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)

Cysteamine administered in a dose of 1.95 mM/kg subcutaneously (SC) markedly reduced several open-field behaviors (locomotion, rearing, grooming and defecation), while pantethine, administered in an equimolar dose, reduced the locomotion only. However, administered in a dose of 3.90 mM/kg (SC), pantethine also markedly reduced all open-field parameters. Cysteamine, and to less extent pantethine, reduced noradrenaline, and increased dopamine and DOPAC concentrations in the hypothalamus. It is discussed whether the lower potency of pantethine on open-field behaviors and hypothalamic catecholaminergic neurotransmission is connected with the limited activity of pantetheinase, the cysteamine-generating enzyme. Intracerebroventricularly (ICV) administered somatostatin did not influence the pantethine-induced (1.95 mM/kg SC) behavioral changes in the open-field test. It is possible that the peptide did not reach at the receptor sites in a sufficient concentration because of the reduced endogenous somatostatin content, or that the pantethine-induced noradrenaline depletion is connected with the ineffectiveness of somatostatin. Furthermore, pretreatment with cysteamine (1.95 mM/kg SC) or pantethine (1.95 mM/kg or 3.90 mM/kg SC) attenuated the somatostatin-induced (10 micrograms ICV) barrel rotation, suggesting that the level of endogenous somatostatin may play a role in the pathogenesis of this motor disturbance.
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PMID:Effects of cysteamine and pantethine on open-field behavior, hypothalamic catecholamine concentrations, and somatostatin-induced barrel rotation in rats. 256

The effects of cysteamine and pantethine were compared on different behavioral tests and neurochemical parameters in rats. Cysteamine, administered in high dose (3.90 mM/kg s.c.), decreased the locomotor and rearing activities of rats, while it slightly but not significantly increased the avoidance latency in a passive avoidance test. Pantethine, 24 hr after its administration, significantly increased the dihydroxyphenyl acetic acid (DOPAC) levels in the striatum. Cysteamine slightly reduced the DOPAC level without influencing the catecholamine levels in this brain area. The striatal somatostatin concentration was reduced 24 hr after the administration of cysteamine, while pantethine did not influence it. After repeated daily injections of pantethine, the drug facilitated the shuttle box learning process and increased the intertrial and open-field activities of the animals. Cysteamine only slightly increased the locomotion and rearing and did not influence the shuttle box learning. Both pantethine and cysteamine slowed the rate of the "body weight increase" of the animals when compared to a saline-treated group. These findings suggest that the locomotor activation induced by pantethine 24 hr after its administration plays an important role in its behavioral effects. It might be that the striatal dopaminergic transmission, modified by administration of pantethine, plays some role in the higher locomotor activity induced by the substance.
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PMID:Cysteamine and pantethine effects on passive avoidance behavior, shuttle box learning, open-field activity, striatal catecholamines and somatostatin. 257 May 53

Cysteamine (CYS) is known to be a quite specific depletor of somatostatin in the rat brain. In the present study we investigated the effect of CYS (100 mg/kg, 300 mg/kg, subcutaneously) on levels of somatostatin-like immunoreactivity (SLI) in the brain and cerebrospinal fluid, on catecholamines in the cortex, and on spectral cortical electroencephalogram (EEG) of rat. SLI was decreased in both the cortex and the striatum (p less than 0.05) of CYS-treated rats, but no change was seen in SLI of CSF. Cortical levels of dopamine, noradrenaline and homovanillic acid were decreased (p less than 0.05) following administration of either dose of CYS. In EEG, during mobility both the frontal and occipital peak (Fp) and mean (Fm) frequencies were slowed (p less than 0.05). Frontally, the amplitude of the frequency bands 1.5-3Hz and 3-5Hz was increased (p less than 0.05). During immobility the Fp and Fm were also slowed. In frequency bands of 3-5Hz, 5-10Hz and 10-20Hz the amplitude was decreased (p less than 0.05), indicating that, in addition to theta frequency, the low voltage fast activity is also affected by CYS. According to our results, both the cortical intrinsic neurons containing somatostatin and also the ascending catecholaminergic systems are affected after the single administration of CYS concomittantly with, but not necessarily related to, changes in different frequency bands in EEG.
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PMID:Effect of cysteamine on levels of somatostatin-like immunoreactivity and catecholamines and on electroencephalogram in the rat brain. 257 Nov 5

