Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distribution of NO synthase (NOS) immunoreactive nerves and the possible co-existence with other neurotransmitters were investigated in the pig lower urinary tract. NOS immunoreactive nerves were found in the muscle layer, in the lamina propria and around blood vessels. The density of NOS immunoreactive nerves was more prominent in the trigone and urethra than in the detrusor. All parts of the lower urinary tract were supplied by numerous acetylcholine esterase (AChE) positive nerves. The number of adrenergic nerves in the trigone and urethra was moderate to rich, whereas only very few adrenergic nerves were demonstrated in the detrusor. A low to moderate number of nerve fibres containing neuropeptide Y (NPY) and vasoactive intestinal polypeptide (VIP) were observed in the trigone and urethra, while very few were found in the detrusor. A small number of nerves, confined to the trigone and urethra, were stained for calcitonin-gene-related peptide, somatostatin and leu-enkephalin. Nerve fibres exhibiting immunoreactivity to bombesin/gastrin releasing peptide, gastrin/cholecystokinin, substance P or neurokinin A were virtually absent. Co-localization studies revealed that some NOS-immunoreactive nerves also stained for NPY, VIP or AChE. The present study shows that nitrergic nerves are present in the pig lower urinary tract in a density lower than the cholinergic, but higher than any of the studied peptidergic nerves. Coinciding localization of NOS-positive nerves with nerves expressing AChE, VIP and NPY suggests that NO may have a role as a messenger in the lower urinary tract directly and by interaction with other transmitters.
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PMID:Co-existence of nitrergic, peptidergic and acetylcholine esterase-positive nerves in the pig lower urinary tract. 761

An impairment of energy metabolism may underlie slow excitotoxic neuronal death in neurodegenerative diseases. We therefore examined the effects of intrastriatal, subacute systemic, or chronic systemic administration of the mitochondrial toxin 3-nitropropionic acid (3-NP) in rats. Following intrastriatal injection 3-NP produced dose-dependent striatal lesions. Neurochemical and histologic evaluation showed that markers of both spiny projection neurons (GABA, substance P, calbindin) and aspiny interneurons (somatostatin, neuropeptide Y, NADPH-diaphorase) were equally affected. Subacute systemic administration of 3-NP produced age-dependent bilateral striatal lesions with a similar neurochemical profile. However, in contrast to the intrastriatal injections, striatal dopaminergic afferent projections were spared. Both freeze-clamp measurements and chemical shift magnetic resonance spectroscopy showed that 3-NP impairs energy metabolism in the striatum in vivo. Microdialysis showed no increase in extracellular glutamate concentrations after systemic administration of 3-NP. The lesions produced by intrastriatal injection or systemic administration of 3-NP were blocked by prior decortication. However, the NMDA antagonist MK-801 did not block the effects of intrastriatal 3-NP, consistent with a non-NMDA excitotoxic mechanism. In contrast to subacute systemic administration of 3-NP, chronic (1 month) administration produced lesions confined to the striatum in which there was relative sparing of NADPH-diaphorase interneurons, consistent with an NMDA excitotoxic process. Chronic administration showed growth-related proliferative changes in dendrites of spiny neurons similar to changes in Huntington's disease (HD). These results are consistent with in vitro studies showing that mild metabolic compromise can selectively activate NMDA receptors while more severe compromise activates both NMDA and non-NMDA receptors. Chronic administration of 3-NP over 1 month produces selective striatal lesions that replicate many of the characteristic histologic and neurochemical features of HD.
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PMID:Neurochemical and histologic characterization of striatal excitotoxic lesions produced by the mitochondrial toxin 3-nitropropionic acid. 769 9

