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Specific changes of somatostatin mRNA expression in the frontal cortex and hippocampus of diabetic rats
Author(s) -
XiaoMing Zhang,
Xi Zhu,
Fang Shen,
Jilin Zhou
Publication year - 2004
Publication title -
journal of anatomy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 118
eISSN - 1469-7580
pISSN - 0021-8782
DOI - 10.1111/j.0021-8782.2004.00273.x
Subject(s) - streptozotocin , endocrinology , medicine , hippocampus , diabetes mellitus , somatostatin , in situ hybridization , biology , messenger rna , biochemistry , gene
Most current studies of diabetic encephalopathy have focused on brain blood flow and metabolism, but there has been little research on the influence of diabetes on brain tissue and the causes of chronic diabetic encephalopathy. The technique of molecular biology makes it possible to explore the mechanism of chronic diabetic encephalopathy by testing the distribution of somatostatin in the brain. We have therefore analysed, by in situ hybridization histochemistry, the changes in somatostatin (SST) mRNA in the frontal cortex and hippocampus of rats made diabetic by the injection of streptozotocin. Ten Sprague–Dawley control rats were compared with ten streptozotocin‐induced diabetic rats. The weight, blood glucose and urine glucose did not differ between the two groups before the injection of streptozotocin. Four weeks after the injection of streptozotocin the weight, blood glucose and urine glucose of the diabetic rats were, respectively, 199.1 ± 15.6 g, 23.7 ± 3.25 mmol L −1 and (++) to (+++) whereas those of the control group were 265.5 ± 30.3 g, 4.84 ± 0.63 mmol L −1 and (–). Somatostatin mRNA was reduced in the diabetic rats. The number of SST mRNA‐positive neurons and the optical density of positive cells in the hippocampus and frontal cortex of the diabetic rats were 80.6 ± 17.5 mm −2 and 76.5 ± 17.6 compared with 150.5 ± 21.1 mm −2 and 115.1 ± 18.5 in the control rats. The induction of diabetes is thus associated with a decreased expression of SST mRNA in the hippocampus and frontal cortex, which might be an important component of chronic diabetic encephalopathy.