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)

Slices (300 microns) of rat caudatoputamen were incubated in Krebs-Henseleit medium and loaded with [3H]glutamine, part of which was converted to [3H]GABA. This conversion takes place only in GABA-neurons most of which probably contribute to the striatonigral pathway. After a 24 min equilibration period, release of radioactivity was stimulated with veratridine (3.1-4 mumol/l) or K+ (15-25 mmol/l) in the absence or presence of somatostatin-14. From the radioactivity released [3H]GABA was separated by cationic exchange chromatography and measured. Somatostatin-14 affected the release of [3H]GABA in a manner which depended on its concentration as well as on the extent of stimulus-evoked release. Somatostatin-14 (1 nmol/l) enhanced the moderate release (2-4% of tissue content) elicited by veratridine (3.1 mumol/l) or K+ (20 mmol/l), but had no effect on the more pronounced release (5-8% of tissue content) elicited by veratridine (4 mumol/l) or K+ (25 mmol/l). Somatostatin-14 (10 nmol/l) had no effect on the moderate release of [3H]GABA, but diminished the pronounced one. Further experiments provided evidence that the somatostatin-14-induced enhancement was not brought about by a direct action on GABA-neurons but was probably indirect, i.e. mediated by other striatal neurons. In contrast, the diminution of the release of [3H]GABA caused by somatostatin-14 may be due to its direct action on releasing neurons. Two antisera against somatostatin lowered the pronounced release indicating that endogenous somatostatin may also enhance the release of [3H]GABA. In addition, endogenous somatostatin seems also to be able to diminish the release under certain experimental conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of somatostatin-14 on the in vitro release of [3H]GABA from slices of rat caudatoputamen. 256 96

We studied the effect of pentylenetetrazol (PTZ)-induced kindling (35 mg/kg, i.p., daily) on somatostatin-like immunoreactivity (SOM) with special attention to the duration of changes (rats were sacrificed either 10 days or 4 months after the development of kindling) and to transmitters or modulators related to somatostatin (neuropeptide Y (NPY), GABA, choline acetyltransferase (ChAT), acetylcholinesterase (AchE]. In rats sacrificed 10 days after the last kindled seizure, SOM was elevated in frontal cortex and striatum (p less than 0.01); NPY was elevated in frontal cortex, striatum and hippocampus (p less than 0.05) of kindled or prekindled rats (i.e., rats which were treated daily with PTZ but did not express three consecutive generalized seizures). ChAT activity was slightly decreased (p less than 0.05) in cortex. GABA levels and AchE activity were unchanged in kindled cortex. In rats sacrificed 4 months after the development of kindling none of the parameters analyzed differed from controls. The present study suggests that the cortical and striatal neurons containing SOM/NPY are affected by PTZ-kindling. The cortical cholinergic system is affected to a much smaller extent. The neuropeptide changes are not persistent, as is the lowered seizure threshold, so they are probably not involved in the maintainance of the latter.
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PMID:Somatostatin, neuropeptide Y, GABA and cholinergic enzymes in brain of pentylenetetrazol-kindled rats. 257 17

In the turtle retina the peptides met-enkephalin (metENK), somatostatin (SS), neurotensin (NT), and the indoleamine serotonin (5-HT) modulate ganglion cell (GC) activity. The predominant action of the peptides is excitatory, generally enhancing spontaneous firing and light-evoked activity. In contrast, 5-HT usually inhibits these GC activities. MetENK has both direct synaptic input onto GC and indirect action possibly via a GABA inhibitory interneuron. The metENK actions appear mediated via a mu-opiate receptor; morphine and D-ala-metENK-amide (DALA), a stable analog of metENK, are agonists. Naloxone antagonizes the actions of metENK and its agonists. DALA occasionally inhibits GC. This inhibition is antagonized by picrotoxin, while concurrent excitatory action on GC is enhanced. DALA enhances GC response at high spatial frequencies; naloxone attenuates it. The enhancement by DALA suggests a narrowed receptive-field (RF) center, possibly due to changes in a GABA-mediated inhibitory surround. 5-HT inhibitory actions are also mediated via direct and indirect synaptic pathways. 5-methoxy-dimethyl-tryptamine and methoxy-phenyl-piperazine are agonists of 5-HT action. They are both specific 5-HT1 agonists. LSD (lysergic acid diethylamide) and cyproheptadine, which act on 5-HT2 receptors, antagonize 5-HT actions in this retina. Strychnine enhances GC activity, probably by antagonizing glycine-mediated inhibitory inputs. It does not block the inhibitory action of 5-HT, which suggests that the indirect 5-HT inhibition is not mediated via a glycinergic interneurone. 5-HT suppresses directional selectivity (DS) and attenuates high spatial frequencies in some GC. This may be mediated via inhibition of GABAergic amacrines subserving DS and the RF inhibitory surround.
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PMID:Pharmacological actions of peptides and indoleamines on turtle retinal ganglion cells. 257 68

