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

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

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

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

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

The cellular abundance of neuronal nitric oxide synthase and somatostatin messenger RNAs was compared in the caudate nucleus, putamen and sensorimotor cortex of Huntington's disease and control cases. Neuronal nitric oxide synthase messenger RNA was significantly decreased in the caudate nucleus and putamen, but not in the sensorimotor cortex in Huntington's disease; the decrease in neuronal nitric oxide synthase messenger RNA became more pronounced with the severity of the disease. Somatostatin gene expression was significantly decreased in the dorsal putamen in Huntington's disease, but was essentially unchanged in all other regions examined. The density of neurons expressing detectable levels of neuronal nitric oxide synthase messenger RNA was reduced in the striata of Huntington's disease cases with advanced pathology; the density of neurons expressing detectable levels of somatostatin messenger RNA was similar in control and Huntington's disease cases. Neuropeptide Y-, somatostatin- and NADPH-diaphorase-positive neurons were consistently present throughout the striatum across all the grades of the disease. Neuronal nitric oxide synthase and NADPH-diaphorase activity (a histochemical marker for nitric oxide synthase-containing neurons) co-localize with somatostatin and neuropeptide Y in interneurons in the human striatum and cerebral cortex. Although the neurodegeneration associated with Huntington's disease is most evident in the striatum (particularly the dorsal regions), neuronal nitric oxide synthase/neuropeptide Y/somatostatin interneurons are relatively spared. Nitric oxide released by neuronal nitric oxide synthase-containing neurons may mediate glutamate-induced excitotoxic cell death, a mechanism proposed to be instrumental in causing the neurodegeneration seen in Huntington's disease. The results described here suggest that although the population of interneurons containing somatostatin, neuropeptide Y and neuronal nitric oxide synthase do survive in the striatum in Huntington's disease they are damaged during the course of the disease. The results also show that the reduction in neuronal nitric oxide synthase and somatostatin messenger RNAs is most pronounced in the more severely affected dorsal regions of the striatum. Furthermore, the loss of neuronal nitric oxide messenger RNA becomes more pronounced with the severity of the disease; thus implying a down-regulation in neuronal nitric oxide synthase messenger RNA synthesis, and potentially neuronal nitric oxide synthase protein levels, in Huntington's disease.
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PMID:Decreased neuronal nitric oxide synthase messenger RNA and somatostatin messenger RNA in the striatum of Huntington's disease. 873 28

Elasmobranchs possess a well-developed cerebellum with an associated cerebellar nucleus. To determine whether the organization of this nucleus is comparable with that of the deep cerebellar nuclei of mammals, we studied the dogfish cerebellar nucleus with light microscopic methods (Nissl stain, Golgi method, reduced silver stain, NADPH-diaphorase histochemistry and immunocytochemistry) and with electron microscopy. We found the dogfish cerebellar nucleus to consist of about 1,050 large neurons, the ratio of Purkinje cells to cerebellar nucleus neurons being about 17:1. Immunocytochemistry showed large glutamatergic neurons in the main portions of the nucleus and small glutamate- and/or alpha-aminobutyric acid (GABA)-immunoreactive cells in the subventricular region of the nucleus. Large glutamatergic neurons corresponded to bipolar or triangular cells revealed by Golgi methods. Application of horseradish peroxidase to the cerebellar cortex produced the labelling of beaded fibres of Purkinje cells in the cerebellar nucleus. Unlike in mammals, GABAergic innervation of the cerebellar nucleus was scare: Purkinje cell axon terminals in the cerebellar nucleus did not appear to be GABA-immunoreactive, most GABAergic fibres being found in the subventricular neuropile. Some fibres immunoreactive to serotonin and somatostatin were also observed in the subventricular neuropile of the cerebellar nucleus. Three neuron types were distinguished with electron microscopy (types A to C). Type A cells were abundant and smooth-surfaced, and appeared to correspond to Golgi-impregnated neurons and large glutamate-immunoreactive cells. Type B neurons were scarce and possessed dendrites covered by sessile or stalked spines. Type C neurons were small cells located mainly in the medialmost region of the nucleus and corresponded to subventricular glutamate- and GABA-immunoreactive cells. Six types of synaptic bouton were observed (types I to VI). The most abundant (type I boutons) made symmetrical contacts and appeared to correspond to Purkinje cell axons. Type I boutons were the only type observed on perikarya and initial axon segments of type A cells. Type IV and type V boutons made complex glomerular-like asymmetrical contacts with spines of type B cells. Type VI boutons appeared to correspond to peptidergic and/or monoaminergic axons. The functional significance of these results is discussed.
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PMID:Organisation of the cerebellar nucleus of the dogfish, Scyliorhinus canicula L.: a light microscopic, immunocytochemical, and ultrastructural study. 874 38

