infralimbic and prelimbic cortices. Other antipsychotic drugs that are D2 receptor antagonists, including haloperidol, raclopride, sulpiride, remoxipride and loxapine, did not alter Fos expression. The clozapine-induced increase in Fos expression was also not attributable to actions at the D1 dopamine receptor, nor to serotonin type 2a/2c receptor antagonism or combined serotonin type 2-D2 dopamine receptor antagonism. The ability of clozapine to block alpha 1-adrenergic or muscarinic cholinergic receptors did not contribute to the unique actions of clozapine. Despite the inability of dopamine receptor antagonists other than clozapine to elicit an increase in Fos expression, both the mixed D1-D2 dopamine agonist apomorphine and the D2-like agonist quinpirole increased Fos protein levels in the prefrontal cortex. However, neither pretreatment with sulpiride to block D2/3/4 dopamine receptors or SCH 23390 to block D1/5 dopamine receptors modified the Fos response to clozapine. Since dopamine receptor antagonist pretreatments did not attenuate the clozapine-elicited Fos expression, but D2 agonists increased cortical Fos expression, clozapine may act in the prefrontal cortex on an as yet undefined dopamine receptor. In contrast to the nucleus accumbens shell, where all antipsychotic drugs increase Fos expression, only clozapine induced Fos in the medial prefrontal cortex. These observations suggest that the ability of clozapine to treat schizophrenic patients who are resistant to the therapeutic benefits of conventional antipsychotic drugs may occur through actions in the prefrontal cortex.
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PMID:The effects of antipsychotic drugs on Fos protein expression in the prefrontal cortex: cellular localization and pharmacological characterization. 884 47

This paper is a light microscopical study describing the detailed morphology and quantitative distribution of local circuit neurones in areas 25, 32, and 24b of the medial prefrontal cortex (mPFC) in the rat. Cortical interneurones were identified immunocytochemically by their expression of calretinin (CR), parvalbumin (PV), and calbindin D-28k (CB) immunoreactivity. Neurones immunoreactive for gamma-aminobutyric acid (GABA) were also investigated, as were interneurones containing reduced nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase activity. Several distinct classes of CR+, PV+, and CB+ neurones were identified; the most frequent were: bipolar/bitufted CR+ cells in upper layer 3; multipolar PV+ neurones in layers 3 and 5; and bitufted/multipolar CB+ neurones in lower layer 3. CB+ neurones resembling Martinotti and neurogliaform cells were also present in layers 5/6. The morphologies and depth distributions of each cell type were consistent across the three areas of mPFC studied. Seven classes of diaphorase-reactive mPFC neurone are described; these cells were composed about 0.8% of the total neurone population and had a peak distribution located in mid- to lower layer 5 in each area. In areas 32 and 25, three defined bands of diffuse NADPH diaphorase staining were located in layer 2 and in upper and deep layer 5. Diaphorase reactivity was very infrequently colocalised with either CR, PV, or CB immunoreactivities. The numerical densities of neurones (N(V), number of cells per mm3) in each layer were calculated stereologically. The mean total neuronal N(V) estimate for areas 25, 32, and 24b was 51,603 +/- 3,324 (mean +/- S.D.; n = 8). Significant interareal differences were detected. From cortical thickness data and neuronal N(V) estimates, the absolute number of neurones under 1 mm2 of cortical surface (N(C)) have been derived. The mean N(C) value for areas 25, 32, and 24b was 57,328 +/- 7,505 neurones. In immunolabelled Nissl-stained sections, CR+ neurones constituted an overall 4.0%, PV+ cells 5.6%, and CB+ 3.4% of the total neurone populations in mPFC. GABA+ cells represented a mean of 16.2% (14.8-17.2%) of neurones in areas 25, 32 and 24b. The absolute numbers of CR+, PV+, CB+, and GABA+ neurones within individual layers in a column of cortex under 1 mm2 of cortical surface (N(L)) have also been derived, with significant interareal differences in N(L) values being detected. The data provide the structural basis for a qualitative and quantitative definition of local cortical circuits in the rat mPFC.
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PMID:Local-circuit neurones in the medial prefrontal cortex (areas 25, 32 and 24b) in the rat: morphology and quantitative distribution. 900 87

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


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