title: A role for Ca2+ stores in kainate receptor-dependent synaptic facilitation and LTP at mossy fiber synapses in the hippocampus.
abstract: Compared with NMDA receptor-dependent LTP, much less is known about the mechanism of induction of NMDA receptor-independent LTP; the most extensively studied form of which is mossy fiber LTP in the hippocampus. In the present study we show that Ca2+-induced Ca2+ release from intracellular stores is involved in the induction of mossy fiber LTP. This release also contributes to the kainate receptor-dependent component of the pronounced synaptic facilitation that occurs during high-frequency stimulation. We also present evidence that the trigger for this Ca2+ release is Ca2+ permeation through kainate receptors. However, these novel synaptic mechanisms can be bypassed when the Ca2+ concentration is raised (from 2 to 4 mM), via a compensatory involvement of L-type Ca2+ channels. These findings suggest that presynaptic kainate receptors at mossy fiber synapses can initiate a cascade involving Ca2+ release from intracellular stores that is important in both short-term and long-term plasticity.
authors.affiliation: MRC Centre for Synaptic Plasticity, Department of Anatomy, School of Medical Sciences, University of Bristol, Bristol BS8 1TD, United Kingdom.
authors.forename: Sari E
authors.initials: SE
authors.lastname: Lauri
authors.forename: Zuner A
authors.initials: ZA
authors.lastname: Bortolotto
authors.forename: Robert
authors.initials: R
authors.lastname: Nistico
authors.forename: David
authors.initials: D
authors.lastname: Bleakman
authors.forename: Paul L
authors.initials: PL
authors.lastname: Ornstein
authors.forename: David
authors.initials: D
authors.lastname: Lodge
authors.forename: John T R
authors.initials: JT
authors.lastname: Isaac
authors.forename: Graham L
authors.initials: GL
authors.lastname: Collingridge
mesh_terms: D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn; D001180:Arthropod Venoms / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D004347:Drug Interactions; D004558:Electric Stimulation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D005110:Extracellular Space; D066298:In Vitro Techniques; D007546:Isoquinolines / Q000494:pharmacology; D007608:Kainic Acid / Q000494:pharmacology; D017774:Long-Term Potentiation / Q000187:drug effects / Q000502:physiology*; D008274:Magnesium / Q000378:metabolism; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D019599:Mossy Fibers, Hippocampal / Q000187:drug effects / Q000502:physiology*; D009543:Nifedipine / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D051381:Rats; D018092:Kainic Acid Receptors / Q000037:antagonists & inhibitors / Q000187:drug effects / Q000378:metabolism*; D012433:Ryanodine / Q000494:pharmacology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D019284:Thapsigargin / Q000494:pharmacology
chemical_list: D015763:2-Amino-5-phosphonovalerate; D001180:Arthropod Venoms; D002118:Calcium; D002121:Calcium Channel Blockers; D004791:Enzyme Inhibitors; D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D007546:Isoquinolines; D007608:Kainic Acid; D008274:Magnesium; D009543:Nifedipine; D018092:Kainic Acid Receptors; D012433:Ryanodine; D019284:Thapsigargin; C400802:LY382884