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)

This paper describes the development of the rat vomeronasal organ from the stage of anlage until adulthood. Groups of four rats were sacrificed daily from prenatal day 13 (E13) until birth; at days 2, 4, 7, 10, 14 and 16 after birth; weekly from day P21 to P42 plus an additional group of adults. The vomeronasal organs were processed for light microscopy, including alcian blue-PAS and NADH-diaphorase reactions, and also for electron microscopy. For summarizing our results we propose the following developmental stages: 1. Anlage (E13). 2. Early morphogenesis (E14-16). 3. Late morphogenesis (E17 to birth). 4. Initiation of secretory activity (First postnatal week). 5. Cytoarchitectural maturity (2nd postnatal week). 6. Complete maturity (From 3rd postnatal week onwards). Our results on the maturation of the histological structure and the histochemical reactions, indicate that there may be some functional activity at birth but the development of the organ still continues during the first three postnatal weeks to acquire its full functional capability.
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PMID:Developmental stages of the vomeronasal organ in the rat: a light and electron microscopic study. 144 18

Serotoninergic and cholinergic neurons are known to appear earlier in the ontogeny (day E12) of the murine gut than those containing substance P or vasoactive intestinal peptide (day E14). It has also been demonstrated that proliferating neural precursors coexist with mature neurons in developing enteric ganglia. These observations have led to the hypotheses that peptidergic neurons develop later than those that utilize small molecule neurotransmitters and that the activity of early developing neurons may affect the phenotypic expression of coexisting neuroblasts. As a partial test of these hypotheses we studied the phenotypic expression of neurons recognized by antisera to neuropeptide Y (NPY) and calcitonin gene-related peptide (CGRP), and of those visualized by the histochemical demonstration of reduced nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase activity. NADPH diaphorase activity, which is coexpressed with NPY immunoreactivity in all submucosal and many myenteric neurons, was first found on day E11 in clusters of cells in the dorsal mesogastrium. These cells also expressed neurofilament reactivity and thus were developing along a neuronal lineage. Enteric neurons that expressed NADPH diaphorase activity were visualized in the stomach one day later, on day E12. At this time, NADPH diaphorase-containing cells could no longer be demonstrated in the dorsal mesogastrium. NPY immunoreactivity first appeared in the wall of the bowel on day E12, when it was seen in cells in the presumptive stomach. By day E13, the entire length of the bowel contained NPY-immunoreactive neurons. Cells that displayed NADPH diaphorase activity were found at this time at both ends of the alimentary tract, but did not appear in the ileum until day E18. In contrast, CGRP immunoreactivity could not be detected anywhere in the gut until day E17, but by day E18 all regions of the bowel contained CGRP-immunoreactive neurons. Endogenous 5-HT was first detected at day E16 in mucosal epithelial cells in all segments of the gut except the stomach, where it appeared at day E18. The NPY/NADPH diaphorase set of neurons thus develop before the acquisition of a detectable level of endogenous 5-HT or enteric neural 5-HT receptors (which arise in the foregut at day E14). These observations demonstrate that enteric neurons that express small molecule neurotransmitters do not necessarily develop earlier than peptidergic neurons as a class; however, various types of enteric neurons do appear in a sequential order.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Time course of expression of neuropeptide Y, calcitonin gene-related peptide, and NADPH diaphorase activity in neurons of the developing murine bowel and the appearance of 5-hydroxytryptamine in mucosal enterochromaffin cells. 278 79

Pancreatic ganglia are formed by neural crest-derived precursors, are innervated by enteric neurons, and contain neuropeptides. In addition, the enzyme NADPH-diaphorase is located in a subset of enteric and pancreatic neurons. The expression of neural markers (GAP-43 and NC-1), neurotransmitter-related markers (including neuropeptide Y (NPY), vasoactive intestinal peptide (VIP), gastrin-releasing peptide (GRP), galanin (GAL), dopamine beta hydroxylase (DBH), substance P (SP), calcitonin gene-related peptide (CGRP)), and NADPH-diaphorase was studied in the fetal and neonatal rat gut and pancreas (E12-P28) in situ and in vitro. NC-1, GAP-43 and DBH-immunoreactive cells were found in the primordial stomach on day E12, and in the pancreas on day E13, along with NPY in endocrine cells. Pancreatic NPY-immunoreactive neurons were detected by day E18. CGRP was seen in the foregut at day E12 but not in the pancreas until day E14. Other neuropeptides (SP, GAL, GRP and VIP) all appeared in the foregut earlier than in the pancreas. NADPH-diaphorase activity was first found in situ in foregut neurons on day E13, and in the pancreas on day E14, but seen in explants a day earlier. These observations show that development of neurons occurs earlier in the gut than in the pancreas, and that NADPH-diaphorase activity appears earlier than the immunoreactivities of the neuropeptides.
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PMID:Appearance of neuropeptides and NADPH-diaphorase during development of the enteropancreatic innervation. 772 Feb 14

