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)

A previous study indicated that in adult rat, a distinctive neuronal group in the dorsomedial division of the subnucleus oralis of the spinal trigeminal nucleus (SpVo) and the rostrolateral part of the nucleus of the solitary tract (Sn) is stained for nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d), and suggested that the labeled structures are involved with sensorimotor reflexive functions. This study aimed to characterize the developmental expression of NADPH-d in SpVo and Sn, including other areas of the lower brainstem and cervical spinal cord, by means of the enzyme histochemical staining technique, from the prenatal through the postnatal period. On embryonic day 12 (E12), no neurons in the brain were stained for NADPH-d, whereas blood vessels were stained. Labeling in the vessels was consistently present throughout pre- and postnatal periods but decreased with development. On E15, labeled neurons appeared in the dorsomedial part of SpVo and the rostrolateral part of Sn, but not in the other nuclei. The labeled neurons in both nuclei increased in numbers drastically to E17. Postnatally, they tended to increase gradually in Sn, but to decrease slightly in SpVo. The cell size of labeled neurons reached a plateau at E17 in SpVo, but at postnatal day 4 (P4) in Sn. In other nuclei on E17, labeling appeared in the lateral paragigantocellular reticular, intermediate reticular, medullary reticular, pedunculopontine tegmental, and spinal vestibular nuclei, and laminae V, VI, and X of the cervical spinal cord. On E20 and P0, labeling appeared in the dorsal column, laterodorsal tegmental, raphe obscurus, parvocellular reticular, ventral gigantocellular reticular, and parahypoglossal nuclei, and laminae IX of the cervical spinal cord. On P4 labeling appeared in the parabrachial and median raphe nuclei, medial and caudolateral Sn, the magnocellular zone of subnucleus caudalis of the spinal trigeminal nucleus (SpVc), and laminae III/IV of the cervical spinal cord. On P10, labeling appeared in the paratrigeminal and dorsal raphe nuclei, the superficial zone of SpVc, and laminae I/II of the cervical spinal cord. No newly labeled neurons appeared in any nuclei after P14. The very early appearance of NADPH-d staining in SpVo and Sn, which precedes the appearance of NADPH-d elsewhere in the brainstem, suggests that the nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) system has an important role for primitive orofacial sensorimotor reflexive functions. Furthermore, the pattern of developmental expression of NADPH-d in SpVo and Sn suggests that the NO/cGMP system is organized in a distinct manner in different nuclei.
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PMID:NADPH-diaphorase in the developing rat: lower brainstem and cervical spinal cord, with special reference to the trigemino-solitary complex. 874 99

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

Nitric oxide (NO) has been implicated as a retrograde signal in the process of refining axonal pathways during brain development. To determine some of the factors involved in this process, we have used two model pathway systems in the rat and mouse superior colliculus (SC). The first, the patch-cluster system, consists of clusters of neurons in the intermediate gray layer (igl) which transiently express NO during development and which receive input from a cholinergic pathway from the parabrachial brainstem as well as from other pathways containing different transmitters. The second system, the retinocollicular pathway, consists of glutamatergic fibers that project to the superficial gray layer. We have used both nitric oxide synthase inhibition (nw-nitro-L-arginine, NoArg) and single (nNOS) and double (nNOS and eNOS) gene knockout mice to examine the effect that reduction in NOS has upon the development of these two systems. The onset of NOS expression in rat, as revealed by nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) labeling, occurred in igl cells as early as postnatal day P5, with clusters being well-established by P14. Cholinergic fibers were first visible at P10 and formed obvious patches and tiers by P14. Intraperitoneal injections of NoArg from P1-P22 had no effect upon the development of these cholinergic patches. The pathway also developed normally in both single and double-knockout mice. In contrast, the ipsilateral retinocollicular pathway was altered in the double, but not in the single knockout mouse. This pathway is exuberant during the first week of life, being distributed across much of the mediolateral axis of the rostral SC. By P8-P15, this pathway has retracted to the most mediorostral SC. This refinement was delayed substantially in the double NOS gene knockout mouse. Ipsilateral fibers were found within 3-5 separate medio-lateral patches within the rostral 600 microns of SC at P15, and patches of abnormal size and extent were also seen at P18. We conclude from these results that NO plays a role in pathway development in the rodent SC, but only in glutamatergic pathways and only when both endothelial and neuronal forms of NOS have been deleted. The mechanism of this effect must involve pathway elimination in situations where there is non-correlated electrical activity. It is likely that NO promotes fiber retraction rather than fiber stabilization in these developing nerve fibers.
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PMID:The role of nitric oxide in development of the patch-cluster system and retinocollicular pathways in the rodent superior colliculus. 993 39

Nitric oxide (NO) has been shown to mediate refinement of glutamatergic axonal pathways during development. In this study, we investigated whether the development of a cholinergic pathway in the intermediate gray layer (IGL) of the mouse superior colliculus (SC) is also mediated by NO. The pathway was labeled using an antibody directed against choline acetyltransferase (ChAT) and its distribution examined in normal C57/BL6 mice and in knockout mice in which the genes for the neuronal isoform of nitric oxide synthase (NOS) or both the endothelial and neuronal isoforms of NOS had been disrupted. We also examined the development of expression of NOS using nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) staining. NADPHd labeled cells were found within the IGL by P8 and formed loose clusters of cells by P12-P15. ChAT and NADPHd labeled fibers were first observed at P12 and gradually established their characteristic two-tiered patchy pattern between P14 and P21. Comparison of the ChAT labeled fiber distribution in normal, single nNOS and double e,nNOS knockout mice revealed no differences between these three groups. We therefore conclude that nitric oxide does not mediate refinement of this cholinergic pathway.
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PMID:Failure to disrupt development of cholinergic fiber patches in the superior colliculus in nitric oxide synthase deficient mice. 1061 22

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 short-lived radical, which modulates synaptic plasticity, neuronal oscillations and cerebral blood flow. NOS-containing neurones can be detected anatomically by nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry or by NOS immunohistochemistry. Neuropeptide Y(NPY) is the most abundant peptide in the brain. NPY is connected with several vital functions, such as a feeding behaviour, sexual maturation, regulation of circadian rhythms, body temperature, blood pressure and neuroendocrine secretions. Neuropeptide Y also modulates anxiety-related disorders, limbic epileptic seizures as well as learning and memory processes. The study was performed on 45 Wistar rats of various ages (PO, P4, P7, P10, P14, P21, P30, P60, and P120; P--postnatal day). The free-floating sections were stained with standard immunohistochemistry methods. Thereafter the histological sections were studied using the confocal laser microscope equipped. For 3D reconstruction the image analysis program LaserSharp 2000v. 2.0 (Bio-Rad, UK) was used. We found that in the newborn rat both NOS- and NPY-immunoreactivity was weak. It had been increasing gradually until the 7th day of postnatal life, after that until P14 it was maintained on the similar level, and then the number of immunolabelled cells deceased. The developmental changes concerned cell morphology as well--until the 10th day of life the immunoreactive cells were immature, with round or oval bodies and had only a few fibres. From P14 the cells' morphology became similar to that in adult.
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PMID:Distribution of nitric oxide synthase and neuropeptide Y neurones during the development of the hippocampal formation in the rat. 1272 88