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)

Nitric oxide may serve as a retrograde messenger to refine or stabilize synapses in the developing nervous system. Whether this action is dependent upon glutamate and the N-methyl-D-aspartate receptor is not yet established. We have used the patch-cluster system in the intermediate gray layer (IGL) of the rat superior colliculus (SC), a system receiving both glutamatergic and cholinergic input, to study this question. The normal distribution and development of nitric oxide synthase (NOS) in SC was examined using nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) histochemistry in Sprague-Dawley rats aged P4 to adulthood. Fibers containing acetylcholine (ACh) were identified using choline acetyltransferase (ChAT) immunocytochemistry. In addition, N omega-nitro-L-arginine, an inhibitor of NOS, was injected intraperitoneally from birth until P10, P14, P18, or P21-22 to determine if NOS inhibition would disrupt the formation of the ACh patches. Control animals were studied from the same age groups. Our results show NADPH-d-labeled cells within the periaqueductal gray and the deep gray layer of SC by P4, the earliest age examined. By P8-P9, cells in the IGL were well labeled by NADPH-d, while few in the superficial layers (SL) were labeled. SL cells were visible by P10 and were intensely labeled by P14. IGL cells transiently expressed NADPH-d in that the number of labeled cells increased from P8 to P35, then decreased in the adult. ChAT-labeled fibers first appeared in the IGL at P10, formed a characteristic two-tier pattern by P14, and established obvious patches by P21. Inhibition of NOS from birth produced no qualitative differences in the distribution or density of either ChAT-labeled fibers or NADPH-d-labeled cells and fibers at any of the ages examined. We therefore conclude that NO does not contribute to the refinement of cholinergic fiber patches in the rat SC, probably because the fiber system is not glutamatergic.
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PMID:Inhibition of nitric oxide synthase fails to disrupt the development of cholinergic fiber patches in the rat superior colliculus. 920 10

We examined the pattern of NADPH-diaphorase (NADPH-d) staining in the lateral geniculate nucleus (LGN) of dorsal thalamus in fetal and newborn kittens, and adult cats. This staining visualizes the synthesizing enzyme of nitric oxide (NO), a neuromodulator associated with central nervous system (CNS) development and synaptic plasticity. In the adult, very few LGN cells stained for NADPH-d, and these were restricted to interlaminar zones and ventral C layers. NADPH-d labeled a dense network of fibers and axon terminals throughout the LGN and adjacent thalamic nuclei. The source of such labelling has been reported to be cholinergic neurons from the parabrachial region of the brain stem (Bickford et al., 1993). A very different pattern of staining was observed in prenatal and early postnatal kittens. Between embryonic (E) day 46-57, lightly stained cells appeared throughout the LGN. From this age, through about the first month of life, the number of stained cells in the LGN rose rapidly. The density (cells/mm2) of labeled cells peaked at postnatal day (P) 28 (P28), and was about 150 times greater than the level measured in the adult LGN. After P28, cell staining declined rapidly, and fell to adult levels at P41. The reduction in cell staining that occurred between P35-41 was accompanied by the appearance of fine-caliber fiber staining, similar to that observed in the adult LGN. NADPH-d staining, which reveals the presence of nitric oxide synthase (NOS), and thus NO activity, may reflect two processes. In the adult LGN, the labeling of cholinergic axons arising from the brain-stem parabrachial region coupled with a paucity of the LGN cellular staining suggests that NO operates in an orthograde manner, being co-released with ACh to influence the gain and efficacy of retinogeniculate transmission. By contrast, in developing kitten, NADPH-d staining of LGN cells suggests that NO acts in a retrograde fashion, perhaps playing a role in maintaining associative processes underlying activity-dependent refinement of retinogeniculate connections.
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PMID:Developmental changes in the pattern of NADPH-diaphorase staining in the cat's lateral geniculate nucleus. 944 96

Nitric oxide (NO) is a neuronal messenger molecule that mediates pathway refinement in some brain regions. We used nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) histochemistry to examine the development of NO expression in the superior colliculus (SC) of kittens aged E28-E58 and P2-P57 and adults in order to determine if NO expression is correlated with pathway refinement. At E28, labeled cells were seen only within the subventricular zone (SVZ). At E36-E41, labeled cells were also found within the deep gray layer (DGL) of SC. At E51 and E58, a few labeled neurons were also present in the intermediate gray layer (IGL). These neurons already had extensive dendritic fields and well-developed morphologies at the time that they first expressed nitric oxide synthase (NOS). The number of neurons labeled in the DGL and IGL increased postnatally, reaching a peak density between P14 and P35. Neurons within the optic (OL) and superficial gray layers (SGL) were first visible at P7 and increased slightly in number until adulthood. However, SGL-labeled neurons were relatively limited in number and lightly labeled at all ages examined. We conclude that (1) NADPHd expression occurs in SC beginning in the second trimester in kittens and progresses in a ventral to dorsal pattern between E36-P35; (2) few neurons in kitten SGL are labeled by NADPHd and these appear relatively late in postnatal development; and (3) there is no correlation between NOS expression and retinocollicular pathway refinement in kittens, a result different from that seen in rodents.
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PMID:Prenatal and postnatal expression of nitric oxide in the developing kitten superior colliculus revealed with NADPH diaphorase histochemistry. 1134 15

Nitric oxide (NO) is a diffusible neurotransmitter that has been implicated in key developmental events, including the refinement of retinogeniculate axons into ON/OFF sublayers in the ferret lateral geniculate nucleus (LGN), and in the formation of eye-specific laminae in other species. To understand the role of NO in the LGN, it is critical to fully characterize the pattern of brain nitric oxide synthase (bNOS) expression within the nucleus, including the phenotype of the neural elements that express it. We have examined the temporal and spatial pattern of bNOS expression in the ferret LGN during the first 6 weeks of postnatal development, and in the adult, by detecting bNOS with a monoclonal antibody as well as beta-nicotinamide adenine dinucleotide phosphate-diaphorase histochemistry. We have found that bNOS is expressed in neurons in the A laminae of the LGN as early as postnatal day 7 (P7), a time coincident with eye-specific segregation of retinal axons. This expression continues through P35, with peak somatodendritic expression at P21. Fluorescent double labeling using antibodies to bNOS and glutamic acid decarboxylase indicate that bNOS is expressed in gamma-aminobutyric acid-ergic interneurons within the A laminae. Electron microscopic examination of bNOS-labeled cells showed synaptic contacts from terminals with two distinct morphologic profiles. Expression of bNOS within interneurons that receive contacts from multiple sources indicates that the synaptic circuitry associated with bNOS activation and the potential targets of NO may be more complex than originally thought and supports a potential new role for interneurons as cellular intermediaries in the refinement of pathways in the LGN. Our findings broaden the window of time that bNOS may be active within the developing LGN, suggesting an expanded role for NO during early postnatal development.
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PMID:Brain nitric oxide synthase expression in the developing ferret lateral geniculate nucleus: analysis of time course, localization, and synaptic contacts. 1279 37