Reopening of Ca2+ channels in mouse cerebellar neurons at resting membrane potentials during recovery from inactivation.
Recordings of single-channel activity from cerebellar granule cells show that a component of Ca2+ entry flows through L-type Ca2+ channels that are closed at negative membrane potentials following a strong depolarization, but then open after a delay. The delayed openings can be explained if membrane depolarization drives Ca2+ channels into an inactivated state and some channels return to rest through the open state after repolarization. Whole-cell recordings show that the charge carried by Ca2+ during the tail increases as inactivation progresses, whereas the current during the voltage step decreases. Voltage-dependent inactivation may be a general mechanism in central neurons for enhancing Ca2+ entry by delaying it until after repolarization, when the driving force for ion entry is large. Modifying the rate and extent of inactivation would have large effects on Ca2+ entry through those channels that recover from inactivation by passing through the open state.
Slesinger
P A
PA
Department of Pharmacology, School of Medicine, University of California, San Francisco 94143-0450.
Lansman
J B
JB
D000818:Animals; D002120:Calcium Channel Agonists / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000378:metabolism*; D002531:Cerebellum / Q000166:cytology / Q000378:metabolism*; D004594:Electrophysiology; D008564:Membrane Potentials; D051379:Mice; D009474:Neurons / Q000378:metabolism* / Q000502:physiology; D009539:Nicotinic Acids / Q000494:pharmacology; D010069:Oxadiazoles; D013237:Stereoisomerism
D002120:Calcium Channel Agonists; D002121:Calcium Channel Blockers; D015220:Calcium Channels; D009539:Nicotinic Acids; D010069:Oxadiazoles; C049834:PN 202-791