Monoclonal antibody VC1.1 is shown to stain selectively a subpopulation of GABAergic neurons in the rat cerebral cortex. Almost all VC1.1 immunoreactive cells were also GABA-like immunoreactive (GABA-LI) and parvalbumin (PV) immunoreactive, whereas they were about 30% and 65% of GABA-LI and PV-positive cells in the parietal cortex and about 13% and 32% in the occipital cortex, respectively. Although a few VC1.1 positive cells showed somatostatin-like and/or cholecystokinin-like immunoreactivities, they were exceptional (less than 1% of VC1.1 positive cells). Furthermore about 90% of VC1.1 positive cells were also stained with a lectin, Vicia villosa agglutinin, with a specific affinity for terminal N-acetylgalactosamine.
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PMID:Monoclonal antibody VC1.1 selectively stains a population of GABAergic neurons containing the calcium-binding protein parvalbumin in the rat cerebral cortex. 259 17

1. NPY is a 36 amino acid tyrosine-rich peptide. It is one of the most abundant and widely distributed neuropeptides known today within the central nervous system with particularly high concentrations in the hypothalamus and in several limbic regions. 2. NPY seems to coexist with other on neurotransmitters like somatostatin, galanin, GABA and the catecholamines noradrenaline and adrenaline in discrete brain regions. 3. NPY binding sites are widely distributed in the brain. However they do not always overlap with the distribution of NPY-like immunoreactivity. 4. NPY is suggested to be involved in a large number of neuroendocrine functions, stress responses, circadian rhythms, central autonomic functions, eating and drinking behaviour, and sexual and motor behaviour. 5. Psychotropic drugs and neurotoxins can alter the NPY concentrations in discrete brain regions. 6. It is possible that NPY is related to various neurological and psychiatric illnesses, like Huntington's chorea, Alzheimer's disease, Parkinson's disease, eating disorders, and major depressive illness.
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PMID:Neuropeptide Y (NPY) and the central nervous system: distribution effects and possible relationship to neurological and psychiatric disorders. 266 85

The therapeutic action of vigabatrin (gamma vinyl GABA, GVG) has been reported to be mediated by GABAergic neurotransmission. In the present study, we evaluated different neurotransmitter systems in the cerebrospinal fluid (CSF) of patients with complex partial epilepsy, before and during GVG treatment. The markers of the GABAergic system (free GABA, total GABA, homocarnosine) showed a two- to threefold elevation. There was also an increase in glycine during the 6 months of GVG treatment. In contrast, we did not find any constant CSF changes in either excitatory amino acids or in markers of the cholinergic (acetylcholinesterase), dopaminergic (homovanillic acid), serotonergic (5-hydroxyindoleacetic acid), or peptidergic (somatostatin, prolactin, beta-endorphin) systems. This finding (except an elevation in glycine) was in agreement with previous studies which suggest a specific action of GVG on the GABAergic system. The role of glycine in antiepileptic efficacy of GVG needs further evaluation.
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PMID:Specificity of vigabatrin for the GABAergic system in human epilepsy. 276 15

