The contribution of intracellular calcium stores to mEPSCs recorded in layer II neurones of rat barrel cortex
Loading slices of rat barrel cortex with 50 μ m 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 Ca 2+ stores with 20 μ m cyclopiazonic acid...
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Veröffentlicht in: | The Journal of physiology 2002-12, Vol.545 (2), p.521-535 |
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Sprache: | eng |
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Zusammenfassung: | Loading slices of rat barrel cortex with 50 μ m 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 Ca 2+ stores with 20 μ m cyclopiazonic acid (CPA), a SERCA pump inhibitor, in conjunction with neuronal depolarisation to activate Ca 2+ stores, results in a similar reduction of mEPSCs to that observed with BAPTA-AM, indicating that the source for intracellular
Ca 2+ is the endoplasmic reticulum. Block or activation of ryanodine receptors by 20 μ m ryanodine or 10 m m caffeine, respectively, shows that a significant proportion of mEPSCs are caused by Ca 2+ release from ryanodine stores. Blocking IP 3 receptors with 14 μ m 2-aminoethoxydiphenylborane (2APB) also reduces the frequency and amplitude of mEPSCs, indicating the involvement of IP 3 stores in the generation of mEPSCs. Activation of group I metabotropic receptors with 20 μ m ( RS) -3,5-dihydroxyphenylglycine (DHPG) results in a significant increase in the frequency of mEPSCs, further supporting the role
of IP 3 receptors and indicating a role of group I metabotropic receptors in causing transmitter release. Statistical evidence is
presented for Ca 2+ -induced Ca 2+ release (CICR) from ryanodine stores after the spontaneous opening of IP 3 stores. |
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ISSN: | 0022-3751 1469-7793 |
DOI: | 10.1113/jphysiol.2002.022103 |