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:1.6.99.1 (NADPH-diaphorase)
3,903 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distribution of nitrergic neurons was investigated by using nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry and nitric oxide synthase (NOS) immunohistochemistry in wholemount preparations of the urinary bladder in guinea pigs. Both NADPH-d+ and NOS+ neurons were located predominantly in the bladder base. Double staining showed that 70.9% of the NADPH-d+ neurons coexpressed NOS. Acetylcholinesterase histochemistry revealed that a majority of the intramural neurons were reactive, and about half of them (51.4%) were double labelled for NOS. Tyrosine hydroxylase-positive neurons were also distributed mainly in the bladder base but in a neuronal population that was separate from the preponderant NADPH-d+ neurons. Vasoactive intestinal polypeptide immunoreactivity was also detected in the some of intramural ganglion cells, in which 21.3% of them coexpressed NADPH-d. Calcitonin gene-related peptide and substance P immunoreactivities were confined to nerve fibers, often in close association with NADPH-d+ cells or extended along the blood vessels. These results have demonstrated the colocalization of NADPH-d and NOS in the majority of intramural ganglion cells. Many of the nitrergic neurons are apparently cholinergic, indicating that they are parasympathetic postganglionic neurons, and this underscores NO as the major neuromodulator in the parasympathetic nerves in the bladder walls. The localization of vasoactive intestinal polypeptide in nitrergic neurons suggests that the peptide may complement NO for regulation of micturition reflex. The close relationship of NADPH-d-reactive intramural neurons with calcitonin gene-related peptide and substance P fibers, most probably derived from dorsal root ganglion cells, suggests that NO released from the local neurons may exert its influence on the sensory neural pathways in the urinary bladder.
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PMID:Colocalization of nitric oxide synthase and some neurotransmitters in the intramural ganglia of the guinea pig urinary bladder. 959 May 57

Adult olivocerebellar axons are capable of vigorous regeneration when provided with growth-permissive environmental conditions. To elucidate the contribution of intrinsic properties to the regenerative capabilities of inferior olivary neurons, we have examined the cellular modifications occurring in these neurons following axotomy and target deprivation in the absence of exogenous growth-promoting influences. Axotomized inferior olivary neurons undergo perikaryal shrinkage, dendritic atrophy and a loss of anti-calbindin immunoreactivity. A conspicuous cell death occurs during the first few weeks after lesion, but about 35% of the affected neurons survive up to 60 days. Coincidentally, a subset of the injured nerve cells become strongly reactive for NADPH diaphorase histochemistry, and this expression is correlated with survival in the medial accessory olive and in the principal olive. In addition, the affected neurons express or maintain the expression of several markers related to regenerative processes, including transcription factors c-Jun, JunD and Krox-24, the growth-associated protein GAP-43 and the developmentally regulated calcitonin gene-related peptide (CGRP). The expression of all these markers is sustained up to two months after lesion, the longest survival time examined. These results show that although adult axotomized inferior olivary neurons undergo severe regressive modifications leading to a conspicuous cell loss, at least a subset of them is resistant to the lesion. In addition, the long-lasting expression of several axon-growth associated markers expressed in these neurons in response to injury reveals that they are endowed with a strong intrinsic regenerative potential.
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PMID:Degenerative phenomena and reactive modifications of the adult rat inferior olivary neurons following axotomy and disconnection from their targets. 962 55

The coexistence of S100beta with calcitonin gene-related peptide (CGRP), substance P (SP), somatostatin (SOM), nicotinamide adenosine dinucleotide phosphate-diaphorase (NADPH-d), and tyrosine hydroxylase (TH) was examined in the glossopharyngeal and vagal sensory ganglia. S100beta immunoreactive (-ir) neurons in the jugular and petrosal ganglia frequently colocalized CGRP- or SP-ir, whereas S100beta-ir neurons in the nodose ganglion infrequently contained CGRP- or SP-ir. No S100beta-ir neurons in the jugular and petrosal ganglia showed SOM-ir while the small number of SOM-ir neurons in the nodose ganglion colocalized S100beta-ir. Many neurons in the nodose ganglion colocalized S100beta-ir and NADPH-d activity, whereas S100beta-ir neurons in the jugular and nodose ganglia infrequently contained NADPH-d activity. S100beta- and TH-ir were frequently colocalized in nodose ganglion but not in petrosal or jugular ganglion neurons. These findings suggest relationships between S100beta and specific putative transmitters in functions of subpopulations of vagal and glossopharyngeal sensory neurons.
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PMID:Coexistence of s100beta and putative transmitter agents in vagal and glossopharyngeal sensory neurons of the rat. 968 88

