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)

We have studied the distribution of the calcium-binding proteins parvalbumin, calbindin and calretinin, the NADPH diaphorase activity and the morphology of the commissural neurons, revealed by the stereotactic applications of fluorogold in the pretectal complex of the rat. The histochemical differentiation of the pretectal complex shows a complementary pattern of parvalbumin and calbindin containing cells. Only a few of the neurons in the pretectal complex contain calbindin. Calretinin immunoreactivity is scant and diffuse. The NADPH-diaphorase activity is restricted to neurons and terminals in the nucleus of the optic tract and the dorsal terminal nucleus. Due to numerous active fibers which traverse these nuclei they display a reticular appearance. Commissural neurons constitute 20% of the cell number of the pretectal complex and are restricted to the dorsal and lateral terminal nuclei.
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PMID:On the structure of the pretectal nuclei of the rat: an immunocytochemical and tracer study. 761 32

Although the gene defect responsible for Huntington disease (HD) has recently been identified, the pathogenesis of the disease remains obscure. One potential mechanism is that the gene defect may lead to an impairment of energy metabolism followed by slow excitotoxic neuronal injury. In the present study we examined whether chronic administration of 3-nitropropionic acid (3-NP), an irreversible inhibitor of succinate dehydrogenase, can replicate the neuropathologic and clinical features of HD in nonhuman primates. After 3-6 weeks of 3-NP administration, apomorphine treatment induced a significant increase in motor activity as compared with saline-treated controls. Animals showed both choreiform movements, as well as foot and limb dystonia, which are characteristic of HD. More prolonged 3-NP treatment in two additional primates resulted in spontaneous dystonia and dyskinesia accompanied by lesions in the caudate and putamen seen by magnetic resonance imaging. Histologic evaluation showed that there was a depletion of calbindin neurons, astrogliosis, sparing of NADPH-diaphorase neurons, and growth-related proliferative changes in dendrites of spiny neurons similar to changes in HD. The striosomal organization of the striatum and the nucleus accumbens were spared. These findings show that chronic administration of 3-NP to nonhuman primates can replicate many of the characteristic motor and histologic features of HD, further strengthening the possibility that a subtle impairment of energy metabolism may play a role in its pathogenesis.
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PMID:Chronic mitochondrial energy impairment produces selective striatal degeneration and abnormal choreiform movements in primates. 762 78

The effect of prenatal cocaine on the anatomical development of the striatum was examined. The distribution and density of dopaminergic innervation of the striatum of animals exposed to cocaine during the second and third week of gestation was not noticeably different from prenatally saline-injected or untreated controls at any age. The patch/matrix organization of the striatum also appeared unaltered: neurons exhibiting dense substance P staining were localized to patches that overlapped dopamine terminal patches early in development, and enkephalin- and calbindin-immunoreactive neurons were found segregated to the matrix. Histochemical staining for acetylcholinesterase and NADPH diaphorase also revealed no differences between prenatally cocaine-treated and control brains. Whereas prenatal cocaine treatment failed to modify the basic compartmental organization of the striatum, it did lead to a hyperinnervation of serotonin-immunoreactive fibers which developed slowly after birth. Thus prenatal exposure to cocaine is capable of altering the ingrowth of serotonergic projections to the striatum while producing no change in the organization of neurons intrinsic to the striatum.
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PMID:Prenatal cocaine increases striatal serotonin innervation without altering the patch/matrix organization of intrinsic cell types. 769 34

