Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.6.5.2 (NQO1)
 6,196 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An anatomical basis was sought for the postulated roles of nitric oxide (NO) as a labile transcellular messenger in the dorsal vagal complex (NTS-X). The diaphorase activity of NO synthase was used as a marker of neurons in NTS-X that are presumed to convert L-arginine to L-citrulline and NO. Nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) staining patterns in the nucleus tractus solitarii (NTS) were spatially related to terminal sites of primary visceral afferents from 1) orosensory receptors (e.g., rostral-central nucleus); 2) soft palate, pharynx, larynx, and tracheobronchial tree (e.g., dorsal, intermediate, and interstitial nuclei); 3) esophagus (nucleus centralis); 4) stomach (nucleus gelatinosus); 5) hepatic and coeliac nerves (nucleus subpostrema); and 6) carotid body and baroreceptors (medial commissural and dorsal-lateral nuclei). Primary visceral afferents were identified as sources of NADPHd-stained fiber plexuses in the NTS-X based on three findings: 1) the presence of NADPHd in nodose ganglion cells with morphological features of first-order sensory relay neurons; 2) retrograde transport of Fluoro-Gold (FG) or cholera toxin B (CT-B) from NTS-X to NADPHd-positive nodose ganglion neurons; and 3) striking reductions of NADPHd-stained processes within primary vagal projection fields ipsilateral to unilateral nodose ganglionectomy. A central origin of NADPHd-stained processes in NTS-X was identified in the medial parvicellular subdivision of the paraventricular hypothalamic nucleus. We conclude that NO of peripheral and central origin may modulate viscerosensory signal processing in the NTS-X and autonomic reflex function.
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PMID:Central and primary visceral afferents to nucleus tractus solitarii may generate nitric oxide as a membrane-permeant neuronal messenger. 878 75

Spinal cord injury results in abnormal sympathetic control of the cardiovascular system, perhaps because of reactions of sympathetic preganglionic neurons to loss of their supraspinal afferent inputs. We investigated morphological changes in sympathetic preganglionic neurons in rats one week after midthoracic spinal cord hemisection or complete transection and one month after complete transection. Morphological changes in adrenal sympathetic preganglionic neurons retrogradely-labelled by cholera toxin were examined as well as changes in other thoracic preganglionic neurons identified by their expression of reduced nicotinamide adenine dinucleotide phosphate-diaphorase. Reactive astrogliosis around these neurons was determined by assessing changes in immunoreactivity to glial fibrillary acidic protein. Changes in immunoreactivity to the synaptic vesicular protein synaptophysin were also evaluated in these areas. One week after transection, a comparison of sympathetic preganglionic neurons rostral and caudal to the lesion revealed significant loss of dendrites and decreased cell size caudal to the injury. Reactive astrocytes surrounded sympathetic preganglionic neurons as far as six segments below the transection. Constitutive expression of synaptophysin was observed rostral to the cord hemisection and synaptophysin expression was increased caudal to the lesion by seven days after the injury. One month after transection, the dendritic arbor of preganglionic neurons was re-established and the intensity of the reactive gliosis around the preganglionic neurons was diminished throughout the thoracic cord. These findings demonstrate that sympathetic preganglionic neurons undergo significant atrophy within a week after deafferentation and that this reaction is reversed within one month. Reactive astrogliosis could contribute to plastic changes in the neuropil that affect the sympathetic neurons, and the enhanced expression of synaptophysin in the gray matter caudal to a cord injury is consistent with fibre outgrowth leading to new synapse formation. Such re-organization could be one of the mechanisms for disorders in blood pressure control that occur after spinal cord injury.
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PMID:Morphological changes in sympathetic preganglionic neurons after spinal cord injury in rats. 884 26

The nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) staining technique was utilized as a marker of nitric oxide synthase (NOS) to map NOS expression in developing and adult rat cerebellum. NADPH-d-positive cells were first visualized in the cerebellar cortex at postnatal day 5 (PND5) which increased to peak levels by PND30 when they began to exhibit a patch-like organization. In order to determine the relationship of the NADPH-d staining pattern with mossy fiber innervation, mossy fiber projections were traced using cholera toxin B subunit or biocytin injected into the lateral reticular nuclei (LRtN) or pontine nuclei (PtN), respectively. Double staining revealed that the clustered mossy fiber terminals projecting from the ventrorostral LRtN and caudal PtN were well matched with NADPH-d-stained patches. This patch-like localization of NOS matched with specific mossy fiber terminals in adult cerebellum implicates these NOS patches as defining distinct anatomical zones.
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PMID:Cerebellar nitric oxide synthase is expressed within granule cell patches innervated by specific mossy fiber terminals: a developmental profile. 920 11

Previous studies have used selective neurochemical markers or retrograde tracers to localize the cells in the brain giving rise to efferents to the turtle retina. Because of the relative selectivity of the neurochemical markers or the lack of sensitivity of the previously employed retrograde tracers, these studies did not locate all the efferent cell bodies, or they could not describe the anatomy of the efferent cells. In the present study, cholera toxin B was used as a highly sensitive retrograde tracer to investigate the distribution, number, and morphology of the retinal efferent or centrifugal cell system in turtle brain. Previous studies of the turtle retina have indicated that nitric oxide synthase may be found in some retinal efferents. Therefore, we also did colocalization studies of the retrograde tracer with reduced nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase histochemistry to investigate nitric oxide as a possible transmitter used by efferent fibers and to localize these NADPH-diaphorase-positive efferent cell bodies in the turtle brain. We found that each eye received projections from approximately 40 efferent cell bodies that were located primarily in the contralateral midbrain. The majority of efferent cell bodies were centered in the isthmic tegmentum; other efferent cells extended more rostrally into the substantia nigra, and some efferent cells extended more caudally into the nucleus raphes superior. The double-label results showed that 30% of the cholera toxin B-like immunoreactive cells were also positive for NADPH-diaphorase. The location of these double-labeled cells around the locus coeruleus corresponded to the NADPH-diaphorase-positive efferent cells in the avian isthmo-optic field. The localization of NADPH-diaphorase in these efferents indicated that they may use nitric oxide to modulate retinal function.
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PMID:Localization of the origin of retinal efferents in the turtle brain and the involvement of nitric oxide synthase. 954 96