Cysteamine (1.95 or 3.90 mM/kg) administered subcutaneously (sc) markedly decreased the open-field activity of the rats, while the structurally related amino acid cysteine had only minor influence. Cysteamine (1.95 or 3.90 mM/kg) reduced the noradrenaline and increased the dopamine and dihydroxyphenyl acetic acid (DOPAC) levels in the hypothalamus. In striatum the drug decreased both the noradrenaline (1.95 or 3.90 mM/kg) and dopamine (3.90 mM/kg) levels without influencing the DOPAC content. Neither the hypothalamic nor the striatal catecholamines are influenced by administration of equimolar doses of cysteine. Cysteamine (1.95 or 3.90 mM/kg) decreased the somatostatin levels both in the hypothalamus and in the striatum without influencing neuropeptide Y (NPY) and corticotropin releasing hormone (CRH) concentrations. Cysteine administered in equimolar doses did not influence the peptide levels in these brain structures. These data suggest that the cysteamine-induced behavioural changes are related to the decrease of brain noradrenaline and somatostatin concentrations. The structurally related amino acid cysteine does not influence the behaviour or the central monoaminergic and peptidergic concentrations in the hypothalamus and striatum of rats.
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PMID:Influence of cysteamine and cysteine on open-field behaviour, and on brain concentrations of catecholamines, somatostatin, neuropeptide Y, and corticotropin releasing hormone in the rat. 257 45

Rats were kindled by intraperitoneal injection of pentylenetetrazol (PTZ) (30 mg/Kg) every 48 h. Once kindled, some of the animals received a single injection of cysteamine (200 mg/Kg). Somatostatin-like immunoreactivity (SLI) and 125 I-Tyr11-somatostatin binding were measured in the frontoparietal cortex and hippocampus of the two experimental groups and the control rats. After PTZ kindling the following was observed: 1) SLI content was increased in the two areas; 2) Somatostatin receptor affinity decreased in the frontoparietal cortex and was unaltered in the hippocampus; 3) The number of somatostatin receptors decreased in the hippocampus and was unaltered in the frontoparietal cortex. Cysteamine, an agent which depletes brain somatostatin and suppresses kindled seizures in PTZ-treated rats, reversed the altered SLI levels and binding in these rats.
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PMID:Cysteamine normalizes cerebral somatostatin level and binding in pentylenetetrazol-kindled rats. 257 2

The effects of cysteamine-induced reductions of somatostatin-like immunoreactivity (SLI) on spatial learning, passive avoidance, and locomotor activity were examined in adult Sprague-Dawley rats. Cysteamine hydrochloride (100 mg/kg, s.c.) produced 54% and 50% reductions in SLI in cortex and hippocampus, respectively, and impaired escape latencies and spatial probe behavior in the Morris water task. Although cysteamine-treated rats displayed hypoactivity in the activity boxes, their swim speed in the Morris water task was unaffected. Cysteamine did not impair passive avoidance retention when administered immediately following training or prior to daily retention testing. These results suggest a role for somatostatin in spatially-mediated behaviors in rats.
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PMID:Morris water task impairment and hypoactivity following cysteamine-induced reductions of somatostatin-like immunoreactivity. 259 42

