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)

Parkinson's disease is characterized by a deficiency of dopamine in the nigrostriatal system. However, changes in dopamine neurons were found also outside the extrapyramidal system, showing that there is a more general brain defect than just the loss of substantia nigra dopamine neurons. With regard to the behavior of striatal D-2 receptors it was possible to divide parkinsonian patients into two subgroups, because either a decrease or an increase in the number of D-2 receptors was found. Clinically, the patients with a decreased number of striatal D-2 receptors were more disabled and had lost the beneficial response to levodopa. D-3 receptor binding sites were decreased in the parkinsonian striatum. Changes in the cholinergic-muscarinic receptors in the striatum seem to be related to changes in D-2 receptors, and muscarinic receptor supersensitivity was found in cortical areas. GABA receptor binding was decreased in the substantia nigra. In the parkinsonian brain there seems to be supersensitivity of a population of enkephalin receptors (delta) in the striatum and in the limbic system and also a loss of others (mu) in the striatum. Furthermore, the Met-enkephalin content was decreased in the parkinsonian substantia nigra. A decreased concentration of substance P was found in the substantia nigra of all parkinsonian patients and in the putamen of those patients who had not received levodopa treatment. The somatostatin level was decreased in the frontal cortex in relation to dementia. There are thus multiple neuronal disturbances in the parkinsonian brain, although those of the nigrostriatal dopamine neurons seem to be the greatest and are more closely related to parkinsonian clinical features and to treatment responses.
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PMID:Brain neurotransmitters and neuropeptides in Parkinson's disease. 609 88

Somatostatin (SRIF) was applied microiontophoretically to neurons in the frontal and parietal neocortex, the hippocampus and the striatum of rats anaesthetized with either urethane or chloral hydrate. Qualitatively identical results were obtained under both anaesthetic conditions. In urethane-treated rats SRIF elicited a dose-dependent increase of the firing rate of 74% of the neurons studied in the frontal cortex and of 46% of the neurons studied in the parietal cortex. All cortical cells identified as pyramidal cells were excited. In the hippocampus SRIF provoked excitatory responses in two thirds of all neurons. Six out of the nine cells identified as pyramidal cells were excited by SRIF. In the striatum 80% of all neurons were excited. Following repeated exposure of central neurons to SRIF, the magnitude of the excitatory response gradually diminished, indicating desensitisation. SRIF in concentrations ranging from 10(-8) to 10(-4) M did not interfere with the binding of (3H)-muscimol to GABA receptor sites. The release of GABA from synapses preloaded with (3H-GABA) was not influenced by SRIF in the concentration range from 10(-6) to 10(-4) M. These results indicated that SRIF does not evoke the excitatory responses through attenuation of GABA-mediated inhibition. In conclusion, the findings support the hypothesis that somatostatin may function as a neurotransmitter in the central nervous system.
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PMID:Central actions of somatostatin. 610 12

Neurotransmitter effects were studied on in vitro release of immunoreactive somatostatin (SRIF) from slices prepared from several regions of the rat brain: mediobasal hypothalamus (MBH), preoptic anterior hypothalamic area (POA) and amygdaloid complex (AMY). Potassium (K+, 56 mM) stimulated SRIF release in all structures tested in a calcium dependent manner. Morphine, dopamine, GABA and serotonin did not modify SRIF release in any structure; noradrenaline (NA) was not effective on MBH slices, but elicited a dose-dependent stimulation of SRIF release from POA and AMY (ED50 = 6.4 +/- 1.4 nM and 3.6 +/- 1.2 nM respectively). Converse orders of potency of adrenergic agonists were observed in both structures (POA, adrenaline greater than noradrenaline greater than isoproterenol; AMY, isoproterenol greater than adrenaline greater than noradrenaline). Phentolamine blocked NA-induced SRIF release in the POA while propranolol was ineffective. On the contrary, propranolol, but not phentolamine, antagonized NA stimulation in the amygdala. The data suggest that NA acting through specific receptors modulate SRIF release from POA and AMY. In POA, NA effect seems mediated through alpha adrenergic receptors while in AMY, beta receptors are involved. The possibility that these interactions of NA with SRIF release are correlated with effects of NA on growth hormone secretion or on epileptic events is discussed.
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PMID:Noradrenaline stimulates somatostatin release from incubated slices of the amygdala and the hypothalamic preoptic area. 611 80