An impairment of energy metabolism may underlie slow excitotoxic neuronal death in neurodegenerative diseases. We therefore examined the effects of intrastriatal, subacute systemic, or chronic systemic administration of the mitochondrial toxin 3-nitropropionic acid (3-NP) in rats. Following intrastriatal injection 3-NP produced dose-dependent striatal lesions. Neurochemical and histologic evaluation showed that markers of both spiny projection neurons (GABA, substance P, calbindin) and aspiny interneurons (somatostatin, neuropeptide Y, NADPH-diaphorase) were equally affected. Subacute systemic administration of 3-NP produced age-dependent bilateral striatal lesions with a similar neurochemical profile. However, in contrast to the intrastriatal injections, striatal dopaminergic afferent projections were spared. Both freeze-clamp measurements and chemical shift magnetic resonance spectroscopy showed that 3-NP impairs energy metabolism in the striatum in vivo. Microdialysis showed no increase in extracellular glutamate concentrations after systemic administration of 3-NP. The lesions produced by intrastriatal injection or systemic administration of 3-NP were blocked by prior decortication. However, the NMDA antagonist MK-801 did not block the effects of intrastriatal 3-NP, consistent with a non-NMDA excitotoxic mechanism. In contrast to subacute systemic administration of 3-NP, chronic (1 month) administration produced lesions confined to the striatum in which there was relative sparing of NADPH-diaphorase interneurons, consistent with an NMDA excitotoxic process. Chronic administration showed growth-related proliferative changes in dendrites of spiny neurons similar to changes in Huntington's disease (HD). These results are consistent with in vitro studies showing that mild metabolic compromise can selectively activate NMDA receptors while more severe compromise activates both NMDA and non-NMDA receptors. Chronic administration of 3-NP over 1 month produces selective striatal lesions that replicate many of the characteristic histologic and neurochemical features of HD.
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PMID:Neurochemical and histologic characterization of striatal excitotoxic lesions produced by the mitochondrial toxin 3-nitropropionic acid. 769 9

Substance P immunoreactivity is localized in discrete subsets of neurons in the human cerebral cortex and basal ganglia. In the normal human cerebral cortex, a subset of aspiny local circuit neurons in deep cortical layers and the cortical subplate contain preprotachykinin mRNA and substance P immunoreactive. These neurons, which contain NADPH diaphorase (NO synthase) activity, are strikingly depleted in Alzheimer's disease--in contrast to other local circuit neurons--suggesting that they may be an early target of the degenerative process. In the human basal ganglia, substance P immunoreactivity and mRNA are localized in a subset of spiny striatal neurons that project to the internal segment of the globus pallidus. These neurons are enriched in D1 dopamine receptors and dynorphin, and are calbindin and DARP 32 immunoreactive. A separate subset of aspiny striatal local circuit neurons also contain substance P immunoreactivity. Fiber and terminal staining is prominent in the matrix compartment of the ventromedial striatum and persists dorsally as a rim outlining patches that contain lesser amounts of immunoreactivity. Intense fiber and terminal staining is found in the pars reticulata of the substantia nigra. In Huntington's disease, substance P is depleted in the striatum in parallel with the dorsoventral gradient of neuronal loss. Terminal staining is progressively depleted in the pallidum and substantia nigra in tandem with striatal atrophy. Substance P receptor immunoreactivity, defined with two polyclonal antisera raised against synthetic peptides derived from the substance P receptor sequence, intensely labels a subset of large neurons in the nucleus basalis and striatum identical to neurons labeled with choline acetyltransferase and nerve growth factor receptor antibodies (although striatal cholinergic neurons do not contain nerve growth factor receptor immunoreactivity in the human). These cholinergic neurons resist degeneration in Huntington's disease but are sensitive to degeneration in Alzheimer's disease. Less intensely labeled neurons include pyramidal neurons in the hippocampal CA2 field, nonpyramidal neurons in CA1-4, pyramidal and nonpyramidal neurons in deep neocortical layers and in the cortical subplate. Substance P receptor immunoreactivity is not well defined in the human globus pallidus or substantia nigra.
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PMID:Substance P and substance P receptor histochemistry in human neurodegenerative diseases. 769 86

This study shows localisation of a second class of calbindin-D28k containing neuron other than the medium-sized spiny neuron in the rat nucleus accumbens, using immunohistochemistry with monoclonal antibodies. Ultrastructural characteristics were used to identify this second population of accumbens neurons within its compartments. Staining with NADPH-diaphorase and calbindin-D28k immunoreactivity revealed that some neurons contained both markers.
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PMID:Calbindin-D28k immunoreactive neurons form two populations in the rat nucleus accumbens: a compartmental study. 780 37

