There is a common belief that the opening of K+-ATP channels during an ischemic episode has protective effects on neuronal functions by inducing a reduction in energy consumption. However, recent studies have also proposed that activation of these channels might have deleterious effects on cell's survival possibly after a stroke or during long-lasting neurodegenerative processes. Considering these contrasting results, we have used a hippocampal in vitro slice preparation in order to investigate the possible effects of K+-ATP channel blockers on the electrophysiological and morphological changes induced by a transient episode of ischemia (oxygen and glucose deprivation) on CA1 pyramidal neurons. Therefore, we found that tolbutamide and glibenclamide, both nonselective K+-ATP channel blockers, produce neuroprotective effects against in vitro ischemia. Interestingly, the mitochondrial K+-ATP channel blocker 5-hydroxydecanoate and various K+ channel blockers did not exert neuroprotection. Our results are consistent with the concept that a decreased activity of the plasmalemmal K+-ATP conductances may have a protective effect during episodes of transient cerebral ischemia.
ASJC Scopus subject areas
- Neuropsychology and Physiological Psychology