Brain extract induces the tetrodotoxin-sensitive action potentials in a rat skeletal muscle cell line (L6)

Yamazaki, Suteo; Satoh, Teikichi; Kano, Masaakira

doi:10.1016/0165-3806(84)90159-7

Cited by 5 publications

(2 citation statements)

References 18 publications

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“…39,46 During differentiation, morphological changes are accompanied by electrical changes; the capability to generate action potentials develops only after fusion into electrically coupled myotubes, and the Na + channel activity underlying the action potential upstroke is tetrodotoxin (TTX)-resistant. 24 Moreover, L6 myotubes are sensitive to neural influences, as exposure to brain extracts induces TTXsensitive action potentials 47 and acetylcholine receptor clustering. 32 The results presented here show that L6 myotubes develop a calcium-activated, apamin-sensitive potassium current not present in myoblasts and contain 10-fold higher levels of apamin binding sites.…”

Section: Discussionmentioning

confidence: 99%

Skeletal muscle and small-conductance calcium-activated potassium channels

et al. 1999

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Section: Discussionmentioning

confidence: 99%

Skeletal muscle and small-conductance calcium-activated potassium channels

et al. 1999

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“…Denervated skeletal muscle and muscle cells in culture without neurons are relatively resistant to blockade of action potentials by tetrodotoxin (TTX). Sensitivity to TTX is increased by spinal cord extract (Kuromi and Hasegawa, 1975;Kuromi et al, 1981) or brain extract (Yamazaki et al, 1984). However, coculture and innervation with retinal neurons does not produce a TTX-sensitive action potential (Suarez-Isla and Thompson, unpublished observations).…”

Section: Introductionmentioning

confidence: 99%

Retinal neurons lack an acetylcholine receptor aggregating factor

Rapoport

1988

Synapse

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Spinal cord neurons form stable synapses on muscle cells in culture, whereas retinal neurons, an inappropriate presynaptic partner for muscle cells, form synapses that are transient. We have hypothesized that a trophic influence of neurons on muscle is involved in the stabilization of synapses. Because other neural tissues that form stable synapses on muscle cells contain factors that aggregate acetylcholine receptors (AChR) into clusters on the surface of muscle cells, it may be that these aggregation factors are necessary for stabilization of neuron-muscle synapses. Therefore, we determined the AChR-aggregating activity of retinal neurons. The results showed that cocultures of retinal neurons and muscle cells and retinal-conditioned medium do not show increases in the number of AChR on muscle cells. Conversely, spinal cord-muscle cocultures and spinal cord-conditioned medium produce increases in the number of AChR clusters. These data, along with previous studies demonstrating that retinal neurons are unable to affect the electrical membrane properties of cultured muscle cells, whereas spinal cord neurons do elicit such changes, add support to the above hypothesis of a trophic influence of neurons in synapse stabilization.

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