Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

The distribution of the enzyme NADPH-diaphorase in the rat basal forebrain was examined in relation to the neuropeptide galanin and the neurotransmitter synthetic enzyme choline acetyltransferase. Immunoperoxidase staining permitted camera lucida mapping of galanin and choline acetyltransferase distributions in serial sections through the basal forebrain for comparison with adjacent sections prepared for NADPH-diaphorase histochemistry. Photographs of sections subjected to indirect immunofluorescence for galanin and choline acetyltransferase were compared to photographs of the same sections taken after NADPH-diaphorase histochemistry. This permitted the direct investigation of co-localization within the cholinergic basal forebrain. The distributions of choline acetyltransferase- and galanin-immunoreactive neurons in the basal forebrain agreed with previous descriptions. NADPH-diaphorase histochemistry selectively stained a population of magnocellular basal forebrain neurons with a distribution similar to that observed with galanin immunohistochemistry. Double and triple staining experiments indicated that NADPH-diaphorase labels a majority of the magnocellular cholinergic neurons in the medial septum and diagonal band nuclei. Most of these neurons also contain galanin immunoreactivity. However, small populations of galanin-positive/diaphorase-negative or diaphorase-positive/galanin-negative cholinergic neurons were also observed. In the more caudal portions of the cholinergic basal forebrain, very few galanin or NADPH-diaphorase-positive neurons were observed. Thus, galanin and NADPH-diaphorase coexist in the majority of cholinergic basal forebrain neurons in the regions innervating limbic structures. The neocortically projecting cholinergic cells in the caudal basal forebrain appear to lack these other neurochemical markers.
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PMID:Galanin and NADPH-diaphorase coexistence in cholinergic neurons of the rat basal forebrain. 171 7

A combination of immunocytochemical and enzyme histochemical methods have been used to study those neurons which survive lesions of the rat striatum, produced by low doses of the excitotoxin quinolinic acid. Nissl-stained sections revealed that following injection of this toxin many large neurons remained within areas of extensive cell loss. These large cells were found to express both the enzyme acetylcholinesterase and choline acetyltransferase-like immunoreactivity. The surviving cells did not contain the enzyme reduced nicotinamide adenine dinucleotide phosphate or the peptides, somatostatin and neuropeptide Y. This pattern of selective cell sparing was also found following lesions induced by low doses of the toxins ibotenic acid and kainic acid. The survival of large neurons indicates that the excitotoxin-lesioned rat striatum shares common features with the pattern of cell loss found in the caudate-putamen in Huntington's disease. The major difference between these two examples of striatal nerve cell degeneration is, however, the selective preservation of somatostatin/neuropeptide Y/nicotinamide adenine dinucleotide phosphate-diaphorase-containing neurons found in Huntington's disease but not observed following quinolinic acid lesions.
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PMID:Sparing of cholinergic neurons following quinolinic acid lesions of the rat striatum. 297 92

The cholinergic neurons located within the pedunculopontine nucleus (Ch5) of patients with Alzheimer's disease (AD; n = 15), Parkinson's disease (PD; n = 2), and neurologically normal (n = 6) subjects were visualized immunohistochemically using choline acetyltransferase, pharmacohistochemically using acetylcholinesterase, or by reduced histochemical methods using nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d). Each histochemical procedure localized a well-delineated, compact lateral group and a more diffuse medial group of neurons within the pedunculopontine nucleus. Co-localization experiments revealed that all three enzymes marked the same population of cholinergic neurons. The extent of pathological alterations associated with the cholinergic neurons within the compact lateral sector of the pedunculopontine nucleus was examined in sections that reacted for NADPH-d, counterstained with thioflavin-S. The average number of neurofibrillary tangles within this portion of the pedunculopontine nucleus was 25.4 (range 0-70) in patients with AD, 1.5 (range 1-2) in those with PD, and 1.2 (range 0-4) in aged control subjects. Of the total number of neurofibrillary tangles counted in AD cases, 72.7% were end-stage ghosts and 27.3% were tangle-bearing neurons. The pathological alteration of cholinergic neurons of the compact lateral aspect of the pedunculopontine nucleus may play a role in some of the behavioral features characteristic of AD.
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PMID:Neurofibrillary tangles in cholinergic pedunculopontine neurons in Alzheimer's disease. 320 15

