ion channels in neuronal injury under hypoxia. Am J Physiol Regul

the current study were to 1) examine the effects of hypoxia and acidosis on cultured cortical neurons and 2) explore the role of transporters and ion channels in hypoxic injury. Cell injury was measured in cultured neurons or hippocampal slices following hyp-oxia (1 % O2) or acidosis (medium pH 6.8) treatment. Inhibitors of transporters and ion channels were employed to investigate their roles in hypoxic injury. Our results showed that 1) neuronal damage was apparent at 5–7 days of hypoxia exposure, i.e., 36–41 % of total lactate dehydrogenase was released to medium and 2) acidosis alone did not lead to significant injury compared with nonacidic, normoxic controls. Pharmacological studies revealed 1) no significant difference in neuronal injury between controls (no inhibitor) and inhibition of Na-K-ATP pump, voltage-gated Na channel, ATP-sensitive K channel, or reverse mode of Na/Ca2 exchanger under hypoxia; however, 2) inhibition of NBCs with 500 M DIDS did not caus