Redox modulation of large conductance calcium-activated potassium channels in CA1 pyramidal neurons from adult rat hippocampus

• Published in: Neuroscience letters Vol. 286; no. 3; pp. 191 - 194
• Main Authors: Gong, Liang-Wei, Gao, Tian M, Huang, Hao, Tong, Zhenqing
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 09.06.2000; Elsevier
• Subjects: 5,5'-Dithio-bis(2-nitrobenzoic acid); Animals; Biological and medical sciences; Calcium - physiology; Central nervous system; Dithionitrobenzoic Acid - antagonists & inhibitors; Dithionitrobenzoic Acid - pharmacology; Dithiothreitol - pharmacology; Electric Conductivity; Electrophysiology; Fundamental and applied biological sciences. Psychology; glutathione disulfide; Glutathione Disulfide - pharmacology; Hippocampus; Hippocampus - cytology; Hippocampus - metabolism; K + channel; Male; Oxidants - antagonists & inhibitors; Oxidants - pharmacology; Oxidation; Oxidation-Reduction; Patch clamp; Patch-Clamp Techniques; Potassium Channels - drug effects; Potassium Channels - metabolism; Potassium Channels - physiology; Pyramidal Cells - metabolism; Rat; Rats; Rats, Wistar; Redox; Reducing Agents - pharmacology; Vertebrates: nervous system and sense organs; Redox; Patch clamp; Oxidation; Rat; Hippocampus; K + channel; Rodentia; Central nervous system; Electrophysiology; Patch clamp method; Ionic channel; Vertebrata; Mammalia; Redox couple; Pyramidal neuron; Potassium; Brain (vertebrata)
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/S0304-3940(00)01121-6

Redox regulation of BK Ca channels was studied in CA1 pyramidal neurons of adult rat hippocampus by using inside-out configuration of patch clamp. Intracellular application of oxidizing agent 5,5′-dithio-bis(2-nitrobenzoic acid) (DTNB) markedly increased activity of BK Ca channels and this stimulating action persisted even after washout. In contrast, the reducing agent dithiothreitol (DTT) had no apparent effects on channel activity but could reverse the pre-exposure of DTNB-induced enhancement. The increase in channel activity produced by DTNB was due to shortened closed time as well as prolonged open time. The effects exerted by another redox couple glutathione disulphide and its reducing form were similar as DTNB and DTT. The present results indicate that BK Ca channels in CA1 pyramidal neurons can be modulated by intracellular redox potential, and that augmentation of BK Ca channels by oxidative stress might contribute to the postischemic electrophysiological alterations of CA1 pyramidal neurons.