In addition to its functions as a neuronal messenger molecule, nitric oxide (NO) has also been implicated in playing a major role in ischemic damage and glutamate neurotoxicity. Using primary cortical cultures from transgenic neuronal NO synthase (NOS) null (nNOS-) mice, we definitively establish NO as a mediator of NMDA and hypoxic neurotoxicity. Neurotoxicity elicited by NMDA is markedly attenuated in nNOS- cortical cultures compared with wild-type cultures. The NOS inhibitor nitro-L-arginine is neuroprotective in wild-type but not nNOS-cultures, confirming the role of nNOS-derived NO in glutamate neurotoxicity. Confirming that the nNOS- cultures lack NMDA-stimulated nNOS activity, NMDA did not stimulate the formation of cGMP in nNOS- cultures, but markedly elevates cGMP in wild-type cultures. Both wild-type and nNOS- cultures are sensitive to toxicity induced by NO donors, indicating that pathways stimulated by NO that result in neuronal cell death are still intact in the transgenic mice. Superoxide dismutase is neuroprotective against NMDA and NO neurotoxicity in both wild-type and nNOS- cultures, highlighting the importance of superoxide anion in subsequent neuronal damage. The unknown cellular factors that endow differential resistance to NMDA neurotoxicity and differential susceptibility to quisqualate neurotoxicity remain intact in the nNOS- cultures, because the response of somatostatin-immunopositive neurons in nNOS- cultures to high-dose NMDA and low-dose quisqualate is identical to the response of NOS-immunopositive neurons in the wild-type cultures. There is no difference in susceptibility to kainate neurotoxicity between nNOS- and wild-type cultures and only a modest resistance to quisqualate neurotoxicity, confirming observations that NO-mediated neurotoxicity is associated primarily with activation of the NMDA receptor. The nNOS- cultures are markedly protected from 60 min of combined oxygen-glucose deprivation neurotoxicity compared with wild-type cultures. Wild-type cultures are protected from neuronal cell death by the NMDA receptor antagonist MK-801 and the NOS inhibitor L-nitroarginine methyl ester, but not its inactive stereoisomer D-nitroarginine methyl ester. nNOS- cultures were not additionally protected. These data confirm that activation of NMDA receptors and production of NO are primary mediators of neuronal damage after ischemic insult.
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PMID:Resistance to neurotoxicity in cortical cultures from neuronal nitric oxide synthase-deficient mice. 878 24

Short axon (SA) cells in the olfactory bulb are subdivided into six types after Golgi impregnation, although their functional significance is not fully elucidated. In the present study, we examined the golden hamster olfactory bulb by immunohistochemistry to localize neurotransmitters, neuron-specific marker, and nitric oxide synthase (NOS) in the SA cells. Enzyme histochemical staining was also performed to detect the activity of nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase, which is identified with NOS. In the main olfactory bulb (MOB), neuropeptide Y (NPY)-, NOS-, and NADPH-diaphorase-positive SA cells were detected in the glomerular layer (GL), vasoactive intestinal polypeptide (VIP)-positive SA cells in the external plexiform layer (EPL), and NPY-, somatostatin (SOM)-, protein gene product 9.5 (PGP 9.5)-, NOS-, and NADPH-diaphorase-positive SA cells in the granule cell layer (GCL). In the accessory olfactory bulb (AOB), VIP- and PGP 9.5-positive SA cells were detected in the mitral/tufted cell layer (MTL), and NPY-, SOM-, NOS-, and NADPH-diaphorase-positive SA cells in the GCL. The common presence of NPY- SOM-, VIP-, PGP 9.5-, NOS-, and NADPH-diaphorase-positive SA cells in both the MOB and the AOB may suggest that respective types of cells with the same immunoreactivity play the same role no matter where these cells are located in the MOB or the AOB.
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PMID:Immunohistochemical and enzyme histochemical characteristics of short axon cells in the olfactory bulb of the golden hamster. 889 91

Nitric oxide synthase is co-localized with somatostatin and neuropeptide Y in a subpopulation of striatal interneurons that stain selectively for NADPH-diaphorase. We studied the ontogeny of diaphorase-positive neurons in striatal serum-free cultures derived from 15-16-day-old CD1 mice. NADPH-diaphorase staining was detected as early as embryological day 18 in vivo and day 5 in vitro. Over the next seven days the number of neurons staining for NADPH-diaphorase increased rapidly and then levelled off at about 0.5-1% of the total neuronal population both in vivo and in vitro. The cultured diaphorase neurons were also similar to their in vivo counterparts in terms of morphology and dendritic branching. Striatal neurons expressing NADPH-diaphorase exhibit similar ontogeny, morphology and neurochemical characteristics in vivo and in serum-free primary neuronal cultures. The culture system may represent a useful model for studying this important subgroup of striatal neurons.
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PMID:The ontogeny of NADPH-diaphorase neurons in serum-free striatal cultures parallels in vivo development. 914 14

Nitric oxide synthase is co-localized with somatostatin and neuropeptide Y in a subpopulation of striatal interneurons that stain selectively for NADPH-diaphorase. We studied the ontogeny of diaphorase-positive neurons in striatal serum-free cultures derived from 15-16-day-old CD1 mice. NADPH-diaphorase staining was detected as early as embryological day 18 in vivo and day 5 in vitro. Over the next seven days the number of neurons staining for NADPH-diaphorase increased rapidly and then levelled off at about 0.5-1% of the total neuronal population both in vivo and in vitro. The cultured diaphorase neurons were also similar to their in vivo counterparts in terms of morphology and dendritic branching. Striatal neurons expressing NADPH-diaphorase exhibit similar ontogeny, morphology and neurochemical characteristics in vivo and in serum-free primary neuronal cultures. The culture system may represent a useful model for studying this important subgroup of striatal neurons.
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PMID:The ontogeny of NADPH-diaphorase neurons in serum-free striatal cultures parallels in vivo development. 902 80


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