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)

Tegmental cholinergic neurons vary their discharge patterns across the sleep-wake cycle, and glutamate is suggested to play an important role in determining these firing patterns. Cholinergic and noncholinergic neurons in the mesopontine tegmentum have different susceptibilities to various excitotoxins, presumably because of heterogeneity in the expression of glutamate receptor subtypes in this area. By using a double-labeling procedure that combines nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-diaphorase) histochemistry and avidin-biotin-peroxidase immunocytochemistry with diaminobenzidine as the chromogen, we compared the colocalization of AMPA receptor subunits GluR1, GluR2/3, and GluR4, kainate receptor subunits GluR5/6/7, and an NMDA receptor subunit NMDAR1 on NADPH-diaphorase-positive (cholinergic) neurons in the mesopontine tegmentum. Throughout the brainstem, neurons immunoreactive for GluR2/3 and NMDAR1 were most numerous, whereas neurons labeled for GluR1, GluR4, and GluR5/6/7 were less common. Specifically within the mesopontine tegmentum, the proportion of double-labeled neurons in the diaphorase-containing cell population was highest with GluR1 (43%) and lowest with GluR5/6/7 (12%). Regardless of the receptor subunit type, the greatest numbers of double-labeled neurons were observed in the pedunculopontine tegmental nucleus pars compacta and the fewest in the dorsal aspect of the laterodorsal tegmental nucleus. In addition, there were regional differences in the relative expression of receptor subunits and diaphorase-positive neurons across the subdivisions of the tegmental cholinergic column. Because each ionotropic subunit confers distinctive properties to a receptor channel, the present results suggest that mesopontine cholinergic neurons have nonuniform responses to glutamate and are also discriminable from basal forebrain cholinergic neurons in terms of glutamate receptor configuration.
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PMID:Colocalization of ionotropic glutamate receptor subunits with NADPH-diaphorase-containing neurons in the rat mesopontine tegmentum. 872 91

Nitric oxide may serve as a neuronal messenger in the regulation of cardiorespiratory function via the N-methyl-D-aspartate (NMDA) receptor-mediated neuronal nitric oxide synthase (nNOS) activation. Since hypoxic stress would drastically influence the cardiorespiratory function, the present study aimed to examine if the expression of nNOS and NMDA receptor subunit 1 (NMDAR1) in the nodose ganglion (NG) would alter under different extents of hypoxia treatment. The nicotinamine adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry, nNOS and NMDAR1 immunofluorescence were used to examine nNOS and NMDAR1 expression in the NG following exposing of adult rats in the altitude chamber (0.27 atm, PO(2)=43 torr) for 2 and 4 h. The present results showed that NADPH-d, nNOS and NMDAR1 reactivities were co-localized in the NG under normoxic and hypoxic environment. Quantitative evaluation revealed that about 43% of neurons in the NG showed positive response for NADPH-d/nNOS and NMDAR1 reactivities. However, in animals subjected to hypoxia, both the percentage and the staining intensity of NADPH-d/nNOS and NMDAR1 labeled neurons were drastically increased. The percentage of NADPH-d/nNOS and NMDAR1-immunoreactive neurons in the NG was raised to 68% as well as 77%, respectively, following 2 and 4 h of hypoxic exposure. The magnitude of up-regulation was positively correlated with the duration of hypoxic periods. No significant cell loss was observed under this experimental paradigm. These findings suggest that different extents of hypoxia might induce the higher expression of nNOS and NMDAR1 in the NG, which could contribute to the neuronal integration as responding to the different physiological demands under hypoxic stress.
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PMID:Upregulation of NMDA receptor and neuronal NADPH-d/NOS expression in the nodose ganglion of acute hypoxic rats. 1266 61