The influence of cortical neurotransmitters and cyclic AMP on the release of immunoreactive somatostatin (IRS)from cultured cortical cells was examined. Cells were obtained by mechanoenzymatic dispersal of telencephalons of 17-day-old rat embryos and were maintained as monolayers in minimum essential medium with 10% heat-inactivated horse serum. After the cultures had stabilized morphologically and in cellular IRS content they were subjected to rapid sequential changes of a buffered salt solution with or without test substances added. The amount of somatostatin released was measured by a specific radioimmunoassay. Acetylcholine and the GABA antagonist, picrotoxin, both stimulated IRS release. The cholinergic stimulation was predominantly muscarinic. GABA and histamine, to a lesser extent, were inhibitory and norepinephrine and serotonin produced no net change in IRS release. Both cAMP and theophylline (DMX) stimulated IRS release. These results confirm the potential of intrinsic cortical somatostatinergic neurons to respond to endogenous neurotransmitters and further establishes somatostatin as a cortical neuromodulator.
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PMID:Effects of neurotransmitters and cyclic AMP on somatostatin release from cultured cerebral cortical cells. 612 Jul 48

The regional distribution and cellular location of GABA-synthesizing enzyme, L-glutamate decarboxylase (GAD), GABA degrading enzyme, GABA-transaminase (GABA-T), taurine synthesizing enzyme, cysteine sulfinic acid decarboxylase (CSAD), aspartate and glutamate converting enzyme, aspartate aminotransferase (AAT), and somatostatin have been visualized in the rat retina by immunocytochemical methods. GAD immunoreactivity was found to be concentrated in the inner plexiform layer. A moderate to weak staining of GAD was found in the inner nuclear layer. The distribution of GABA-T immunoreactivity was similar to that of GAD with the exception that a weak to moderate staining of GABA-T was also observed in the outer plexiform layer. CSAD immunoreactivity was seen in every layer with the heaviest staining in the inner plexiform layer, and moderate staining in the inner and outer nuclear layers and ganglion cell layer. AAT immunoreactivity was mostly concentrated in the outer nuclear layer; there was weak staining in the inner nuclear layer and inner and outer plexiform layer. Dense somatostatin staining was seen in the inner plexiform layer and moderate staining was present in the inner nuclear layer, outer plexiform layer and ganglion cell layer. These findings suggest that in rat retina, GABA-containing cells occur in some types of amacrine cells only, while taurine and somatostatin appear in both amacrine and horizontal cells. AAT immunoreactivity was primarily associated with the photoreceptor cells suggesting that AAT may be used as a marker for aspartergic/glutamergic cells and their endings in the central nervous system.
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PMID:Immunocytochemical localization of L-glutamate decarboxylase, gamma-aminobutyric acid transaminase, cysteine sulfinic acid decarboxylase, aspartate aminotransferase and somatostatin in rat retina. 613 12

We examined the ability of several putative amino acid neurotransmitters to influence immunoreactive somatostatin (IRS) release from cultured rat cerebral cortical cells. The cells were exposed to either or sequential incubations in various concentrations of glutamate (Glu), aspartate (Asp), GABA, glycine, taurine and arginine. Glu and Asp were stimulatory to IRS release, whereas GABA was inhibitory. Glu-induced IRS release was calcium-dependent. Glycine and taurine were weak stimulants.
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PMID:Somatostatin release from cerebral cortical cells: influence of amino acid neurotransmitters. 613 67

Neuropeptides are found in dense networks of neuronal perikarya, fibers and terminals within numerous brain regions. Among the more striking of these collections are sites within the central nervous system that are presumed to regulate either endocrine or autonomic function. A recent example of a neuropeptide which is likely to play a significant role in endocrine regulation is cortocotropin releasing factor (CRF). Immunohistochemical studies revealed that CRF immunoreactivity was found in many brain regions, including the paraventriculo-infundibular pathway. CRF released from nerve terminals belonging to this pathway presumably regulates ACTH release. Treatment of rats with reserpine depletes CRF as well as vasopressin from the external layer of the median eminence, suggesting tonic, monoaminergic inhibition of CRF and vasopressin containing neurons. CRF antisera were found which stain urotensin I immunoreactivity within the caudal neurosecretory system of fish. Numerous putative neurotransmitters impinge upon preganglionic sympathetic neurons within the intermediolateral cell column of the spinal cord. Preganglionic sympathetic neurons which innervate the adrenal medulla appear to have a specific input from somatostatin immunoreactive fibers. In addition, binding sites for serotonin and alpha-2 adrenergic ligands are more highly concentrated over sympathoadrenal neurons. Finally, the pancreatic islet contains peptide producing endocrine cells which possess several neuron-like properties. Some of these properties are reviewed, especially the finding that the insulin producing cells contain glutamate decarboxylase immunoreactivity, the biosynthetic enzyme for GABA. Further studies revealed that GABA agonists inhibit somatostatin release from islet cells.
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PMID:Peptidergic regulation in neuroendocrine and autonomic systems. 614 35