Nitric oxide (NO) has been implicated in the pathogenesis of brain injury from hypoxia-ischaemia. In the brain, the enzyme responsible for NO synthesis is neuronal nitric oxide synthase (nNOS). Using in situ hybridization, immunohistochemistry and NADPH diaphorase histochemistry, we examined the spatial and temporal expression of nNOS during development of the rat brain to determine whether the expression of nNOS delineates the areas of the brain that are selectively vulnerable to hypoxic-ischaemia injury. The expression of nNOS was localized to discrete areas of the brain. nNOS could be detected in the developing forebrain in the 10-day-old embryo (E10). From E14 to E18, the highest level of expression was in the cortical plate, where the majority of neurons were positive. However, this expression diminished with time; in the adult there were only a few nNOS-positive neurones in the deep layers of the cortex. Expression of nNOS was not detected prenatally in the basal ganglia. There was transient high-level expression during the first postnatal week. Thereafter, the basal ganglia exhibited the adult pattern of expression. Expression of nNOS could be detected in the hippocampus at E16. This expression remained constant with regional localization in layers CA1 and CA3 in the adult. Similarly, nNOS expression in the developing cerebellum was observed only after birth. From the first day after birth (P1) to P6, expression was limited to the molecular cell layer. As the cerebellum matured, nNOS expression could be detected in the inner granular layer. By P21, the adult distribution of nNOS expression was observed. All regions expressing nNOS mRNA also demonstrated nNOS protein expression and NADPH diaphorase catalytic activity. Our results demonstrate that nNOS expression in the developing brain correlates with regions of selective vulnerability to hypoxic-ischaemic injury, and, therefore, supports a role for NO in hypoxic-ischaemic injury in the developing brain.
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PMID:Expression of neuronal nitric oxide synthase corresponds to regions of selective vulnerability to hypoxia-ischaemia in the developing rat brain. 917 98

Neurotrophin-3 (NT-3) is known to promote enteric neuronal and glial development. Ciliary neurotrophic factor (CNTF) and leukemia inhibitory factor (LIF) were investigated to test the hypothesis that the development of subsets of enteric neurons and/or glia is also affected by a neuropoietic cytokine, by itself, or together with NT-3. Crest-derived cells, immunoselected from the fetal rat gut (E14) with antibodies to p75NTR, were found by RT-PCR and immunocytochemistry (after culture) to express both alpha (CNTER alpha) and beta components (gp130 and LIFR beta) of the tripartite CNTF receptor. In situ, myenteric ganglia below the esophagus were CNTFR alpha-immunoreactive by E16-E18. In vitro, CNTF and LIF induced in crest-derived cells nuclear translocation of STAT3 (signal transducer and activator of transcription 3), a concentration-dependent increase in expression of neuronal or glial markers, and a decrease in expression of the precursor marker, nestin. LIFR beta was expressed by more cells than CNTFR alpha; therefore, although the factors were equipotent, the maximal effect of LIF > CNTF. The cytokines and NT-3 were additive in promoting neuronal but not glial development. Specifically, the development of neurons expressing NADPH-diaphorase activity (an early marker found in inhibitory motor neurons) was promoted by CNTF and NT-3. These observations support the idea that a ligand for the tripartite CNTF receptor complex plays a role in ENS development.
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PMID:Promotion of the development of enteric neurons and glia by neuropoietic cytokines: interactions with neurotrophin-3. 965 38

Interactions of developing neurons with their postsynaptic targets play a significant role in neuronal differentiation. The goal of the present study was to determine if target contact affected the migration or differentiation of autonomic motor neurons (AMNs) in developing rat spinal cord. The peripheral targets of AMNs were excised microsurgically from histotypic spinal slices before the arrival of AMN axons. The migration of AMNs was assessed in DiI retrogradely labeled preparations, and the differentiation of these cells was evaluated by beta-nicotinamide adenine dinucleotide phosphate reduced diaphorase (NADPH-d) histochemistry. In target-deprived specimens, NADPH-d expression in AMNs was virtually eliminated. In addition, DiI-labeled AMNs were scattered throughout the intermediate spinal gray matter instead of being aggregated in the intermediolateral nucleus as in control slices. This observation indicated that migration of AMNs had occurred, but that it had been disorganized significantly by target removal on embryonic day 13 (E13). In sham, "incision-only" specimens from which peripheral target tissue was not removed, AMNs expressed NADPH-d and migrated normally, indicating that axotomy alone was not sufficient to disrupt AMN development. Previous studies have shown that target removal after the arrival of AMN axons at their postsynaptic targets on E14 has no affect on the organized migration of AMNs (Barber et al. [1993] J. Neurosci. 13:4898-4907). This observation together with the present results indicate that initial target contact is necessary for both the differentiation and directed migration of AMNs, and that this contact does not need to be sustained for these developmental events to progress normally.
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PMID:Autonomic motor neuron migration and expression of nicotinamide adenine dinucleotide phosphate reduced diaphorase are dependent upon peripheral target. 971 10

