title: Synaptic activation of kainate receptors gates presynaptic CB(1) signaling at GABAergic synapses.
abstract: Glutamate can control inhibitory synaptic transmission through activation of presynaptic kainate receptors. We found that glutamate released by train stimulation of Schaffer collaterals could lead to either short-term depression or short-term facilitation of inhibitory synaptic transmission in mouse CA1 pyramidal neurons, depending on the presence of cannabinoid type 1 (CB(1)) receptors on GABAergic afferents. The train-induced depression of inhibition (t-Di) required the mobilization of 2-arachidonoylglycerol through postsynaptic activation of metabotropic glutamate receptors and [Ca(2+)] rise. GluK1 (GluR5)-dependent depolarization of GABAergic terminals enabled t-Di by facilitating presynaptic CB(1) signaling. Thus, concerted activation of presynaptic CB(1) receptors and kainate receptors mediates short-term depression of inhibitory synaptic transmission. In contrast, in inhibitory connections expressing GluK1, but not CB(1), receptors, train stimulation of Schaffer collaterals led to short-term facilitation. Thus, activation of kainate receptors by synaptically released glutamate gates presynaptic CB(1) signaling, which in turn controls the direction of short-term heterosynaptic plasticity.
authors.affiliation: INSERM U862 NeuroCentre Magendie, Endocannabinoids and Neuroadaptation, Bordeaux, France.
authors.forename: Joana
authors.initials: J
authors.lastname: Lourenço
authors.forename: Astrid
authors.initials: A
authors.lastname: Cannich
authors.forename: Mario
authors.initials: M
authors.lastname: Carta
authors.forename: Françoise
authors.initials: F
authors.lastname: Coussen
authors.forename: Christophe
authors.initials: C
authors.lastname: Mulle
authors.forename: Giovanni
authors.initials: G
authors.lastname: Marsicano
mesh_terms: D000818:Animals; D001095:Arachidonic Acids / Q000378:metabolism; D056547:CA1 Region, Hippocampal / Q000502:physiology; D002118:Calcium / Q000378:metabolism; D063388:Endocannabinoids; D018698:Glutamic Acid / Q000378:metabolism; D005989:Glycerides / Q000378:metabolism; D066298:In Vitro Techniques; D051379:Mice; D008822:Mice, Transgenic; D009433:Neural Inhibition / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology*; D017729:Presynaptic Terminals / Q000502:physiology*; D017966:Pyramidal Cells / Q000502:physiology; D043884:Receptor, Cannabinoid, CB1 / Q000235:genetics / Q000378:metabolism*; D018092:Kainic Acid Receptors / Q000235:genetics / Q000378:metabolism*; D018094:Receptors, Metabotropic Glutamate / Q000378:metabolism; D013569:Synapses / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology; D013997:Time Factors; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
chemical_list: D001095:Arachidonic Acids; D002118:Calcium; D063388:Endocannabinoids; D018698:Glutamic Acid; D005989:Glycerides; D043884:Receptor, Cannabinoid, CB1; D018092:Kainic Acid Receptors; D018094:Receptors, Metabotropic Glutamate; D005680:gamma-Aminobutyric Acid; C094503:glyceryl 2-arachidonate