It is now clear that a variety of neuropeptides interact with the more classically defined neurotransmitters to stimulate or inhibit feeding. An extensive peripheral peptide satiety system has been identified. Peptides involved in this system include cholecystokinin, bombesin, gastrin-releasing peptide, glucagon, somatostatin, and possibly thyrotropin-releasing hormone and calcitonin. Some of these peptides appear to inhibit feeding by activating ascending fibers in the vagus, whereas others exert their actions independent of the vagus. In addition, neuropeptides appear to play a role in producing the neuromodulatory effects of taste on appetite, and hormones from the endocrine system modulate neuropeptide effects on feeding. The central appetite regulatory system appears to be arranged in a cascade, with an interaction between dynorphin and dopamine producing a part of the feeding drive. This drive is held in check by a variety of neuropeptides including calcitonin, corticotropin-releasing factor, and bombesin. In turn, these peptides are modulated by a norepinephrine-alpha-aminobutyric acid (GABA) system. Neurotensin, serotonin, cyclohistidyl proline diketopiperazine, and the peripheral satiety system appear to modulate the norepinephrine-GABA disinhibitory system. By the judicious use of neuropharmacological modeling we have developed a model of the neurotransmitter interactions involved in appetite regulation that can act as a springboard for the design of future experiments to unravel the mysteries of appetite regulation.
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PMID:Neuropeptides and appetite: contribution of neuropharmacological modeling. 614 55

Pyriform Ab amacrine cells in the goldfish retina take up [3H]GABA and show somatostatin-like immunoreactivity (SLIR), leading to the question of whether these two markers are labeling the same or different types of Ab amacrine cells. We used a double-label radio/immuno-technique at the electron microscopical level to visualize the comparative location of [3H]GABA uptake and SLIR in Ab amacrine cells and their processes. SLIR was restricted to large dense-cored vesicles in processes of Ab amacrine cells. In no case were processes labeled with SLIR observed to take up [3H]GABA. Thus, there are at least two types of pyriform Ab amacrine cells: one that takes up [3H]GABA and one that shows SLIR. These may correspond to the two types of Ab amacrine cells described by Cajal in his classic studies on the retina.
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PMID:Two types of pyriform Ab amacrine cells in the goldfish retina: an EM analysis of [3H]GABA uptake and somatostatin-like immunoreactivity. 614 93

The control of prolactin (PRL) cell activity in Salmo gairdneri was investigated in vivo and in vitro. In some in vivo experiments treatment was followed by estimation of pituitary PRL content by gel electrophoresis or of PRL cell nuclear area by light microscopy. In the remainder, treatment was followed by incubation of the pituitary glands in drug-free medium for estimation of PRL synthesis and release. The dopamine precursor, L-dopa (20 mg/kg), reduced pituitary PRL content. Conversely, the dopamine-receptor blocker, domperidone (10 mg/kg), increased total PRL content and amount released in the subsequent incubation. The initial serotonin precursor, L-tryptophan (75 mg/kg), increased pituitary PRL content and PRL cell nuclear area. 5-HTP (20 mg/kg), the immediate serotonin precursor, increased both percentage PRL release and total PRL levels during subsequent incubation. Pargyline (25 mg/kg) treatment to inhibit serotonin catabolism elevated PRL levels in pituitary and medium during subsequent incubation. The serotonin synthesis blocker, parachlorophenylalanine (pCPA; 100 mg/kg), nonsignificantly reduced PRL cell nuclear area. When this was followed by incubation, percentage PRL release and total PRL fell significantly. During in vitro incubation, dopamine (2 micrograms/ml) reduced the release of PRL into the medium, while serotonin (10(-5) M) increased PRL release. These results suggest that both an inhibitory dopaminergic and a stimulatory serotonergic system may be involved in PRL cell regulation in S. gairdneri. The lack of any significant effect of cortisol (1 microgram/ml), somatostatin (300 ng/ml). GABA (100 mg/ml) and TRH 100 ng/ml) on PRL release in vitro suggested little or no involvement of these putative regulatory factors in PRL cell regulation.
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PMID:Evidence for dopaminergic and serotonergic regulation of prolactin cell activity in the trout Salmo gairdneri. 615 Aug 77


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