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Facilitation of Acetylcholine Secretion in Mouse Motor Synapses Caused by Calcium Release from Depots upon Activation of L-Type Calcium Channels

  • Physiology
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Bulletin of Experimental Biology and Medicine Aims and scope

Pharmacological disinhibition of L-type Ca2+ channels by two ways (with agonist S(-) BAY K 8644 and iberiotoxin, a Ca2+-activated BK-type K+-channel blocker) increases quantal content of evoked end-plate potentials, which was completely prevented by ryanodine (2 μM) blockade of ryanodine receptors. We conclude that increased quantal secretion of the transmitter induced by L-type Ca2+ channel functioning requires activation of ryanodine receptors and calcium release from depots in motor terminals in mice.

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Authors and Affiliations

  1. Department of Human and Animal Physiology, Biological Faculty, M. V. Lomonosov Moscow State University, Moscow, Russia

    A. E. Gaydukov, S. N. Melnikova & O. P. Balezina

Authors
  1. A. E. Gaydukov
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  2. S. N. Melnikova
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  3. O. P. Balezina
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Correspondence to A. E. Gaydukov.

Additional information

Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 148, No. 8, pp. 124-128, August, 2009

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Gaydukov, A.E., Melnikova, S.N. & Balezina, O.P. Facilitation of Acetylcholine Secretion in Mouse Motor Synapses Caused by Calcium Release from Depots upon Activation of L-Type Calcium Channels. Bull Exp Biol Med 148, 163–166 (2009). https://doi.org/10.1007/s10517-009-0678-9

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  • DOI: https://doi.org/10.1007/s10517-009-0678-9

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