ReviewMetabolic brain disease2000
Reconstitution of mediatophore-supported quantal acetylcholine release.
Review in Metabolic brain disease, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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0 citing papers in PubMed, 4 citations in OpenAlex.
No citing paper in PubMed yet.
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synaptic transmission of a nerve impulse is an extremely rapid event relying on transfer of brief chemical impulses from one cell to another. This transmission is dependent upon Ca2+ and known to be quantal, which led to the widely accepted vesicular hypothesis of neurotransmitter release. However, at least in the case of rapid synaptic transmission the hypothesis has been found difficult to reconcile with a number of observations. In this article, we shall review data from experiments dealing with reconstitution of quantal and Ca2+-dependent acetylcholine release in: i) proteoliposomes, ii) Xenopus oocytes, and iii) release-deficient cell lines. In these three experimental models, release is dependent on the expression of the mediatophore, a protein isolated from the plasma membrane of cholinergic nerve terminals of the Torpedo electric organ. We shall discuss the role of mediatophore in quantal acetylcholine release, its possible involvement in morphological changes affecting presynaptic membrane during the release, and its interactions with others proteins of the cholinergic nerve terminal.
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