Single Presynaptic Neurone mediates a Two Component Postsynaptic Inhibition

A TWO component postsynaptic inhibition recorded from a group of identifiable neurones of the pleural ganglia of Aplysia has been recently described. It is composed of a rapidly decaying, chloride dependent component, and a more slowly decaying, potassium dependent component 1,2 . An ionophoretic in...

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Bibliographic Details
Published in:Nature (London) 1969-03, Vol.221 (5183), p.866-868
Main Author: KEHOE, JACSUE
Format: Article
Language:English
Subjects:
Action Potentials
Animals
Humanities and Social Sciences
letter
Membrane Potentials
Mollusca
multidisciplinary
Neurons - physiology
Neurotransmitter Agents - physiology
Receptors, Drug
Science
Science (multidisciplinary)
Synapses - physiology
Synaptic Transmission
Tetraethylammonium Compounds - pharmacology
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Summary:A TWO component postsynaptic inhibition recorded from a group of identifiable neurones of the pleural ganglia of Aplysia has been recently described. It is composed of a rapidly decaying, chloride dependent component, and a more slowly decaying, potassium dependent component 1,2 . An ionophoretic injection of acetylcholine (ACh) onto cells showing this two component inhibition produces a response which also has two components. As with the synaptic potential, the initial, more rapid phase is chloride dependent and the delayed, more slowly decaying phase is potassium dependent 1 . That ACh is the transmitter responsible for both phases of the synaptic inhibition was further indicated by the fact that the chloride dependent component of both the synaptic and ACh potentials was completely blocked by d -tubocurarine or strychnine 1,2 , whereas the potassium dependent component—unaffected by these drugs—was selectively suppressed by the addition of tetra-ethyl-ammonium chloride (TEA-Cl) to the external medium 2 . These data suggest that the two component inhibition is caused by a single transmitter (ACh) acting on two pharmacologically distinct receptors and triggering two different permeability changes in the postsynaptic cells.
ISSN:0028-0836
1476-4687
DOI:10.1038/221866a0