Vagal afferent neurons contain a variety of neurochemical markers and neuroactive substances, most of which are present also in dorsal root ganglion cells. To test for the suitability of the calcium-binding protein calretinin as a specific marker for vagal afferent fibers in the periphery, immunocytochemistry for this protein was combined with retrograde tracing. Nerve fibers in the rat esophagus, as well as vagal and spinal sensory neurons innervating the esophagus, were investigated for co-localization of calretinin with calbindin, calcitonin gene-related peptide, and NADPH diaphorase. The results indicated that calretinin immunocytochemistry demonstrates neuronal structures known as vagal afferent from other studies, in particular intraganglionic laminar endings. A few enteric neurons whose distribution was unrelated to intraganglionic laminar endings also stained for calretinin. Strikingly, calretinin immunoreactivity was absent from spinal afferent neurons innervating the rat esophagus. In intraganglionic laminar endings and nodose ganglion cells calretinin was highly co-localized with calbindin but not with calcitonin gene-related peptide. On the other hand, calbindin was also found in spinal afferents to the esophagus where it was co-localized with calcitonin gene-related peptide. Vagal afferent neurons innervating the esophagus were never positive for NADPH diaphorase. Thus, calretinin appears to be a more specific marker for vagal afferent structures in the esophagus than calbindin, which is expressed by both vagal and spinal sensory neurons. Calretinin immunocytochemistry may be utilized as a valuable tool for investigations of subpopulations of vagal afferents in certain viscera.
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PMID:Vagal and spinal afferent innervation of the rat esophagus: a combined retrograde tracing and immunocytochemical study with special emphasis on calcium-binding proteins. 970 May 72

In isolated canine lingual arteries denuded of the endothelium, transmural electrical stimulation (2-20 Hz) produced a frequency-related contraction which was not significantly influenced by prazosin but which was reversed to a relaxation by alpha,beta-methylene ATP. The responses were abolished by tetrodotoxin. The stimulation-induced relaxation was abolished by treatment with NG-nitro-L-arginine (L-NA, 10(-6) M) and restored by the addition of L-arginine. Neurogenic relaxation resistant to L-NA was not observed after electrical stimulation, even though the pulse width and stimulus intensity were raised. Under treatment with prazosin, alpha,beta-methylene ATP and indomethacin, the arterial strips responded to nicotine (10(-4) M) with a marked relaxation that was abolished by hexamethonium. The relaxation was significantly inhibited but not abolished by L-NA (10(-5) M), and raising the concentration of the inhibitor to 10(-4) M, did not produce additional inhibition. In the strips treated with L-NA, the nicotine-induced relaxation was abolished or markedly reduced under desensitization with vasoactive intestinal peptide (VIP) or calcitonin gene-related peptide (CGRP) and by treatment with high concentrations of beraprost, a stable analog of prostaglandin I2, but was unaffected by CGRP or VIP receptor antagonists. Relaxant responses to a low concentration of nicotine (5 x 10(-6) M) were abolished by L-NA and restored by L-arginine. Histochemical study demonstrated many nerve fibers and bundles containing NADPH diaphorase in the adventitia of the arteries. It is concluded that the neurogenic arterial contraction is induced mainly by ATP via stimulation of P2X purinoceptors, and that the relaxation induced by electrical stimulation or a low concentration of nicotine is mediated by nitric oxide (NO) released from perivascular nerves. In high concentrations, nicotine elicits marked relaxations possibly due to the liberation of NO from the nerve and also vasodilator substances that increase the content of cyclic AMP in the tissue. CGRP and VIP are unlikely to be involved.
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PMID:Mechanisms underlying constrictor and dilator responses to perivascular nerve stimulation in canine lingual arteries. 972 29