To determine if the putative amino acid transmitter taurine could affect the release of somatostatin (SRIF) from median eminence fragments, median eminences were incubated in vitro in the presence of various concentrations of taurine and its precursors, hypotaurine, cysteamine, cysteic acid, and L-cysteine sulfinic acid. Taurine was effective in releasing SRIF at doses of 50 microM and higher. Surprisingly, cysteic acid was the most potent stimulant of SRIF release, with a minimal effective dose of 0.1 microM. Cysteamine was effective at a dose of 50 microM, hypotaurine was effective only at 200 microM, and cysteine sulfinic acid was ineffective in stimulating SRIF release at any of the doses tested. To determine if the effect of taurine was mediated by the dopaminergic system, the dopamine receptor blocker pimozide (1 microM) was added to the medium containing either taurine or cysteic acid. Pimozide did not prevent the stimulatory effect of the amino acids. In conclusion, these investigations suggest that taurine and related amino acids may be involved in SRIF release by a nondopaminergic pathway. In view of the high concentrations of taurine in the hypothalamus it must be considered a putative transmitter releasing SRIF.
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PMID:Stimulation of somatostatin release from median eminence tissue incubated in vitro by taurine and related amino acids. 285 39

Cysteamine (CSH) and its close derivatives deplete immunoreactive somatostatin (SS) in rat organs. The effect of CSH is dose and time dependent and reversible. Structural requirements of the analogs are the presence of either -SH or -NH2 on a two- or three-carbon alkyl molecule; both radicals together increase, whereas insertion of carboxyl abolishes potency. The duodenal ulcerogenic potency of CSH derivatives is correlated significantly with their SS-depleting activity in the gastric mucosa. The mechanism of this action of CSH is poorly understood, but it is not caused by increased release, enhanced degradation of the peptide, or selective necrosis of SS cells. It is likely that in the intracellular environment CSH causes a conformational change in the peptide that affects the antigenic and functional properties of SS.
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PMID:Somatostatin depletion by cysteamine: mechanism and implication for duodenal ulceration. 286 15

Cysteamine (2-aminoethanethiol [CSH], given in vivo or in vitro, rapidly but reversibly depletes immunoreactive somatostatin (irSS) in the central nervous system and gut as well as biological and immunological prolactin (PRL) activity in both the anterior pituitary and blood of the rat. This depletion of irSS and PRL is dose dependent and cannot be accounted for by release of either compound. Basal and potassium-stimulated SS release is reduced from hypothalamic tissue in vitro in CSH-treated animals. PRL secretion induced both pharmacologically and physiologically is abolished after CSH administration. Furthermore, CSH reduces cellular PRL content in a number of hyperprolactinemic states. The mechanism by which CSH reduces PRL levels is not clear, but it does not appear to act through the dopamine receptor nor does it alter the morphological structure of the lactotrope in normal animals. Most likely, CSH acts by interacting with the disulfide bonds of PRL, thus rendering the molecule both immunologically and biologically inactive.
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PMID:Cysteamine-induced depletion of somatostatin and prolactin. 286 16

We have studied the effects by cysteamine in vitro and in vivo on hormone production and islet cell metabolism in isolated pancreatic islets and perfused pancreas of the rat. In isolated islets, cysteamine dose-dependently depleted somatostatin immunoreactivity by 50% after 60 min exposure to 1 mmol/l of the compound. This effect appeared to be independent of interaction of the drug with secretion of somatostatin from the pancreatic D-cells. Cysteamine, however, interacted acutely not only with the D-cells, but also markedly suppressed glucose-induced insulin release. Moreover, cysteamine inhibited islet glucose oxidation, an effect which reflects interference with the metabolism mainly of the B-cells. The effect of cysteamine on glucose-induced insulin release was prolonged, since it was still observed in the isolated rat pancreas perfused 24 h after in vivo treatment with cysteamine. In contrast to the effects on glucose-induced insulin release, the response to glibenclamide remained unaffected by a previous exposure to cysteamine in vivo. However, both glucose- and glibenclamide-induced somatostatin secretion was reduced by 50%, whereas basal glucagon secretion was significantly enhanced in pancreata from cysteamine-treated rats vs. control rats. We conclude that (1) cysteamine does not specifically affect the D-cells of the islets, and (2) the multiple effects by cysteamine on islet cell function, particularly on B-cell metabolism and secretion, renders the compound unsuitable for the study of paracrine interactions in the islets.
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PMID:Cysteamine exerts multiple effects on the endocrine cells of the rat pancreas. 286 20


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