Retinal neurons that express the immediate early gene c-fos after light exposure were characterized by neurotransmitter content using histochemical and immunocytochemical staining. In Northern blots the amount of c-fos mRNA peaked at 30 min, but remained detectable 60 min following light stimulation. Fos proteins were seen in the inner nuclear and ganglion cell layers, and the staining was most intense two and three hours after beginning the light exposure. In the ganglion cell layer 30-40% of Fos-immunoreactive cells were cholinergic displaced amacrine cells and 3-5% were ganglion cells. In the inner nuclear layer 24% of Fos-immunoreactive cells were Type I and 7% Type II NADPH-diaphorase-reactive (nitric oxide synthase) amacrine cells, 11% were tyrosine hydroxylase-containing cells, and 10-15% cholinergic amacrine cells. No Fos immunoreactivity was seen in serotoninergic, somatostatin- or VIP-immunoreactive cells, bipolar, horizontal or photoreceptor cells. Nicotine, kainic acid, NMDA and SCH 38393, a dopamine D1 receptor agonist, induced Fos immunostaining in the inner nuclear and ganglion cell layers, but administration of the corresponding receptor blockers mecamylamine, kynuretic acid, MK-801, haloperidol and SCH 23990 did not prevent light-induced Fos expression.
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PMID:Light-induced c-fos expression in amacrine cells in the rabbit retina. 777 1

We analyzed the distribution and light-microscopic features of the NADPH diaphorase-containing structures in the lizard hippocampus, likely to correspond to nitric oxide synthase-containing cells and fibers, and thus likely to release nitric oxide. We also studied co-localization of NADPH diaphorase with the neurotransmitter GABA, the calcium-binding protein parvalbumin, and the neuropeptide somatostatin, in order to examine whether putative nitric oxide-synthesizing neurons represent a different subpopulation of GABA cells, on which the authors recently reported in lizards. We also studied co-localization of NADPH diaphorase with parvalbumin or somatostatin in mice to ascertain whether the characteristics of this population in reptiles parallel the situation in mammals. Most of the positive NADPH diaphorase neurons were stained in a Golgi-like manner and were in the plexiform layers of the lizard hippocampus with morphologies ranging from bipolar to multipolar. Co-localization with GABA was 100%, and NADPH diaphorase-positive neurons in the lizard hippocampus did not contain parvalbumin or somatostatin. The results indicate that putative nitric oxide-synthesizing neurons represent a distinct subpopulation of GABA interneurons in the lizard hippocampus. Two different types of fibers were described in the plexiform layers: one type bearing thick varicosities, and the other thinner ones. We discuss the possibility that at least part of the positive fibers arise from a hypothalamic aminergic nucleus contacting the third ventricle, the periventricular hypothalamic organ. Most radial glia were stained almost completely and formed typical end-feet both at the pia and around capillaries. The results of this study confirm that the capacity for synthesizing nitric oxide is linked to a determined set of neuronal markers depending on the specific brain region, and they provide new resemblances between hippocampal regions in different classes of vertebrates.
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PMID:NADPH diaphorase-positive neurons in the lizard hippocampus: a distinct subpopulation of GABAergic interneurons. 778 47

Lesions of the nucleus basalis of Meynert (NBM) have been used to mimic, in part, cholinergic deficits occurring in age-related neurodegenerative disorders, i.e., Alzheimer's disease. In our study, the effect of a persistent cholinergic denervation of the fronto-parietal cortex on neuropeptide Y (NPY) and somatostatin (SOM) was examined in young adult (3 months old) and aging (> 18 months old) rats, 1, 3 and 6 months after bilateral stereotaxic NBM lesions with quisqualic acid. In aging, non-lesioned rats a significant decrease in radioimmunologically and immunohistochemically detectable NPY and SOM was found with no further changes after lesions. Morphological markers for these peptidergic populations (cell size and number, NADPH-diaphorase histochemistry, electron microscopy) demonstrated no signs of alterations in both age groups after lesion. Densitometric analysis of peptide fibre networks displayed a heterogeneous response with a significant rarefication in young rats 1 month after the lesion, followed by restoration and a tendency towards increase 6 months post lesioning in individual animals. These findings were confirmed by radioimmunological measurements. Examination of synaptic and cytoskeletal markers, i.e., synaptophysin, GAP-43, MAP-2, Tau-1 and amyloid precursor protein, did not reveal any signs for neuronal reorganization or sprouting. These data are discussed in the context of plasticity and pathology in age-related neurodegenerative disorders with cholinergic impairment.
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PMID:Neuropeptide Y and somatostatin in the neocortex of young and aging rats: response to nucleus basalis lesions. 780 68