The distribution of nitric oxide synthase (NOS)-, choline acetyltransferase (ChAT)-, and vasoactive intestinal polypeptide (VIP)-immunoreactivities, and nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd)-reactivities in the sphenopalatine ganglia (SPG), and perivascular nerves in middle cerebral arteries of the pig was investigated by double-staining techniques using combined immunofluorescence and histochemistry methods. In the SPG, almost all ganglionic cells were NOS-immunoreactive (I) and NADPHd-positive, and both NOS immunoreactivities and NADPHd reactivities were completely co-localized. ChAT-I ganglionic cells accounted for 75%, while VIP-I ganglionic cells represented 42% of all ganglionic cells. Almost all VIP immunoreactivities were co-localized with ChAT immunoreactivities, and all ganglionic cells that were VIP-I and/or ChAT-I were NOS-I and NADPHd-reactive. None of the ganglionic cells in the SPG were immunoreactive to calcitonin gene-related peptide (CGRP). CGRP immunoreactivities, however, were found to surround some ganglionic cells. In middle cerebral arteries, all adventitial NOS-I bundles and fine fibers were coincident with NADPHd fibers. Almost all adventitial ChAT-I bundles and thin fibers, and VIP-I mesh-like fibers stained positively for NADPHd, while the mesh-like NADPHd fine fibers were not ChAT-I. Simultaneous labeling using antibodies against VIP and ChAT further indicated that VIP-I fibers were closer than ChAT-I fibers to the smooth muscle. In rare occasions, perivascular fibers were found to be stained for both ChAT and VIP, showing that most ChAT-I and VIP-I fibers were not coincident. These results suggest that ChAT and VIP are rarely co-localized in perivascular nerves in middle cerebral arteries, and point out that the neurotransmitter and the modulator that are co-localized within the same nerve cell body may distribute totally independently and differently at the terminal level. The present results also indicate that in cerebral perivascular nerves, the combination of nitric oxide (NO) and acetylcholine (ACh), as well as the combination of NO and VIP, are localized in the same nerve with different axons containing either NO plus ACh, or NO plus VIP. These findings support the hypothesis that ACh and VIP may act as modulators in regulating presynaptic release of NO, and therefore, cerebral neurogenic vasodilation, from their respective perivascular cholinergic-nitric oxidergic and VIPergic-nitric oxidergic nerves.
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PMID:Segregation of VIPergic-nitric oxidergic and cholinergic-nitric oxidergic innervation in porcine middle cerebral arteries. 972 90

The rat heart receives its blood supply not only from the coronary arteries but also from the accessory coronary arteries that supply mainly the atria. The distribution and chemical nature of nitric oxide synthase-containing nerve fibers in the conduction system as well as the coronary and accessory coronary arteries were investigated using immunohistochemistry and NADPH diaphorase (NADPH-d) histochemistry. A few NADPH-d-positive nerve fibers were observed mainly around the main trunk of the coronary arteries, while NADPH-d-positive fibers were found along the entire course of the accessory coronary arteries from their main branches to the arteriolar level. A double-staining method demonstrated that NADPH-d-positive fibers innervating both the coronary and accessory coronary arteries contained vasoactive intestinal polypeptide or neuropeptide Y. NADPH-d-positive fibers were relatively abundant in the sinus node and penetrating bundle but were very sparse in the atrioventricular node and right bundle branch. No NADPH-d-positive fibers were detected in the left bundle branch. Some of the NADPH-d-positive fibers innervating the penetrating bundle exhibited distinct immunoreactivity to calcitonin gene-related peptide. These results suggest that nitric oxide may play a role as a neurotransmitter and/or neuromodulator in the neural control of the cardiac blood flow and impulse conduction.
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PMID:Distribution and neuropeptide content of nitric oxide synthase-containing nerve fibers in arteries and conduction system of the rat heart. 973 24

We have made an immunohistochemical study of the vomeronasal (VN) complex of 12-day-old rats to characterize the innervation of its blood vessels. The VN complex can be subdivided into rostral, middle and caudal segments, each one with a particular vascularization pattern. Several small vessels were associated with the rostral segment, whereas a large venous sinus ran along the middle and caudal segments. Immunostaining for alpha-smooth muscle actin demonstrated that the muscular sheath was asymmetric, with more cells layers in its lateral than in its medial walls. Nerves were demonstrated with antisera against protein gene product 9.5 (PGP), and against several molecules associated with specific classes of nerve fibers: the C-terminal peptide of neuropeptide Y (CPON), calcitonin gene-related peptide (CGRP), substance P (SP), galanin (GAL), vasoactive intestinal peptide (VIP) and neuronal nitric oxide synthase (NOS). The latter, was also studied with NADPH-diaphorase. Vascular associated fibers exhibited NOS-, CPON-, GAL-, CGRP-, SP- and VIP-immunoreactivity. Only the vessels of the rostral segment showed VIP-immunoreactive fibers. Each wall of the venous sinus exhibited different types of nerve fibers. CPON-, GAL-, CGRP- and SP-immunoreactive fibers concentrated in the medial wall, whereas NOS-immunoreactive ones concentrated in the lateral wall. This distribution of vascular fibers, plus the presence of sensory fibers exhibiting CGRP-, SP- and GAL-immunoreactivity within the pseudostratified epithelium of the VN tube, would be relevant to understand the operation of the pumping mechanism regulating influx and efflux from the VN tube.
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PMID:Innervation of blood vessels in the vomeronasal complex of the rat. 980 88