In Parkinson's disease the progressive loss of nigrostriatal dopamine neurons leads to striatal dopamine deficiency and correlates with the severity of parkinsonian disability. The findings concerning dopamine receptors both in vitro and in vivo are not consistent, possibly reflecting differences in patient populations, but the presynaptic defect in dopaminergic neurotransmission is greater than that seen in postsynaptic receptor binding studies. The cholinergic neurons in the extrapyramidal nuclei are relatively well preserved, but subcortico-cortical and -hippocampal cholinergic neurons degenerate in relation to the degree of dementia. The decreased GABA receptor binding in the parkinsonian substantia nigra possibly reflects the loss of nigral dopamine neurons, since nigral GABA receptors are located on these neurons. Of the various neuropeptides, the concentration of met- and leu-enkephalin seems to be reduced in the striatum. In the substantia nigra the concentration of substance P decreases, together with the met-enkephalin and cholecystokinin levels. The concentration of somatostatin decreases in the frontal cortex and hippocampus of demented patients. With the exception of the association between cortical somatostatin deficiency and intellectual deterioration, the role of the neuropeptides in the pathophysiology and clinical features of Parkinson's disease are not yet fully understood.
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PMID:Chemical neurotransmission in the parkinsonian brain. 282 31

The study of neurotransmitter receptors aids in the understanding of the normal anatomy, pharmacology, therapeutics and pathophysiology of disease processes involving the basal ganglia. Receptors may be studied in vitro by homogenate binding experiments, enzyme analysis or quantitative autoradiography and in vivo with positron emission tomography. In the substantia nigra (SN), receptors have been identified for somatostatin, neurotensin, substance P, glycine, benzodiazepine and GABA, opiates, dopamine, angiotensin converting enzyme (ACE) and serotonin. The striatum has receptors for dopamine, GABA and benzodiazepines, acetylcholine, opiates, substance P, glutamate and cholecystokinin. GABA and benzodiazepine receptors are also located in the globus pallidus. In Parkinson's disease, striatal dopamine D-2 receptors are elevated in patients that have not received L-DOPA therapy. This supersensitivity is reversed with agonist therapy. Muscarinic binding to cholinergic receptors seems to correlate with dopamine receptors. Delta opiate receptors are increased in the caudate and mu binding is reduced in the striatum. In the SN of patients with Parkinson's disease, there is reduced binding of somatostatin, neurotensin, mu and kappa opiates, benzodiazepine and GABA and glycine. In Huntington's disease, there is reduced binding of GABA and benzodiazepines, dopamine, acetylcholine, glutamate and CCK. There is increased binding of GABA in both the SN and globus pallidus. Glycine binding is increased in the substantia nigra and ACE is reduced.
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PMID:Receptors in the basal ganglia. 282 9

The functional role of three putative neurotransmitter systems in the visual cortex is compared; the GABAergic inhibitory interneurons, the interneurones containing somatostatin and the cholinergic input originating from the nucleus basalis of Meynert (nbM). Evidence is presented to support the role of GABAergic processes in the generation of the functional structure of the visual cortex and the view that the cholinergic input exerts a neuromodulatory influence enhancing stimulus selective responses. Although the neuropeptide somatostatin produces facilitatory and inhibitory effects on visual cortical cells there is no clear functional pattern to its action. The possible significance of this data and the interaction of SSt with GABA is discussed in the light of evidence that they may coexist in some cells.
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PMID:Modulatory and inhibitory processes in the visual cortex. 286 40

Immunohistochemical studies with antisera to somatostatin have, in many instances, led the way to our present understanding of the peptidergic nervous system. Somatostatin was among the first of the hypophysiotropic hormones shown to be contained in diverse neuronal circuits outside of the hypothalamus. For example, somatostatin is found within neurons ranging in location from the cerebral cortex to primary sensory neurons to enteric neurons within the gut wall. Somatostatin was also the first neuropeptide demonstrated to coexist within vertebrate neurons that also produce a classical neurotransmitter. Since this initial demonstration in sympathetic ganglionic neurons, somatostatin and numerous other neuropeptides have been demonstrated to coexist with a variety of classical neurotransmitters. The "rules" for coexistence are not clear, since somatostatin coexist in some instances with norepinephrine, in other cases with GABA, and probably with other classical transmitters as well. In some neurons, somatostatin also coexists with certain other neuropeptides. Finally, the specificity of immunohistochemical localizations of somatostatin has now been confirmed by virtue of the co-staining of somatostatin neurons with antisera to other portions of the biosynthetic precursor to somatostatin.
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PMID:Immunocytochemical studies of somatostatin neurons in brain. 286 29


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