The mesencephalic locomotor region (MLR) was identified physiologically by inducing controlled locomotion on a treadmill in the precollicular rat following application of low amplitude current pulses to areas of the pontomesencephalic tegmentum. The same brains were processed using either of two techniques known to label neurons of the pedunculopontine nucleus (PPN)-choline acetyltransferase (ChAT) immunocytochemistry or nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase histochemistry. Histological reconstruction of locomotion-inducing sites were localized within or adjacent to ChAT or NADPH-diaphorase labeled cell groups. Three dimensional reconstructions of the PPN were used to visualize the colocalization of low threshold locomotion-inducing stimulation sites within PPN neuronal aggregates. These findings lend further support to the suggestion that the PPN is part of the MLR. A theoretical framework is proposed to account for results derived from various lines of research on this area.
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PMID:Locomotion-inducing sites in the vicinity of the pedunculopontine nucleus. 330 44

A major group of cholinergic neurons is present in the midbrain and pontine tegmentum. These cells could be selectively stained using either monoclonal antibodies to choline acetyltransferase, the pharmacohistochemical acetylcholinesterase procedure, or reduced nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase histochemistry. Using these three techniques, the precise distribution of this cell group was determined. By combining these techniques with immunohistochemical staining for various neuropeptides, examples of peptide-cholinergic coexistence could be demonstrated in this cell group. Approximately 30% of these cholinergic neurons displayed substance P immunoreactivity. Most of these cells also showed corticotropin-releasing factor immunoreactivity and bombesin/gastrin-releasing peptide immunoreactivity. These results therefore provide evidence for the coexistence of various neuropeptides together with NADPH-diaphorase activity in the ascending cholinergic reticular system.
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PMID:Neuropeptides and NADPH-diaphorase activity in the ascending cholinergic reticular system of the rat. 396 Mar 9

The carotid body is an arterial chemoreceptor organ sensitive to blood levels of O2, CO2 and pH. The present immunocytochemical and neurochemical study has demonstrated the presence of an extensive plexus of nitric oxide (NO)-synthesizing nerve fibers in this organ. These nitric oxide synthase (NOS)-containing axons are closely associated with parenchymal type I cells and with blood vessels in the carotid body. Denervation and retrograde tracing experiments have revealed that these fibers arise from NOS-immunoreactive and nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase-positive neuronal cell bodies located in the petrosal ganglion and the carotid body, and dispersed along the glossopharyngeal and carotid sinus nerves (CSN). Within the petrosal ganglion, these neurons are topographically segregated from the catecholaminergic cells, and they contain the neuropeptide, substance P. NOS-positive autonomic microganglial cells in the carotid body and CSN also exhibit choline acetyltransferase (ChAT) immunoreactivity. Our results suggest that nitric oxide may be a novel neuronal messenger in the mammalian carotid body involved in the modulation of chemosensory transduction and transmission in this organ.
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PMID:Neurons synthesizing nitric oxide innervate the mammalian carotid body. 750 96

