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)

To elucidate the mechanism by which carbamazepine lowers somatostatin concentration in cerebrospinal fluid of humans, the effect of carbamazepine on secretion of this peptide was studied in rat cerebral cell cultures. Concentrations of carbamazepine within the therapeutic range (4 x 10(-5) M) inhibited spontaneous release of somatostatin and blocked secretory responses to the epileptogen, picrotoxin, and to the cyclic cAMP stimulator forskolin. One of the proposed mechanisms of carbamazepine action is that it binds to adenosine receptors, but in this study, aminophylline, an adenosine antagonist, in a concentration as high as 2.4 x 10(-4) M, did not reverse carbamazepine effects. Carbamazepine suppression of picrotoxin, however, was overcome by exposure to veratridine, a sodium channel-active compound. This finding supports the hypothesis that carbamazepine acts by binding to sodium channels. Phenytoin, another anticonvulsant with many similar properties, also blocked picrotoxin-induced somatostatin release at a concentration of 10(-4) M, and its effects were also reversed by veratridine at a concentration of 10(-5) M. These findings clarify the mechanism by which carbamazepine and phenytoin act in epilepsy and trigeminal neuralgia.
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PMID:Carbamazepine and phenytoin inhibit somatostatin release from dispersed cerebral cells in culture. 168 80

The concentrations of central neuropeptides, somatostatin (SS) and substance-P (SP), were determined in the different brain regions of young-aged male rats after a long-term administration of anticonvulsants Qingyangshen (QYS), Diphenylhydantoin (DPH), and Carbamazepine (CBZ). The results were compared with Pentylenetetrazol (PTZ)-induced seizure model and normal saline-treated controls. No effects of QYS on the concentrations of SS and SP were found in the rats of four-week or eight-week group. Both of DPH and PTZ increased the SS levels in the midbrain of rats in four-week group. DPH, CBZ, and PTZ also increased the SP levels in the cerebral cortex, striatum, and brain stem of rats in eight-week group. Our present data indicated that the central neuropeptides SS and SP were involved in the processes of epilepsy and antiepilepsy. Since QYS did not influence the contents of SS and SP after a long-term administration, it suggested that the anticonvulsant mechanism of QYS may be different from those of DPH and CBZ, i.e. it may be not due to its effect on the central neuropeptide pathway.
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PMID:The investigation of antiepileptic action of qingyangshen (QYS)--effect of QYS on the concentrations of neuropeptides in rat brain. 171 32

Somatostatin and gamma-aminobutyric acid (GABA) concentrations were evaluated in the brain of kindled rats treated chronically with carbamazepine and valproic acid. Kindled seizures were almost completely blocked by treatment with carbamazepine, whereas the effect of valproic acid was partial, suppressing only generalized seizures. The duration of after-discharge in amygdala was suppressed by carbamazepine not by valproic acid. Carbamazepine induced a decrease in immunoreactive somatostatin concentration and an increase in GABA concentration in the temporal cortex of kindled rats. Valproic acid induced only an increase in GABA concentration. The results suggest that somatostatin may be associated with the suppression of focal seizure in amygdala and GABA may have a role in the suppression of generalized seizures.
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PMID:Effects of carbamazepine and valproic acid on brain immunoreactive somatostatin and gamma-aminobutyric acid in amygdaloid-kindled rats. 287 90