The genesis of the cuneothalamic neurons (CTNs) in the rat cuneate nucleus was determined by a double-labeling method using 5'-bromodeoxyuridine (BrdU), the thymidine analogue, and Fluoro-Gold (FG), a retrograde fluorescent tracer. BrdU-positive cells were observed in the cuneate nucleus in all rats receiving BrdU injection at embryonic days (E) E13--E16; none was detected in rats given BrdU injection at E12. At E13 and E14, BrdU-positive cells were randomly distributed. However, at E15, the number of BrdU-positive cells was clearly reduced and the majority of them was located at the dorsolateral or peripheral region of the nucleus. FG/BrdU double-labeling study showed the existence of BrdU-labeled CTNs when the mother rat received BrdU injection at E13 and E14, being more numerous at E13 in which the neurons were scattered throughout the nucleus. At E14, however, the majority of the BrdU-labeled CTNs were located superficially in the nucleus. Double-labeled cells were undetected in rats that had been exposed to BrdU at E15 and E16. Quantitative data showed that the majority (ca 70-80%) of the CTNs were generated at E13, and were markedly decreased at E14 (ca 4-6%). Using nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry coupled with BrdU immunohistochemistry, we have shown the NADPH-d/BrdU double-labeled neurons in the nucleus between E13 and E15, with the majority of them occurring at E14, but absent at E16. The present results suggest that the CTNs are generated prior to the NO-containing neurons in the cuneate nucleus.
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PMID:Neurogenesis of cuneothalamic neurons and NO-containing neurons in the cuneate nucleus of the rat. 1181 40

Reelin, the extracellular matrix protein missing in reeler mice, plays an important role in neuronal migration in the central nervous system. We examined the migratory pathways of phenotypically identified spinal cord neurons to determine whether their positions were altered in reeler mutants. Interneurons and projection neurons containing choline acetyltransferase and/or NADPH diaphorase were studied in E12.5-E17.5 reeler and wild-type embryos, and their final locations were assessed postnatally. While three groups of dorsal horn interneurons migrated and differentiated normally in reeler mice, the migrations of both sympathetic (SPNs) and parasympathetic preganglionic neurons (PPNs) were aberrant in the mutants. Initially reeler and wild-type SPNs were detected laterally near somatic motor neurons, but by E13.5, many reeler SPNs had mismigrated medially. Postnatally, 79% of wild-type SPNs were found laterally, whereas in reeler, 92% of these neurons were positioned medially. At E13.5, both reeler and wild-type PPNs were found laterally, but by E14.5, reeler PPNs were scattered across the intermediate spinal cord while wild-type neurons correctly maintained their lateral location. By postnatal day 16, 97% of PPNs were positioned laterally in wild-type mice; in contrast, only 62% of PPNs were found laterally in mutant mice. In E12.5-E14.5 wild-type mice, Reelin-secreting cells were localized along the dorsal and medial borders of both groups of preganglionic neurons, but did not form a solid barrier. In contrast, Dab1, the intracellular adaptor protein thought to function in Reelin signaling, was expressed in cells having positions consistent with their identification as SPNs and PPNs. In combination, these findings suggest that, in the absence of Reelin, both groups of autonomic motor neurons migrate medially past their normal locations, while somatic motor neurons and cholinergic interneurons in thoracic and sacral segments are positioned normally. These results suggest that Reelin acts in a cell-specific manner on the migration of cholinergic spinal cord neurons.
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PMID:Evidence for a cell-specific action of Reelin in the spinal cord. 1190 Apr 67

The superficial dorsal horn of birds as well as mammals contains both cholinergic and nitrergic neuronal structures as evident from the presence of the synthesizing enzymes such as choline acetyltransferase and nitric oxide synthase, which is an NADPH diaphorase. In the rat, both systems develop only postnatally. Rats are altricial at birth whereas pigeons and chickens are semiprecocial or precocial, respectively, at the time of hatching. Immunocytochemical studies of choline acetyltransferase and nitric oxide synthase in the developing avian spinal cord (starting with embryonic day 12 of 18 in the pigeon and 14 of 21 in the chicken) showed that both systems are well developed in the superficial dorsal horn at the time of hatching in both avian species. In the pigeon, choline acetyltransferase-positive superficial dorsal horn neurons appear only on the day of hatching (E18), whereas nitric oxide synthase-positive neurons can be first detected at stage E14. In the chicken, nitric oxide synthase-positive neurons are present already at stage E14, whereas choline acetyltransferase-positive neurons appear at stage E20. Autonomic and somatic motor neurons show adult-like choline acetyltransferase-immunoreactivity and/or nitric oxide synthase-immunoreactivity at the earliest stages investigated. It is concluded that the stage of maturation at birth or hatching plays an important role in the development of superficial dorsal horn cholinergic and nitrergic systems.
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PMID:Embryonic development of choline acetyltransferase and nitric oxide synthase in the spinal cord of pigeons and chickens with special reference to the superficial dorsal horn. 1604 18