The morphology and distribution of perikarya positive for choline acetyltransferase, somatostatin, calcium binding protein (calbindin D28K) and nicotinamide adenine dinucleotide phosphate diaphorase were surveyed in the human striatum. Choline acetyltransferase and somatostatin antibodies labeled separate populations of large striatal interneurons. Somatostatin immunoreactivity and nicotinamide adenine dinucleotide phosphate diaphorase (nitric oxide synthase) activity were completely co-localized. Calbindin antibody identified two distinct groups of striatal neurons: (1) numerous medium-sized, lightly stained neurons, probably analogous to striatopallidal projection neurons in the rat, and (2) much less numerous, large, darkly stained neurons. Half of the latter group, but none of the former, were also nicotinamide adenine dinucleotide phosphate diaphorase-positive. Somatostatin-positive and medium-sized, calbindin-positive neurons were more numerous in the caudate nucleus than in the putamen or ventral striatum. By contrast, large calbindin-immunoreactive neurons were more frequently encountered in the putamen. Choline acetyltransferase-positive neurons were evenly distributed across striatal components. In aged control subjects, the size of large, darkly stained calbindin-positive neurons was reduced relative to young subjects. Aging had no effect on somatostatin-, medium-sized calbindin-, or choline acetyltransferase-positive neurons. However, in histologically confirmed cases of Alzheimer's disease, there was a selective, 75% loss of choline acetyltransferase-immunoreactive perikarya from the ventral striatum, but not from the dorsal striatum, compared to aged controls. Furthermore, the remaining cholinergic neurons in the ventral striatum of Alzheimer's disease cases were significantly smaller than similar neurons in controls. These results indicate that various striatal components which have been shown to differ in their anatomical connectivity and functional specialization, also differ in their neurochemical signatures. The specific and marked loss of choline acetyltransferase-positive neurons from the ventral striatum in Alzheimer's disease is consistent with the characteristic cholinergic and 'limbic' pathology in this disease.
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PMID:Human striatum: chemoarchitecture of the caudate nucleus, putamen and ventral striatum in health and Alzheimer's disease. 752 83

To characterize the specificity of a novel cholinergic immunotoxin (conjugate of the monoclonal antibody 192IgG against the low-affinity nerve growth factor receptor with the cytotoxic protein saporin), coronal sections through the basal forebrain of adult rats, that received a single intracerebro-ventricular injection of 4 micrograms of 192IgG-saporin conjugate, were subjected to histochemical and immunocytochemical procedures to evaluate cholinergic (choline acetyltransferase (ChAT)-immunoreactive, acetylcholinesterase-positive, NADPH-diaphorase-positive) and GABAergic structures (parvalbumin-immunoreactive, labeling of perineuronal nets with Wisteria floribunda agglutinin) as well as microglia (visualized with Griffonia simplicifolia agglutinin) and astrocytes (immunostaining for glial fibrillary acidic protein). Seven days following injection of the immunotoxin, ChAT-immunoreactive cells nearly completely disappeared throughout the magnocellular basal forebrain complex, including globus pallidus, as compared to vehicle-injected controls. However, there was no significant difference in the number of ChAT-positive cells in the adjacent ventral pallidum and in the caudate-putamen of immunolesioned and control animals. NADPH-diaphorase-containing cells, including a significant subpopulation of cholinergic cells, also strikingly decreased in number by more than 90% in the magnocellular basal forebrain complex following immunolesion, and only a few noncholinergic diaphorase-positive cells survived in the medial septum, vertical and horizontal diagonal band, and nucleus basalis of Meynert. In contrast, the number of parvalbumin-containing GABAergic projection neurons in the septum-diagonal band of Broca complex and nucleus basalis of Meynert from immunolesioned rats was not different from that of vehicle-injected control animals. Immunolesioning also did not result in any change in either number or shape of cells surrounded by perineuronal nets, which are frequently associated with parvalbumin-containing GABAergic neurons. Seven days following injection of the immunotoxin, a very strong activation of microglia with an identical distribution pattern was observed in all experimental animals. Large numbers of activated microglia were found in all magnocellular basal forebrain nuclei, corresponding to the distribution of degenerating cholinergic cells. Additionally, immunolesioning also resulted in a dramatic activation of microglia in the lateral septal nuclei, which are known to be almost free of cholinergic cells, but not of penetrating cholinergic dendrites in adjacent zones, and in the ventral pallidum, where there was no observed loss of cholinergic cells. There was no significant increase in microglia activation in striatum and cortical areas, and no astrocytic response in any of the basal forebrain nuclei at this particular time point of survival. These results suggest that 192IgG-saporin specifically destroys basal forebrain cholinergic neurons and does not suppress their neuronal activity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:192IgG-saporin immunotoxin-induced loss of cholinergic cells differentially activates microglia in rat basal forebrain nuclei. 756 26

