Rodriguez-Sanchez M N, Colas B, Prieto J C, Arilla E
Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Alcalá de Henares, Madrid, Spain.
Brain Res. 1989 Aug 7;494(1):36-41. doi: 10.1016/0006-8993(89)90141-8.
The effects of severe insulin-induced hypoglycemia on somatostatin level and specific binding in the cerebral cortex and hippocampus were examined using 125I-Tyr11-somatostatin as a ligand. Severe insulin-induced hypoglycemia did not affect the level of somatostatin-like immunoreactivity in the brain areas studied. However, the number (but not the affinity) of specific somatostatin receptors was significantly decreased in membrane preparation from the hippocampus but not in the cerebral cortex at the onset of hypoglycemic coma (5-10 min). Administration of glucose at the onset of hypoglycemic coma brought about extensive recovery of hippocampal somatostatin receptor number. These results suggest that glucose modulates the somatostatin receptor in the rat hippocampus. The physiological significance of these findings remains to be clarified.
以125I-Tyr11-生长抑素为配体，研究了严重胰岛素诱导的低血糖对大脑皮质和海马中生长抑素水平及特异性结合的影响。严重胰岛素诱导的低血糖并未影响所研究脑区中生长抑素样免疫反应性的水平。然而，在低血糖昏迷发作时（5 - 10分钟），海马膜制剂中特异性生长抑素受体的数量（而非亲和力）显著减少，而大脑皮质中则未减少。在低血糖昏迷发作时给予葡萄糖可使海马生长抑素受体数量大量恢复。这些结果表明，葡萄糖可调节大鼠海马中的生长抑素受体。这些发现的生理意义仍有待阐明。