Recent studies of autonomic ganglia have shown that specific combinations of neuropeptides and other potential neurotransmitters distinguish different functional types of neurons. In the present paper the patterns of coexistence of neurochemicals in guinea-pig cardiac ganglion cells was examined, using multiple-labelling immunohistochemistry. Many neurons were found to contain somatostatin immunoreactivity with various combinations of immunoreactivity for dynorphin B, substance P, neuropeptide Y and nitric oxide synthase. There were several small populations of neurons without somatostatin immunoreactivity, which contained combinations of immunoreactivity for vasoactive intestinal peptide, neuropeptide Y, dynorphin B, substance P and nitric oxide synthase. Possible synaptic inputs to these populations of ganglion cells were identified using multiple-labelling immunohistochemistry combined with long-term organ culture. These experiments demonstrated that cardiac ganglia contain prominent pericellular baskets of varicose nerve terminals of sympathetic and sensory origin. In addition, populations of intrinsic intraganglionic nerve terminals were identified which were immunoreactive for vasoactive intestinal peptide, neuropeptide Y or both peptides. These terminals presumably originate from intrinsic neurons, with the same combinations of neuropeptides, located in other cardiac ganglia. These results have demonstrated that there are diverse populations of cardiac ganglion cells in the guinea-pig and that some of these neurons may act as interneurons within the intrinsic cardiac plexuses. Therefore it is highly likely that vagal transmission in the heart is modified by sympathetic, sensory and intrinsic neurons and that cardiac ganglia are complex integrators of convergent neuronal activity rather than simple relays.
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PMID:Multiple populations of neuropeptide-containing intrinsic neurons in the guinea-pig heart. 781 2

Previous work has shown that growth hormone-releasing factor (GRF) stimulates cGMP production and somatostatin [somatotropin (growth hormone)-release-inhibiting factor, SRIF] release without altering cAMP accumulation by fragments of median eminence incubated in vitro. Therefore, this study was undertaken to evaluate the effect of GRF and cGMP on SRIF mRNA and SRIF release in the periventricular nuclei of male rats in vitro. SRIF mRNA levels were determined in explants of periventricular nuclei incubated for 6 hr in Waymouth's medium in the presence of various substances. Steady-state levels of SRIF mRNA were measured by an S1 nuclease protection assay using a 32P-labeled rat SRIF RNA probe. SRIF release and cGMP formation were measured at 30 min and 6 hr by RIA. SRIF mRNA levels and SRIF release were significantly (P < 0.025) increased (approximately 2-fold) by 1 microM dibutyryl cGMP, whereas sodium butyrate had no effect. This augmentation was not influenced by cycloheximide, an inhibitor of protein synthesis. Sodium nitroprusside (10 microM), an activator of the guanylate cyclase pathway via its release of nitric oxide, augmented (P < 0.001) SRIF mRNA levels and significantly increased (P < 0.05) SRIF release. GRF (1 nM) increased SRIF mRNA (P < 0.001) and stimulated the release of SRIF at 30 min (P < 0.05) and 6 hr (P < 0.01). This stimulation was abolished by 10 microM NG-monomethyl-L-arginine (L-NMMA), a specific inhibitor of nitric oxide synthase, but not by NG-monomethyl-D-arginine (D-NMMA, the inactive isomer). GRF also increased cGMP formation. This effect was completely blocked by incubation with L-NMMA but not D-NMMA. These results indicate that GRF releases nitric oxide. The nitric oxide diffuses to the adjacent SRIF neurons, where it activates guanylate cyclase, leading to increased formation of cGMP. This cGMP increases SRIF mRNA and SRIF release in the periventricular nuclei of male rats.
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PMID:Growth hormone-releasing factor increases somatostatin release and mRNA levels in the rat periventricular nucleus via nitric oxide by activation of guanylate cyclase. 790 58

