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J Physiol Volume 545, Number 2, 521-535, December 1, 2002 DOI: 10.1113/jphysiol.2002.022103
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Journal of Physiology (2002), 545.2, pp. 521-535
© Copyright 2002 The Physiological Society
DOI: 10.1113/jphysiol.2002.022103

The contribution of intracellular calcium stores to mEPSCs recorded in layer II neurones of rat barrel cortex

Christopher R. L. Simkus and Christian Stricker

Institute of Neuroinformatics, University of Zürich and Federal Institute of Technology (ETH), Winterthurerstrasse 190, CH-8057 Zürich, Switzerland

Loading slices of rat barrel cortex with 50 µM BAPTA-AM while recording from pyramidal cells in layer II induces a marked reduction in both the frequency and amplitudes of mEPSCs. These changes are due to a presynaptic action. Blocking the refilling of Ca2+ stores with 20 µM cyclopiazonic acid (CPA), a SERCA pump inhibitor, in conjunction with neuronal depolarisation to activate Ca2+ stores, results in a similar reduction of mEPSCs to that observed with BAPTA-AM, indicating that the source for intracellular Ca2+ is the endoplasmic reticulum. Block or activation of ryanodine receptors by 20 µM ryanodine or 10 mM caffeine, respectively, shows that a significant proportion of mEPSCs are caused by Ca2+ release from ryanodine stores. Blocking IP3 receptors with 14 µM 2-aminoethoxydiphenylborane (2APB) also reduces the frequency and amplitude of mEPSCs, indicating the involvement of IP3 stores in the generation of mEPSCs. Activation of group I metabotropic receptors with 20 µM (RS)-3,5-dihydroxyphenylglycine (DHPG) results in a significant increase in the frequency of mEPSCs, further supporting the role of IP3 receptors and indicating a role of group I metabotropic receptors in causing transmitter release. Statistical evidence is presented for Ca2+-induced Ca2+ release (CICR) from ryanodine stores after the spontaneous opening of IP3 stores.



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