Disturbances in memory, concentration, and problem solving are common after even mild to moderate traumatic brain injury. Because these functions are mediated in part by forebrain cholinergic and catecholaminergic innervation, in this study the authors sought to determine if experimental concussive injury produces detectable morphological damage to these systems. Fluid-percussion head injury, sufficient to cause a 13- to 14-minute loss of righting reflex, was produced in rats that had been anesthetized with halothane. Injury was delivered either at midline or 2 mm off midline and compared with appropriate sham-injured controls. After 11 to 15 days, the rat brains were stained in serial sections for choline acetyltransferase, tyrosine hydroxylase, dopamine beta-hydroxylase, acetylcholinesterase, and nicotinamide adenine dinucleotide phosphate diaphorase. Cell counts were determined for the entire population of ventrobasal forebrain cholinergic cells. Midline injury produced a bilateral loss of cholinergic neurons averaging 36% in area Ch1 (medial septal nucleus), 45% in Ch2 (nucleus of the diagonal band of Broca), and 41% in Ch4 (nucleus basalis of Meynart), (p < or = 0.05). Lateralized injury resulted in cholinergic neuron loss of similar magnitude ipsilaterally (p < or = 0.05), but a smaller contralateral loss of between 11% and 28%. No loss of neurons was detected in the pontomesencephalic cholinergic groups Ch5 and Ch6. There was no visible effect of head injury on forebrain dopamine or noradrenergic innervation. A significant and apparently selective loss of ventrobasal forebrain cholinergic neurons following brief concussive injury in rats is demonstrated in this study. This type of injury is known to produce significant disturbance in cognitive tasks linked to neocortical and hippocampal cholinergic function. It remains to be determined how this neuron loss occurs, whether it can be prevented with neuroprotective agents, how it affects innervation in target tissues, and whether it occurs in human victims of traumatic brain injury.
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PMID:Loss of forebrain cholinergic neurons following fluid-percussion injury: implications for cognitive impairment in closed head injury. 766 29

Phenotypic diversity underlies the complex functioning of the nervous system. One characteristic in which neurons differ from one another is the kind of molecules that they use for intercellular signalling. The classical neurotransmitter acetylcholine, synthesized by the enzyme choline acetyltransferase, is used by five groups of neurons in the rat spinal cord. Another messenger is nitric oxide, which is synthesized by nitric oxide synthase. Neurons that express nitric oxide synthase can be stained specifically by NADPH diaphorase histochemistry. In the spinal cord, approximately five groups of neurons are labeled by the diaphorase reaction, and some of these populations overlap with cholinergic groups. To determine the proportions of neurons that co-express choline acetyltransferase and nitric oxide synthase, we performed choline acetyltransferase immunocytochemistry and diaphorase histochemistry on single sections of rat spinal cord. Some cell types were single-labeled: somatic motor neurons were choline acetyltransferase-immunoreactive only, and neurons in lamina II were diaphorase-positive only. Four cell groups included double-labeled cells. Autonomic motor neurons were either double-labeled (62%) or choline acetyltransferase-only (37%), partition cells in lamina VII were double-labeled (54%) or choline acetyltransferase-only (45%), neurons in laminae III-V of the dorsal horn were double-labeled (70%) or diaphorase-only (27%), and neurons surrounding the central canal were double-labeled (56%), choline acetyltransferase-only (23%) or diaphorase-only (21%). These data indicate that certain spinal cord populations may be heterogeneous with regard to the intercellular messenger phenotypes involving acetylcholine and nitric oxide.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Choline acetyltransferase and NADPH diaphorase are co-expressed in rat spinal cord neurons. 770 May 13


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