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)

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

The neuron morphology and distribution of four putative transmitters were investigated in the myenteric plexus of frog (Rana esculenta) midgut. The gross morphology was revealed by NADH-diaphorase histochemistry, and the shape of the neurons by silver impregnation. Nerve cells had heterogeneous distribution: they either formed ganglia or placed as solitary neurons in the duodenum, while in the rest of the midgut only solitary neurons were observed. Three morphologically distinct cell types were revealed by silver impregnation: mainly type I and type II neurons cells were seen in the duodenum, while the rest of the intestine contained type II and III cells. Catecholamine fluorescence was revealed in nerve fibres in the duodenum, while few small nerve cells were observed in the small intestinal region. Acetylcholinesterase histochemistry showed strongly reactive nerve cells that were associated with the main fibre bundles in the duodenum. Only longitudinally oriented fibres and occasionally stained neurons were seen in the small intestine. Substance P immunocytochemistry revealed an extensive plexus, which contained a moderate number of stained perikarya in the full length of the midgut. Gamma-aminobutyric acid showed non-uniform distribution in the two parts of the midgut: a stronger and more regular fibre staining was found in the duodenum then in the rest of the intestine. Ultrastructural observations demonstrated that intrinsic neurons received synaptic inputs from the profiles contained agranular vesicles, while "P"-type profiles established close contacts with neurons. Both profile types formed close contacts with the smooth muscle cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Some morphological and histochemical features of the midgut myenteric plexus of the common European frog, Rana esculenta. 137 78

The present study describes the patterns of NADPH-diaphorase reactivity in the ventral and dorsal lateral geniculate nuclei of rats. In the ventral lateral geniculate nucleus, two distinct populations of NADPH-diaphorase reactive cells are apparent. One population is deeply stained, generally larger in somal size and located in the more superficial or dorsolateral regions of the nucleus. The second population of reactive cells in the nucleus is lightly labeled, small in somal size, and found in deeper or more ventromedial regions of the nucleus. Double labeling with an antibody to GABA revealed that neither cell class is GABAergic. In the dorsal lateral geniculate nucleus, reactivity is apparent in lightly labeled small cells only, most of which are GABA immunoreactive also. The NADPH-diaphorase reactive cells, however, form only a small proportion of the total population of GABAergic cells in the nucleus. The striking feature of the NADPH-diaphorase reactive cells in the dorsal lateral geniculate nucleus is their spatial distribution. Most cells are located in the more superficial or dorsolateral areas: very few are apparent in deeper or more ventromedial areas of the nucleus. This distribution closely parallels the location of the outer "shell" region of the nucleus (see Reese, 1988), which receives most of its afferents from the smaller class II and III ganglion cells of the retina and from the superior colliculus.
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PMID:NADPH-diaphorase reactivity in the ventral and dorsal lateral geniculate nuclei of rats. 150 29

Neuronal degeneration that occurs in both ischemia and degenerative neurologic illnesses may involve excitotoxic mechanisms. In the present study, we examined whether cortical lesions with agonists acting at subtypes of glutamate receptors result in selective patterns of neuronal death. Injections of quinolinic acid, NMDA, homocysteic acid, kainic acid (KA), and alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA) were made at 2 sites in the dorsolateral frontoparietal cortex in rats. After 1 week, the cerebral cortex was either dissected for neurochemical studies, or animals were perfused for histologic evaluation. Concentrations of somatostatin (SS), neuropeptide Y (NPY), substance P (SP), cholecystokinin (CCK), and vasoactive intestinal polypeptide (VIP) were measured by radioimmunoassay, while amino acids and catecholamines were measured by high-performance liquid chromatography (HPLC) with electrochemical detection. NMDA agonists (quinolinic acid, homocysteic acid, and NMDA itself) resulted in dose-dependent reductions in glutamate and GABA, while SS, NPY, SP, CCK, and VIP were either unchanged or significantly increased in concentration. KA and AMPA at doses that resulted in comparable GABA depletions caused significant reductions in SS concentrations. Markers of cortical afferents were spared. All excitotoxins resulted in dose-dependent marked increases in uric acid concentrations. Histologic examination verified that lesions with NMDA agonists produced relative sparing of NADPH-diaphorase, SS, VIP, and CCK neurons. These results show that NMDA excitotoxin lesions result in a pattern of selective neuronal damage in the cerebral cortex that is similar to that which occurs in both ischemia and Huntington's disease.
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PMID:Neurochemical characterization of excitotoxin lesions in the cerebral cortex. 167 Jul 82

NADPH-diaphorase positive cells were described in the visual cortex of the rat in layers II-VI and in the white matter. Their somata were large or medium-sized, oval or elongated, and their cytoplasm was accumulated at the poles. Some proximal thickened coarse dendrites formed a bitufted dendritic field. These features showed a cell type impregnated with the Golgi-Kopsch-method and a Golgi-deimpregnation-method described as Martinotti cell (sparsely spined polarized neurons with ascending axons). The immunocytochemical evidence of GABA in NADPH-diaphorase positive neurons (double labeling) showed the GABA ergic nature of these cells, but an attempt for a double labelling of NADPH-diaphorase and Parvalbumin was negative.
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PMID:[Gabaergic NADPH-diaphorase-positive Martinotti cells in the visual cortex in rats]. 170 86

