Regulation of the Hippocampal Network by VGLUT3-Positive CCK-GABAergic Basket Cells
Regulation of the Hippocampal Network by VGLUT3-Positive CCK-GABAergic Basket Cells
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DOI：
10.3389/fncel.2017.00140
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发表时间：
2017-05-16
影响因子：
5.3
通讯作者：
El Mestikawy, Salah
中科院分区：
文献类型：
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作者：
Fasano, Caroline;Rocchetti, Jill;El Mestikawy, Salah
海马中间神经元释放抑制性递质GABA来调节兴奋、节律产生和突触可塑性。GABA能篮状细胞的亚群共表达GABA/甘氨酸囊泡转运蛋白（VIAAT）和非典型III型囊泡谷氨酸转运蛋白（VGLUT 3）;因此，这些细胞具有用GABA和谷氨酸发出信号的能力。篮状细胞的GABA能传递已被广泛表征，但对这些细胞释放的VGLUT 3依赖性谷氨酸的功能意义一无所知。在这里，使用VGLUT 3缺失的小鼠，我们观察到VGLUT 3的缺失导致Shaeffer外侧-CA 1突触处突触可塑性的化生移位和改变的θ振荡。CA 1锥体层GABA能电流的VGLUT 3依赖性抑制作用消失，这些变化也随之消失。因此，突触前III型代谢型可被VGLUT 3阳性中间神经元释放的谷氨酸激活。这种假定的突触前异源反馈机制抑制局部GABA能紧张并调节海马神经元网络。
Hippocampal interneurons release the inhibitory transmitter GABA to regulate excitation, rhythm generation and synaptic plasticity. A subpopulation of GABAergic basket cells co-expresses the GABA/glycine vesicular transporters (VIAAT) and the atypical type III vesicular glutamate transporter (VGLUT3); therefore, these cells have the ability to signal with both GABA and glutamate. GABAergic transmission by basket cells has been extensively characterized but nothing is known about the functional implications of VGLUT3-dependent glutamate released by these cells. Here, using VGLUT3-null mice we observed that the loss of VGLUT3 results in a metaplastic shift in synaptic plasticity at Shaeffer'scollaterals-CA1 synapses and an altered theta oscillation. These changes were paralleled by the loss of a VGLUT3-dependent inhibition of GABAergic current in CA1 pyramidal layer. Therefore presynaptic type III metabotropic could be activated by glutamate released from VGLUT3-positive interneurons. This putative presynaptic heterologous feedback mechanism inhibits local GABAergic tone and regulates the hippocampal neuronal network.