| First Author | Lourenço J | Year | 2010 |
| Journal | Nat Neurosci | Volume | 13 |
| Issue | 2 | Pages | 197-204 |
| PubMed ID | 20081851 | Mgi Jnum | J:156676 |
| Mgi Id | MGI:4421220 | Doi | 10.1038/nn.2481 |
| Citation | Lourenco J, et al. (2010) Synaptic activation of kainate receptors gates presynaptic CB(1) signaling at GABAergic synapses. Nat Neurosci 13(2):197-204 |
| abstractText | 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. |
