abstract
- The effect of the adenosine triphosphate (ATP)-sensitive potassium (KATP) channel blocker, glibenclamide, on adenosine-induced postsynaptic hyperpolarization was studied by means of intracellular recording techniques in TTX-treated CA1 neurones in the rat hippocampal slice. Glibenclamide applied in the CSF perfusion fluid at 30 microM reversibly depressed the 2-chloroadenosine-induced hyperpolarization and the increase in the membrane conductance. It is suggested that adenosine induces the opening of potassium channels in the postsynaptic membrane of CA1 neurones, including KATP channels in the mammalian central nervous system (CNS).