title: The contribution of intracellular calcium stores to mEPSCs recorded in layer II neurones of rat barrel cortex.
abstract: Loading slices of rat barrel cortex with 50 microM 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 microM 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 microM ryanodine or 10 mM caffeine, respectively, shows that a significant proportion of mEPSCs are caused by Ca(2+) release from ryanodine stores. Blocking IP(3) receptors with 14 microM 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 microM (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.
authors.affiliation: Institute of Neuroinformatics, University of Zürich and Federal Institute of Technology (ETH), Winterthurerstrasse 190, CH-8057 Zürich, Switzerland.
authors.forename: Christopher R L
authors.initials: CR
authors.lastname: Simkus
authors.forename: Christian
authors.initials: C
authors.lastname: Stricker
mesh_terms: D000818:Animals; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000502:physiology*; D002120:Calcium Channel Agonists / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D000252:Calcium-Transporting ATPases / Q000037:antagonists & inhibitors / Q000378:metabolism; D000697:Central Nervous System Stimulants / Q000494:pharmacology; D002614:Chelating Agents / Q000494:pharmacology; D004533:Egtazic Acid / Q000031:analogs & derivatives*; D004594:Electrophysiology; D004721:Endoplasmic Reticulum / Q000187:drug effects / Q000378:metabolism; D019706:Excitatory Postsynaptic Potentials / Q000502:physiology*; D066298:In Vitro Techniques; D007293:Inosine Triphosphate / Q000494:pharmacology; D007478:Iontophoresis; D009474:Neurons / Q000502:physiology*; D018408:Patch-Clamp Techniques; D051381:Rats; D017208:Rats, Wistar; D017661:Receptors, Presynaptic / Q000187:drug effects; D019837:Ryanodine Receptor Calcium Release Channel / Q000187:drug effects / Q000378:metabolism; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D013003:Somatosensory Cortex / Q000166:cytology / Q000502:physiology*
chemical_list: D002120:Calcium Channel Agonists; D002121:Calcium Channel Blockers; D000697:Central Nervous System Stimulants; D002614:Chelating Agents; D017661:Receptors, Presynaptic; D019837:Ryanodine Receptor Calcium Release Channel; D007293:Inosine Triphosphate; D002110:Caffeine; D004533:Egtazic Acid; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D000252:Calcium-Transporting ATPases; C025603:1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid; D002118:Calcium