title: Priming of long-term potentiation mediated by ryanodine receptor activation in rat hippocampal slices.
abstract: Administration of the Group 1 metabotropic glutamate receptor (mGluR) agonist (R,S)-3,5-dihydroxyphenylglycine (DHPG) facilitates ("primes") subsequent long-term potentiation (LTP) through a phospholipase C signaling cascade that may involve release of Ca2+ from the endoplasmic reticulum (ER). We investigated the intracellular calcium pathways involved in this priming effect, recording field potentials from area CA1 of rat hippocampal slices before and after high-frequency stimulation. The priming of LTP by DHPG was prevented by co-administration of cyclopiazonic acid, which depletes ER Ca2+ stores. The priming effect was also blocked by the ryanodine receptor (RYR) antagonist ryanodine (RYA, 100 microM). In contrast, a low dose of RYA (10 microM) which opens the RYR channel, by itself primed LTP. In addition to RYR activation, entry of extracellular calcium through store-operated channels appears necessary for priming, since diverse treatments known to impede store-operated channel activity completely blocked both RYA and DHPG priming effects. Thus, RYR activation plays a critical role in the priming of LTP by Group 1 mGluRs, and this effect is coupled to the entry of extracellular calcium, probably through store-operated calcium channels.
authors.affiliation: Department of Medical Physiology, Panum Institute, University of Copenhagen, Denmark; Department of Psychology, University of Otago, Otago, New Zealand. cmellentin@mfi.ku.dk
authors.forename: C
authors.initials: C
authors.lastname: Mellentin
authors.forename: H
authors.initials: H
authors.lastname: Jahnsen
authors.forename: W C
authors.initials: WC
authors.lastname: Abraham
mesh_terms: D000818:Animals; D001896:Boron Compounds / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004307:Dose-Response Relationship, Radiation; D004347:Drug Interactions; D004558:Electric Stimulation / Q000379:methods; D004791:Enzyme Inhibitors / Q000494:pharmacology; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D006624:Hippocampus / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D066298:In Vitro Techniques; D007211:Indoles / Q000494:pharmacology; D017774:Long-Term Potentiation / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D008297:Male; D008734:Methoxyhydroxyphenylglycol / Q000031:analogs & derivatives / Q000494:pharmacology; D009570:Nitriles; D018408:Patch-Clamp Techniques / Q000379:methods; D051381:Rats; D017207:Rats, Sprague-Dawley; D012433:Ryanodine / Q000494:pharmacology; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism*; D020032:Tyrphostins / Q000494:pharmacology
chemical_list: D001896:Boron Compounds; D004791:Enzyme Inhibitors; D018690:Excitatory Amino Acid Agonists; D007211:Indoles; D009570:Nitriles; D019837:Ryanodine Receptor Calcium Release Channel; D020032:Tyrphostins; D012433:Ryanodine; C001784:SF 6847; D008734:Methoxyhydroxyphenylglycol; C109986:2-aminoethoxydiphenyl borate; D002118:Calcium; C010117:3,4-dihydroxyphenylglycol; C000543:cyclopiazonic acid