title: Calcium current activated by potassium ions in voltage-clamped rat hippocampal pyramidal neurones.
abstract: 1. Neuronal activity results in local elevation of extracellular K+ concentration ([K+]o). 2. Using the patch-clamp technique in the whole-cell configuration, we investigated whether extracellular K+ activates non-voltage-operated Ca2+ channels in pyramidal cells cultured from rat embryonic hippocampi. 3. K+ (12 mM) reversibly activated a sustained inward current at a holding potential of -100 mV. Membrane conductance and variance of noise were significantly increased by K+. This current could be observed at membrane potentials negative to +60 mV. 4. Inhibitors of inward rectifier K+ channels and hyperpolarization-induced cation current reduced the current only at potentials negative to -50 mV. 5. The K+-induced current was activated in Na+-free but not in Ca2+-free medium, did not depend on cytosolic [Cl-], and was blocked by Cd2+ but not by organic channel inhibitors. 6. Half-maximal activation of the current (at -100 mV) was attained at [K+]o approximately 20 mM. 7. The current is similar to Igl, a K+-induced Ca2+ current described in glomerulosa cells. It was also present in pyramidal cells from prefrontal cortex but not in hippocampal bipolar and glial cells. 8. Activation of K+-induced Ca2+ current may elevate cytoplasmic [Ca2+] at [K+]o levels which are insufficent to activate voltage-dependent Ca2+ channels.
authors.affiliation: Department of Physiology and Laboratory of Cellular and Molecular Physiology, Semmelweis University of Medicine, Budapest, Hungary.
authors.forename: F
authors.initials: F
authors.lastname: Deák
authors.forename: G
authors.initials: G
authors.lastname: Nagy
authors.forename: P
authors.initials: P
authors.lastname: Várnai
authors.forename: E
authors.initials: E
authors.lastname: Madarász
authors.forename: A
authors.initials: A
authors.lastname: Spät
mesh_terms: D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000818:Animals; D017609:Barium Compounds / Q000494:pharmacology; D002104:Cadmium / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000502:physiology; D002478:Cells, Cultured; D002586:Cesium / Q000494:pharmacology; D002712:Chlorides / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005260:Female; D005333:Fetus / Q000166:cytology; D006624:Hippocampus / Q000737:chemistry / Q000166:cytology; D015640:Ion Channel Gating / Q000187:drug effects / Q000502:physiology; D009543:Nifedipine / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D010455:Peptides / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology*; D017397:Prefrontal Cortex / Q000737:chemistry / Q000166:cytology; D011247:Pregnancy; D017966:Pyramidal Cells / Q000737:chemistry* / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology; D020866:omega-Conotoxin GVIA
chemical_list: D017609:Barium Compounds; D002121:Calcium Channel Blockers; D015220:Calcium Channels; D002712:Chlorides; D018691:Excitatory Amino Acid Antagonists; D010455:Peptides; D002104:Cadmium; C024986:barium chloride; D002586:Cesium; D013779:Tetrodotoxin; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; D015763:2-Amino-5-phosphonovalerate; D020866:omega-Conotoxin GVIA; D012964:Sodium; C028019:cesium chloride; D009543:Nifedipine; D011188:Potassium; D002118:Calcium