INSERM U862 NeuroCentre Magendie, Endocannabinoids and Neuroadaptation, Bordeaux, France.
Nat Neurosci. 2010 Feb;13(2):197-204. doi: 10.1038/nn.2481. Epub 2010 Jan 17.
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.
谷氨酸可以通过激活突触前 kainate 受体来控制抑制性突触传递。我们发现，通过 Schaffer 侧支的串刺激释放的谷氨酸可以导致 CA1 锥体神经元的抑制性突触传递产生短期抑制或短期易化，这取决于 GABA 能传入上是否存在大麻素 1 型（CB1）受体。这种由串刺激引起的抑制性易化（t-Di）需要通过突触后代谢型谷氨酸受体的激活和 [Ca(2+)]的上升来动员 2-花生四烯酸甘油。GluK1（GluR5）依赖性 GABA 能末梢去极化通过促进突触前 CB1 信号来实现 t-Di。因此，协同激活突触前 CB1 受体和 kainate 受体介导了抑制性突触传递的短期抑制。相比之下，在表达 GluK1 但不表达 CB1 受体的抑制性连接中，Schaffer 侧支的串刺激会导致短期易化。因此，突触释放的谷氨酸激活 kainate 受体，从而控制突触前 CB1 信号的传递，进而控制短期异突触可塑性的方向。
