Kinetics of acetylcholine-activated cation channel blockade by the calcium antagonist D-600 in Aplysia neurons

The effects of the calcium channel blocker D-600 on the cation channels activated by acetylcholine (ACh) was studied in voltage-clamped Aplysia neurons by voltage-jump relaxation analysis. D-600 blocked the steady-state ACh current in a highly voltage-dependent manner, the degree of antagonism incre...

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Bibliographic Details
Published in:Cellular and molecular neurobiology 1983-12, Vol.3 (4), p.329-344
Main Authors: TRAVERSE SLATER, N, HAAS, H. L, CARPENTER, D. O
Format: Article
Language:English
Subjects:
acetylcholine
Acetylcholine - pharmacology
Animals
Aplysia
Biological and medical sciences
calcium
Calcium - metabolism
cations
channels
Dose-Response Relationship, Drug
Fundamental and applied biological sciences. Psychology
Gallopamil - pharmacology
Ganglia - drug effects
inhibitors
Ion Channels - drug effects
Isolated neuron and nerve. Neuroglia
Kinetics
Membrane Potentials - drug effects
neurons
Neurons - drug effects
neurotransmitters
Receptors, Cholinergic - drug effects
Synaptic Transmission - drug effects
Verapamil - pharmacology
Vertebrates: nervous system and sense organs
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Summary:The effects of the calcium channel blocker D-600 on the cation channels activated by acetylcholine (ACh) was studied in voltage-clamped Aplysia neurons by voltage-jump relaxation analysis. D-600 blocked the steady-state ACh current in a highly voltage-dependent manner, the degree of antagonism increasing with membrane hyperpolarization. In the presence of D-600 the current relaxations following hyperpolarizing command steps became biphasic. The time constants of ACh-induced current relaxations (tau f), which approximate the mean channel lifetime, were reduced in a voltage-dependent manner, the degree of reduction of tau f increasing with increasing membrane potential. In addition to the acceleration of tau f, a slow, inverse kinetic component (tau s) of the relaxation appeared in the presence of D-600. The rate of this inverse kinetic component was accelerated either by increasing the agonist or antagonist dose or by increasing the membrane potential. These results suggest that D-600 acts to antagonize the acetylcholine response through a blockade of the open state of the transmitter-activated cation channel. Possible kinetic schemes for this interaction are discussed.
ISSN:0272-4340
1573-6830
DOI:10.1007/BF00734714