We previously found a relative sparing of somatostatin and neuropeptide Y neurons 1 week after producing striatal lesions with NMDA receptor agonists. These results are similar to postmortem findings in Huntington's disease (HD), though in this illness there are two- to threefold increases in striatal somatostatin and neuropeptide Y concentrations, which may be due to striatal atrophy. In the present study, we examined the effects of striatal excitotoxin lesions at 6 months and 1 yr, because these lesions exhibit striatal shrinkage and atrophy similar to that occurring in HD striatum. At 6 months and 1 yr, lesions with the NMDA receptor agonist quinolinic acid (QA) resulted in significant increases (up to twofold) in concentrations of somatostatin and neuropeptide Y immunoreactivity, while concentrations of GABA, substance P immunoreactivity, and ChAT activity were significantly reduced. In contrast, somatostatin and neuropeptide Y concentrations did not increase 6 months after kainic acid (KA) or alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA) lesions. At both 6 months and 1 yr, QA lesions showed striking sparing of NADPH-diaphorase neurons as compared with both AMPA and KA lesions, neither of which showed preferential sparing of these neurons. Long-term QA lesions also resulted in significant increases in concentrations of both 5-HT and 5-hydroxyindoleacetic acid (HIAA), similar to findings in HD. Chronic QA lesions therefore closely resemble the neurochemical features of HD, because they result in increases in somatostatin and neuropeptide Y and in 5-HT and HIAA. These findings strengthen the possibility that an NMDA receptor-mediated excitotoxic process could play a role in the pathogenesis of HD.
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PMID:Chronic quinolinic acid lesions in rats closely resemble Huntington's disease. 171 Jun 57

Heritable neurodegenerative diseases may be associated with one or more endogenous neurotoxins whose actions on neurons lead to the degenerative changes. One metabolite of tryptophan, the amino acid L-kynurenic acid (L-KYN), was chronically injected into the striatum of the male rat to test its potential as an endogenous neurotoxin. L-KYN, at concentrations of approximately five times its normal brain levels, produced a large lesion with relative selective neuron sparing. The L-KYN-induced lesion presented three concentric regions: a central necrotic zone, a thin pyknotic zone, and an outermost spongiose zone. The number of GABA-ergic neurons were markedly reduced (approximately 76%), while cholinesterase-positive neurons were also lost. The NADPH diaphorase-positive neurons were the most resistant to L-KYN neurotoxicity and were spread throughout the spongiose zone. The brain levels of L-KYN are abnormal in patients with the neurodegenerative disorder Huntington's disease and as a neurotoxin L-KYN may play a role in the etiology of this disease. Of further significance, the fact that L-KYN is neurotoxic contraindicates the use of this excitatory amino acid receptor antagonist as a therapeutic agent in the treatment of neurodegenerative disorders.
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PMID:Chronic intrastriatal injection of the excitatory amino acid receptor antagonist L-kynurenic acid in rat produces selective neuron sparing lesions. 173 68

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 purpose of this study was to determine the nature of the neurochemical signals which impinge on the mesencephalic locomotor region (MLR) to produce locomotion in the rat. Injections of GABA antagonists into NADPH diaphorase-positive regions (PPN) were found to induce locomotion for short episodes (5-30 sec) which were repeated for several minutes (1-40 min). Such activity was blocked by injections of GABA and the GABA agonist, muscimol. Locomotion was induced by injection of substance P (SP), which also produced short, repeated episodes of locomotion. The more potent excitatory amino acid agonist, n-methyl-d-aspartic acid (NMDA), however, did produce dose-dependent, long-lasting (20 sec-5 min) locomotor episodes which were repeated over prolonged periods at the higher concentrations used (2-24 min). Additional injections of NMDA could drive stepping from a walk to a trot to a gallop. The effects of NMDA were blocked by injections of the excitatory amino acid antagonist, aminophosphonovalerionic acid (APV) (1-10 mM). Preliminary evidence suggests that carbachol (10-50 mM), a cholinergic agonist, inhibits NMDA-induced increases in muscle tone and episodes of stepping. The effect of carbachol was blocked by the cholinergic antagonist, atropine.
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PMID:Posterior midbrain-induced locomotion. 197 Sep 47

Neurons in long-term striatal grafts were examined to determine if they retain the neurotransmitter characteristics of cells in younger grafts. In addition, calbindin-d28k, a ubiquitous marker of medium spiny neurons, was used to examine the overall frequency and ultrastructural characteristics of spiny neurons in the older grafts. Grafts from 17-day fetal striata were injected into the quinolinic acid-lesioned caudate nucleus in 5 adult rats. After 16 months, the neostriatum was processed for the localization of immunoreactive GABA, calbindin, enkephalin and NADPH-diaphorase (-d) activity. The proportions of GABA-, enkephalin- and NADPH-d-labeled neurons to total Nissl-stained neurons in the 16-month-old grafts (25 +/- 6, 13 +/- 4, and 3 +/- 3, respectively) were similar to findings in 2-month-old grafts. Calbindin-positive cells formed the highest proportion (36.3 +/- 3) of labeled neurons in the older grafts. Nuclear and spine morphology of immunoreactive calbindin cells varied more in the grafts than in host caudate. Results show that there is long-term survival and stability of GABA, enkephalin and NADPH-d cell populations in the grafts and that some grafted spiny neurons may exhibit altered phenotype from those of host striatum.
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PMID:Long-term survival of GABA-, enkephalin-, NADPH-diaphorase- and calbindin-d28k-containing neurons in fetal striatal grafts. 198 Aug 52


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