The Blockade of K+-ATP Channels has Neuroprotective Effects in an In Vitro Model of Brain Ischemia

Robert Nisticò, Silvia Piccirilli, L. Sebastianelli, Giuseppe Nisticò, G. Bernardi, N. B. Mercuri

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)383-395
Number of pages13
JournalInternational Review of Neurobiology
Publication statusPublished - 2007

ASJC Scopus subject areas

  • Neuroscience(all)
  • Neuropsychology and Physiological Psychology
  • Physiology


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