2-Deoxyglucose (2-DG) uptake is an index of regional glucose utilization which reflects predominantly activity in the axonal terminal of neuronal pathways. The present experiments showed that somatostatin elevated 2-DG uptake in rat cortex and hippocampus slices. Treatment with somatostatin-14 and somatostatin-28 markedly enhanced 2-DG uptake, whereas the amino-terminal fragment of somatostatin-28 did so only slightly. This effect appearef to the mediated by an interaction with somatostatin receptors because cyclo-somatostatin, a somatostatin antagonist, abolished the effect of somatostatin-14. The increase in 2-DG uptake caused by somatostatin-14 was blocked by the calcium channel antagonist, nifedipine, but not by tetrodotoxin, suggesting that the action of somatostatin does not require the initiation of impulse activity. somatostatin enhaced the KCl-induced release of acetylcholine, suggeting that a cholingic mechanism is involved in teh somatostatin-induced cellular responses. We therefore examined whether acetylcholine receptor antagonists block the somatostatin-induced increase in 2-DG uptake. Neither muscarinic nor nicotinic receptor antagonists affected the somatostatin-14-induced response. The present results suggest that somatostatin has a stiomulatory effecton energy metabolism and that this effect is independent of acetylcholine receptor mechanism.
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