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)

In rats, on the 25th day after the start of a thiamine-deficient (TD) diet, impairment of avoidance learning was significantly induced in proportion to the decrease somatostatin (SST) fluorescence intensity in the cortex, amygdala, thalamus, hypothalamus, and hippocampus, including the CA1, CA2, and dentate gyrus (DG). Only a single injection of thiamine HCl (0.5 mg/rat, subcutaneous) on the 14th day after the start of a TD diet improved the amnesia to the level of the pair-fed control and prevented the decrease in the SST level. Whereas these reversal effects of thiamine treatment were not found when the treatment was given on the 21st day after the start of a TD diet. These results indicate that, after a certain degree of thiamine deficiency, TD-induced behavioral effects might be reversible, but some neuronal fibers might be irreversibly damaged, probably due to the reduction of thiamine-dependent enzymes in brain mitochondria. The results also suggest the possibility that SST in the brain may be closely related to the avoidance learning impairment induced by TD.
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PMID:Immunohistochemical estimation of rat brain somatostatin on avoidance learning impairment induced by thiamine deficiency. 1065 80

We produced thiamine deficiency by treating mice with a thiamine deficient (TD) diet, but not with pyrithiamine, a thiamine antagonist. Twenty days after TD feeding, a significant antinociceptive effect was observed in the formalin test. A single injection of thiamine HCl (50 mg/kg, s.c.) on the 19th day after TD feeding (on the late TD stage) failed to reverse the antinociceptive effect, the muricide effect, and impairment of avoidance learning induced by TD feeding, as compared to pair-fed controls. These results indicate the possibility that the TD-induced antinociceptive effect may result from irreversible changes in the spinal and/or brain neurons. To clarify the involvement of substance P (SP) and somatostatin (SST) systems in the spinal cord, we examined the effect of intrathecal (i.t.) injections of these agonists on TD feeding-inducd elevation of pain threshold. I.t. injection of SP and SST elicited a behavioral response consisting of reciprocal hindlimb scratching, biting and/or licking of hindpaws. There was no significant difference in the behavioral response to SP between TD mice and PF mice on the 5th day after feeding. However, on the 10th and 20th day after TD feeding the response to SP was significantly increased compared with PF mice. This phenomenon was also observed with SST on the 20th day after TD feeding. These results indicate the possibility that TD feeding may produce an increased behavioral response to SP and SST through an enhanced sensitivity of neurokinin-1 and SST receptors in the spinal cord. Taken together, the antinociceptive effect following TD feeding may result from a decrease in spinal SP and SST contents.
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PMID:Antinociceptive effect following dietary-induced thiamine deficiency in mice: involvement of substance P and somatostatin. 1150 48