ATP reduces voltage-activated K+ current in cultured rat hippocampal neurons.
Effects of extracellular ATP were investigated in cultured rat hippocampal neurons using whole-cell voltage-clamp techniques. When a depolarizing step to +10 mV was applied from a holding potential of -60 mV, an outward K+ current was activated. ATP (3 to 300 microM) reduced the K+ current. Among adenosine derivatives, ADP (100 microM) slightly inhibited the K+ current, and AMP or adenosine (100 microM) was ineffective. UTP was as potent as ATP and alpha,beta-methylene ATP was less effective than ATP. The inhibition by ATP of the K+ current was abolished by inclusion of 2 mM GDP beta S in the intracellular solution. The results indicate that ATP inhibits K+ channels in rat hippocampal neurons through UTP-responsive P2-purinoceptors coupled with GTP-binding proteins.
Nakazawa
K
K
Division of Pharmacology, National Institute of Health Sciences, Tokyo, Japan.
Inoue
K
K
Inoue
K
K
D000241:Adenosine / Q000031:analogs & derivatives / Q000494:pharmacology; D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000818:Animals; D002478:Cells, Cultured; D004594:Electrophysiology; D019204:GTP-Binding Proteins / Q000378:metabolism; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D018408:Patch-Clamp Techniques; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism*; D058919:Purinergic P2 Receptor Antagonists; D051381:Rats
D015221:Potassium Channels; D058919:Purinergic P2 Receptor Antagonists; D000255:Adenosine Triphosphate; D019204:GTP-Binding Proteins; D000241:Adenosine