The substantia gelatinosa of the spinal cord (lamina II) is the major site of integration for nociceptive information. Activation of NMDA glutamate receptor, production of nitric oxide (NO), and enhanced release of substance P and calcitonin gene-related peptide (CGRP) from primary afferents are key events in pain perception and central hyperexcitability. By combining reduced nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase histochemistry for NO-producing neurons with immunogold labeling for substance P, CGRP, and glutamate, we show that (1) NO-producing neurons in lamina IIi are islet cells; (2) these neurons rarely form synapses onto peptide-immunoreactive profiles; and (3) NADPH diaphorase-positive dendrites are often in close spatial relationship with peptide-containing terminals and are observed at the periphery of type II glomeruli showing glutamate-immunoreactive central endings. By means of confocal fluorescent microscopy in acute spinal cord slices loaded with the Ca2+ indicator Indo-1, we also demonstrate that (1) NMDA evokes a substantial [Ca2+]i increase in a subpopulation of neurons in laminae I-II, with morphological features similar to those of islet cells; (2) a different neuronal population in laminae I-IIo, unresponsive to NMDA, displays a significant [Ca2+]i increase after slice perfusion with either substance P and the NO donor 3morpholinosydnonimine (SIN-1); and (3) the responses to both substance P and SIN-1 are either abolished or significantly inhibited by the NK1 receptor antagonist sendide. These results provide compelling evidence that glutamate released at type II glomeruli triggers the production of NO in islet cells within lamina IIi after NMDA receptor activation. The release of substance P from primary afferents triggered by newly synthesized NO may play a crucial role in the cellular mechanism leading to spinal hyperexcitability and increased pain perception.
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PMID:Nitric oxide-producing islet cells modulate the release of sensory neuropeptides in the rat substantia gelatinosa. 985 75

Stimulation of extrinsic nerves markedly alters pancreatic endocrine and exocrine secretion, yet little is known of the neurochemical organization and physiologic roles of specific neural pathways within the pancreas. Here we report histochemical staining for acetylcholinesterase (AChE), NADPH-diaphorase (NADPH-d), nitric oxide synthase (NOS), and several neuropeptides to identify the neurotransmitter content of rabbit pancreatic nerves. An extensive network of AChE-positive nerve fibers was found throughout the islets, acini, ducts, ganglia, and blood vessels. All pancreatic neurons were AChE positive, two thirds were NADPH-d positive, and many were NOS positive. Ganglia in the head/neck region were connected to the duodenal myenteric plexus by AChE- and NADPH-d-positive fibers, and NADPH-d-positive pancreatic neurons appeared to send processes toward both the duodenum and pancreas. Many pancreatic neurons were vasoactive intestinal peptide (VIP) positive, and VIP nerve terminals were abundant in ganglia, acini, islets, and ducts. Pituitary adenylate cyclase-activating peptide (PACAP-38)-positive fibers also were observed within acini and passing through ganglia. Substance P (SP)-, calcitonin gene-related peptide (CGRP)-, and dopamine beta-hydroxylase (DBH)-positive fibers were abundant along blood vessels and ducts, and varicose fibers were observed in pancreatic ganglia. Fine galanin-positive fibers were also occasionally observed running with blood vessels and through ganglia. Thus the rabbit pancreas receives a dense, diverse innervation by cholinergic, adrenergic, and peptidergic nerves and cholinergic pancreatic neurons, most also containing VIP or NOS or both, appear to innervate both endocrine and exocrine tissue, and may mediate local communication between the duodenum and pancreas.
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PMID:Morphology and histochemistry of the rabbit pancreatic innervation. 988 61


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