Synaptic activation of kainate receptors gates presynaptic CB(1) signaling at GABAergic synapses.

Joana Lourenço, Astrid Cannich, Mario Carta, Françoise Coussen, Christophe Mulle, Giovanni Marsicano
Nat Neurosci. 2010-01-17; 13(2): 197-204
DOI: 10.1038/nn.2481

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1. Nat Neurosci. 2010 Feb;13(2):197-204. doi: 10.1038/nn.2481. Epub 2010 Jan 17.

Synaptic activation of kainate receptors gates presynaptic CB(1) signaling at
GABAergic synapses.

Lourenço J(1), Cannich A, Carta M, Coussen F, Mulle C, Marsicano G.

Author information:
(1)INSERM U862 NeuroCentre Magendie, Endocannabinoids and Neuroadaptation,
Bordeaux, France.

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.

DOI: 10.1038/nn.2481
PMID: 20081851 [Indexed for MEDLINE]


Auteurs Bordeaux Neurocampus