We examined the projection from the basal forebrain to thalamic and cortical regions of the visual system in cats, with particular reference to the visual sector of the thalamic reticular nucleus, the lateral geniculate nucleus, and the striate cortex. First, we made injections of wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP) into the visual sector of the thalamic reticular nucleus and found cells labeled by retrograde transport in the lateral nucleus basalis magnocellularis. Injection of biocytin into the basal forebrain resulted in the anterograde labeling of a dense band of fibers and terminals within the entire thalamic reticular nucleus; this labeling extended through the visual sector including the perigeniculate nucleus. No orthograde labeling was found in the lateral geniculate nucleus. Next, we addressed the issue of putative neurotransmitters used by this pathway using a variety of immunocytochemical and histochemical markers. In this fashion, we identified two populations of cells in the nucleus basalis magnocellularis of the cat; large cholinergic cells that contain choline acetyltransferase, NADPH-diaphorase, and calbindin and that project to striate cortex and smaller cells that contain gamma-aminobutyric acid (GABA), glutamic acid decarboxylase, and parvalbumin and that project to the visual sector of the thalamic reticular nucleus. We also examined at the electron microscopic level terminals in the visual sector of the thalamic reticular nucleus that were labeled from a biocytin injection in the basal forebrain. Most of these terminals form symmetric contacts onto dendrites and were revealed by postembedding immunocytochemical staining to be positive for GABA.
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PMID:GABAergic projection from the basal forebrain to the visual sector of the thalamic reticular nucleus in the cat. 783 59

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

In order to examine the localisation of calbindin D28k in the normal striatum of the rat, immunocytochemistry using monoclonal antibodies was carried out at both the light and electron microscopic levels. As has previously been shown, many striatal spiny neurones were immunopositive, however, a small population of neurones with smooth dendrites and indented nuclei were also identified. At least some of these cells also displayed NADPH-diaphorase activity. These findings indicate that, in common with the primate striatum and grafted striatal tissue in the rat, the normal rat striatum contains at least two populations of neurones that express calbindin D28k.
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PMID:Two populations of calbindin D28k-immunoreactive neurones in the striatum of the rat. 810 Apr 72

The striatum is especially vulnerable to hypoxic-ischemic injury, both in adulthood and during development. Striatal injury is likely to play a major role in the chronic abnormalities of motor control which occur as a consequence of developmental hypoxia-ischemia. Previous studies have shown that two striatal neuron phenotypes, cholinergic and NADPH-diaphorase-positive, are resistant to developmental hypoxia-ischemia, but little is otherwise known of patterns of vulnerability among other striatal neurons. In particular, there has been no data available about patterns of vulnerability within the major striatal neuron group, the medium-sized neurons. Since a major anatomical and functional organization of these neurons is in their localization to either the striosome or the matrix compartments, we have examined the effect of developmental hypoxia-ischemia on these compartments using a quantitative morphologic analysis of immunostaining for the calcium-binding protein calbindin-D28k. We have found that there is a predominant loss of the striosome compartment; in the presence of a mean loss of 33% of total striatal area, there was a 49% decrease in striosomal area. There was also a 41% reduction in the number of striosomes, and a small (14%) but significant decrease in the mean area of individual striosomes. The striosome loss was uniform in the rostrocaudal dimension. At a cellular level, the density of calbindin-positive neurons, expressed as number per unit area, was preserved. While there are several possible explanations for the selective loss of the striosome compartment, one hypothesis is that the lower level of calbindin within these neurons makes them more vulnerable to increases in intracellular calcium, which has been postulated to play a role in hypoxic-ischemic injury. The predominant loss of the striosome compartment following hypoxic-ischemic injury may lead to an imbalance with the functionally distinct matrix system. Such an imbalance may contribute to the abnormalities of motor control observed after this form of injury.
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PMID:Relative loss of the striatal striosome compartment, defined by calbindin-D28k immunostaining, following developmental hypoxic-ischemic injury. 824 62


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