Altered prevalence of gating modes in neurotransmitter inhibition of N-type calcium channels.
G protein-mediated inhibition of voltage-activated calcium channels by neurotransmitters has important consequences for the control of synaptic strength. Single-channel recordings of N-type calcium channels in frog sympathetic neurons reveal at least three distinct patterns of gating, designated low-Po, medium-Po, and high-Po modes according to their probability of being open (Po) at -10 millivolts. The high-Po mode is responsible for the bulk of divalent cation entry in the absence of neurotransmitter. Norepinephrine greatly decreased the prevalence of high-Po gating and increased the proportion of time a channel exhibited low-Po behavior or no activity at all, which thereby reduced the overall current. Directly observed patterns of transition between the various modes suggest that activated G protein alters the balance between modal behaviors that freely interconvert even in the absence of modulatory signaling.
Delcour
A H
AH
Department of Molecular and Cellular Physiology, Beckman Center, Stanford University Medical Center, CA 94305.
Tsien
R W
RW
D000818:Animals; D001001:Anura; D015220:Calcium Channels / Q000187:drug effects* / Q000502:physiology*; D002413:Cations, Divalent; D004558:Electric Stimulation; D004594:Electrophysiology; D019204:GTP-Binding Proteins / Q000502:physiology; D015640:Ion Channel Gating / Q000502:physiology*; D007700:Kinetics; D009474:Neurons / Q000502:physiology; D018377:Neurotransmitter Agents / Q000494:pharmacology*; D009638:Norepinephrine / Q000494:pharmacology; D013564:Sympathetic Nervous System / Q000166:cytology / Q000502:physiology; D013569:Synapses / Q000502:physiology
D015220:Calcium Channels; D002413:Cations, Divalent; D018377:Neurotransmitter Agents; D019204:GTP-Binding Proteins; D009638:Norepinephrine