Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.6.5.2 (NQO1)
 6,196 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

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