Calcium Currents Recorded from a Vertebrate Presynaptic Nerve Terminal are Resistant to the Dihydropyridine Nifedipine

The influx of Ca ions into the presynaptic nerve terminal through ion channels is a key link between the action potential and the release of chemical transmitters. It is not clear, however, which types of Ca channel are involved in neurosecretion at vertebrate synapses. In particular, there is disag...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 1990-12, Vol.87 (24), p.9683-9687
Main Authors: Stanley, Elis F., Atrakchi, Aisar H.
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Calcium Channel Blockers - pharmacology
Calcium Channels - drug effects
Calcium Channels - physiology
Calyx
Central nervous system
Chick Embryo
chick embryos
Dihydropyridines
Electric current
Electric potential
Electrophysiology
Fundamental and applied biological sciences. Psychology
Ganglia
Ganglia, Parasympathetic - drug effects
Ganglia, Parasympathetic - physiology
In Vitro Techniques
Kinetics
membrane currents
Nerves
Neurons
Neurons - drug effects
Neurons - physiology
nifedipine
Nifedipine - pharmacology
Oculomotor Nerve - physiology
omega-Conotoxin GVIA
Peptides, Cyclic - pharmacology
Pipettes
Synapses
Synapses - drug effects
Synapses - physiology
Synaptic transmission
Synaptic Transmission - drug effects
Vertebrates: nervous system and sense organs
Citations: Items that cite this one
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Summary:The influx of Ca ions into the presynaptic nerve terminal through ion channels is a key link between the action potential and the release of chemical transmitters. It is not clear, however, which types of Ca channel are involved in neurosecretion at vertebrate synapses. In particular, there is disagreement as to whether these channels are sensitive to dihydropyridine blockers, characteristic of L-type Ca channels. We have used the chicken ciliary ganglion calyx synapse to test the effect of the dihydropyridine nifedipine on Ca current recorded directly from a cholinergic presynaptic nerve terminal. We used a control neuron to define the experimental conditions under which L-type Ca channels are blocked by 10 μM nifedipine. We then tested the effect of the dihydropyridine on Ca currents recorded from the presynaptic terminal using the same conditions. Nifedipine did not reduce the calyx Ca current nor did it block chemical transmission through the ganglion. The lack of effect of the dihydropyridine was not due to restricted access since ω-conotoxin GVIA, a peptide toxin that blocks transmission at this synapse, rapidly blocked the calyx Ca current. Thus, the predominant Ca channel in this presynaptic nerve terminal is not dihydropyridine sensitive and, hence, cannot be characterized as L-type.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.87.24.9683