In the present study, histochemical techniques combined with more conventional anatomical methods were used to refine the identification of the nucleus of the optic tract and the nuclei of the accessory optic system in the opossum. The distribution of the enzyme cytochrome oxidase (CO) was examined in the cells and the neuropil of the opossum's mesodiencephalic region. Strong CO labeling was present in the nucleus of the optic tract (NOT)-dorsal terminal nucleus (DTN). Alternate sections, taken from animals that had received bilateral injections of horseradish peroxidase centered in the region of the inferior olive, were subjected to assays for CO and horseradish peroxidase. The region occupied by CO-labeled cells in the NOT-DTN superimposed with the one defined by retrogradely labeled cells. Cell counts along the NOT-DTN anteroposterior axis revealed that although the olivary and CO-positive cells were confined within similar boundaries, the latter are up to twofold more numerous than the former. As revealed by cytochrome oxidase histochemistry, the outlines of the NOT-DTN, the other pretectal nuclei and the nuclei belonging to the accessory optic system coincided with those revealed by the histochemistry for nicotinamide dinucleotide phosphate diaphorase (NADPH-d). After an intraocular injection of cholera toxin beta subunit and alternate sections processing for NADPH-d and CO, the distribution of labeled retinal terminal fields in the mesodiencephalic region was shown to be coincident with regions of high levels of histochemical labeling. These results are discussed in the light of previous anatomofunctional assessments of the pretectum and accessory optic system.
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PMID:Cytochrome oxidase and NADPH-diaphorase on the afferent relay branch of the optokinetic reflex in the opossum. 970 May 67

Intravenous administration of phenylephrine provokes a pattern of cellular activation in the nucleus of the solitary tract that resembles the central distributions of primary baroreceptor afferents supplied by the carotid sinus and aortic depressor nerves. Transganglionic transport and denervation methods were used in an experimental setting to test the dependence of phenylephrine-induced Fos immunoreactivity on the integrity of buffer nerve afferents, and to identify the subregions of the nucleus of the solitary tract supplied by each. Cholera toxin B-horseradish peroxidase injections into either or both nerves revealed terminal labeling concentrated in, but not restricted to, the dorsal commissural part of the nucleus of the solitary tract at the level of the apex of calamus scriptorius, and extending into the dorsal subnucleus at the level of the area postrema. Preferential ramifications of carotid sinus and aortic depressor nerve afferents at the levels of the commissural part of the nucleus and the area postrema, respectively, were reflected in the extent to which labeled fibers comingled with neurons exhibiting phenylephrine-induced Fos in dual labeling experiments. Complete sinoaortic denervation reduced by 90% the number of neurons exhibiting drug-induced Fos expression. Selective carotid and aortic sinus denervations effected partial reductions manifest preferentially in the caudal and rostral foci of the distribution, respectively. Reduced activational responses at the level of the area postrema of aortic sinus-denervated rats were accompanied by a reduction in cellular nicotinamide adenine dinucleotide phosphate-diaphorase activity in this region. Animals killed 30 days after complete sinoaortic denervation displayed no evidence of recovery of phenylephrine-induced Fos, while the strength and distribution of the response in rats that received selective carotid sinus denervation were indistinguishable from those seen in controls. These findings (i) support the dependence of phenylephrine-induced Fos expression on the integrity of carotid sinus and aortic depressor nerve afferents, (ii) provide anatomical and functional evidence that the two buffer nerves distribute differentially within the nucleus of the solitary tract, and (iii) implicate central reorganization as a likely basis for functional recovery of baroreflex mechanisms following partial sinoaortic denervation.
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PMID:Effects of selective sinoaortic denervations on phenylephrine-induced activational responses in the nucleus of the solitary tract. 1106 45

Vibrio cholerae and many other marine and pathogenic bacteria possess a unique respiratory complex, the Na(+)-pumping NADH:quinone oxidoreductase (Na(+)-NQR), which pumps Na(+) across the cell membrane using the energy released by the redox reaction between NADH and ubiquinone. To function as a selective sodium pump, Na(+)-NQR must contain structures that (1) allow the sodium ion to pass through the hydrophobic core of the membrane and (2) provide cation specificity to the translocation system. In other sodium-transporting proteins, the structures that carry out these roles frequently include aspartate and glutamate residues. The negative charge of these residues facilitates binding and translocation of sodium. In this study, we have analyzed mutants of acid residues located in the transmembrane helices of subunits B, D, and E of Na(+)-NQR. The results are consistent with the participation of seven of these residues in the translocation process of sodium. Mutations at NqrB-D397, NqrD-D133, and NqrE-E95 produced a decrease of approximately >or=10-fold in the apparent affinity of the enzyme for sodium (Km(app)(Na+)), which suggests that these residues may form part of a sodium-binding site. Mutation at other residues, including NqrB-E28, NqrB-E144, NqrB-E346, and NqrD-D88, had a strong effect on the quinone reductase activity of the enzyme and its sodium sensitivity, but a weaker effect on the apparent sodium affinity, consistent with a possible role in sodium conductance pathways.
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PMID:Acid residues in the transmembrane helices of the Na+-pumping NADH:quinone oxidoreductase from Vibrio cholerae involved in sodium translocation. 1969 31