ATP-sensitive potassium channels mediate the effects of a peripheral injection of glucose on memory storage in an inhibitory avoidance task.

A peripheral injection of glucose has been found to improve memory in rats, but the underlying mechanisms are unknown. One possible mechanism by which peripheral glucose might act on memory storage is by regulating ATP-sensitive potassium (K-ATP) channels. The present study investigated the effects of K-ATP channel modulators (minoxidil, a K-ATP channel opener and glibenclamide, a K-ATP channel closer) on memory enhancement induced by peripheral injection of glucose in an inhibitory avoidance task. Rats were trained in a one trial inhibitory avoidance task (50 Hz, 1 mA, 3 s footshock), and minoxidil (12.5,25 or 50 mg/kg) or glibenclamide (2.5,5,10 or 20 mg/kg) was injected interaperitoneally (I.P) 30 min before training. Immediately after training the rats were injected with glucose (100 mg/kg, I.P). Retention was tested 2 days later. The results indicate that systemic post-training injection of glucose improved memory storage and this effect was attenuated and enhanced by pretreatment of minoxidil and glibenclamide, respectively. The drug minoxidil or glibenclamide alone did not significantly affect memory storage. This shows that K-ATP channels mediate the memory improving effects of systemic glucose.