NADPH-diaphorase activity (NADPH-DA), a marker of neural nitric oxide synthase, was found in many postganglionic nerve cell bodies in the adult rat superior cervical ganglion (SCG) after colchicine treatment, postganglionic nerve trunk ligation or ganglion culture. NADPH-DA colocalized with immunoreactivity to tyrosine hydroxylase (TH), serotonin, vasoactive intestinal peptide (VIP), neuropeptide Y (NPY), methionine-enkephalin and somatostatin. Almost all cells showing NADPH-DA were TH-immunoreactive, although several TH-immunoreactive cells lacked NADPH-DA. While suggesting that nitric oxide has an important role in the neuronal modulation in the synaptic transmission in the rat SCG, our results point out that nitric oxide synthesis is confined to a subpopulation of ganglion neurons. Our findings confirm the idea that the superior cervical ganglion consists of several subpopulations in which noradrenaline is colocalized with other transmitter or neuropeptide. Only about one-fourth of serotonin-immunoreactive neurons contained NADPH-DA. Similarly, the neuropeptides studied showed only partial colocalization with NADPH-DA. Our results thus suggest that nitric oxide is not associated with any particular transmitter or peptide.
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PMID:NADPH-diaphorase activity and its colocalization with transmitters and neuropeptides in the postganglionic neurons of the rat superior cervical ganglion. 795 6

Using in situ hybridization, the expression of the mRNA for a neuropeptide Y (NPY) receptor, was studied in lumbar (L) 4 and 5 dorsal root ganglia (DRGs) of normal rats and at various intervals after unilateral sciatic nerve transection. Twenty percent of all normal DRG neurons were NPY receptor mRNA-positive, and the majority of these neurons were of the small type, with only a few labelled medium-sized and large neurons. In L5 normal ganglia NPY receptor mRNA colocalized with substance P, calcitonin gene-related peptide and galanin mRNAs in small neurons, but not in medium-sized or large neurons containing these peptides. NPY receptor mRNA was not observed in somatostatin or nitric oxide synthase mRNA-positive neurons. Sciatic nerve transection induced a marked decrease in NPY receptor mRNA levels. However, in parallel there was a transient increase in the number of NPY receptor mRNA-positive small neuron profiles, but the intensity of labelling was mostly very low, although a few strongly labelled, small neuron profiles were also encountered. In addition, axotomy caused a marked increase in the number of NPY receptor mRNA-positive large neuron profiles in the ipsilateral DRGs, and they constituted 15-20% of counted DRG neuron profiles and 45-65% of counted large neuron profiles, 7-28 days after axotomy. In L5 DRGs, ipsilateral to the axotomy, NPY receptor mRNA colocalized with NPY mRNA in many large and some medium-sized neuron profiles, with galanin mRNA in some small, medium-sized and large neuron profiles and with vasoactive intestinal polypeptide mRNA in some small and medium-sized neuron profiles and a few large profiles. Occasionally, NPY receptor mRNA was observed in nitric oxide synthase mRNA-positive small neurons. In the dorsal horn, NPY receptor mRNA-positive small neurons were concentrated in lamina II at L4 and L5 levels, and were scattered in deeper laminae. No marked changes were observed ipsilateral to the axotomy. No NPY receptor mRNA-positive cells were found in the normal rat gracile nucleus, or in this nucleus after axotomy. These results show that a NPY receptor may be a prejunctional receptor in primary afferent neurons and play a role in the modulation of somatosensory information, both in normal and lesioned primary afferent DRG cells. However, axotomy induced a distinct shift in NPY receptor mRNA expression from small to large neurons, indicating that sensitivity to NPY is switched from one modality to another.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effect of peripheral axotomy on expression of neuropeptide Y receptor mRNA in rat lumbar dorsal root ganglia. 813 Sep 32

Histochemical staining was used to demonstrate that intramural neurons of the gallbladder contain NADPH-diaphorase, and therefore are likely to produce nitric oxide. A subset of the neurons in the gallbladders of the guinea pig, gerbil, opossum, dog, and human stained positively for the enzyme. In the guinea pig, all neurons that were immunoreactive for vasoactive intestinal peptide (VIP), also contained NADPH-diaphorase. Furthermore, neurons that were immunoreactive for neuropeptide Y, which have been shown to be immunoreactive for substance P and somatostatin as well, rarely contained NADPH-diaphorase. It is suggested that the VIP/NADPH-diaphorase-containing neurons represent intrinsic inhibitory motor neurons of the gallbladder, and that these neurons may have a role in the relaxation of the muscularis during gallbladder filling.
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PMID:NADPH-diaphorase and VIP are co-localized in neurons of gallbladder ganglia. 831 13


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