ArticleNeurochemical research1987
Depolarization of brain synaptosomes activates opposing factors involved in regulating levels of cytoskeletal actin.
Article in Neurochemical research, 1987. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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1 citing paper in PubMed, 12 citations in OpenAlex.
- Mechanisms in the regulation of neurotransmitter release from brain nerve terminals: current hypotheses.Neurochemical research · 1993Review
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2 authors at 1 institution in 1 country.
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Abstract
Depolarization of mouse brain synaptosomes elicits transmitter release and modifies factors that regulate cytoskeletal actin (C-actin) levels. We previously reported (Bernstein and Bamburg, J. Neurosci. 1985. 5:2565-2569) that depolarization causes a release of about 25% of the actin associated with the cytoskeleton of synaptosomal lysates. From our current studies we conclude that depolarization only transiently perturbs the balance in opposing factors which regulate C-actin levels in lysates. Prolonged incubation of the lysates permits the actin to reequilibrate so that no difference between C-actin levels of resting and depolarized synaptosomes is observed. Both the initial transient release of actin from the cytoskeleton and its reassociation with the cytoskeleton during prolonged incubation are calcium dependent and involve factors in both the cytoskeletal and soluble fractions. Depolarization initiates modifications that both increase and decrease the C-actin level probably through mechanisms involving calcium sensitive actin binding proteins.
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