GluR5 kainate receptor activation in interneurons increases tonic inhibition of pyramidal cells
GluR5 kainate receptor activation in interneurons increases tonic inhibition of pyramidal cells
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DOI：
10.1038/2185
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发表时间：
1998-10-01
影响因子：
25
通讯作者：
Ben-Ari, Y
中科院分区：
文献类型：
--
作者：
Cossart, R;Esclapez, M;Ben-Ari, Y
我们研究了谷氨酸和红藻氨酸作用于CA1海马区含GluR5的红藻氨酸受体对GABA能抑制的调制。谷氨酸盐、红藻氨酸盐或ATPA是含GluR5受体的选择性激动剂，在抑制性中间神经元中产生内向电流并引起重复动作电位放电。这导致锥体神经元的胞体和顶树突中的紧张性GABA能抑制大量增加。GluR5拮抗剂LY 293558可阻止这些作用。兴奋性传入神经的电刺激产生红藻氨酸受体介导的兴奋性突触后电流（EPSC）和动作电位，在确定的中间神经元，项目的树突和锥体神经元的胞体。因此，作用于含有GluR5亚基的红藻氨酸受体的谷氨酸可能提供针对过度兴奋的保护机制。
We studied the modulation of GABAergic inhibition by glutamate and kainate acting on GluR5-containing kainate receptors in the CA1 hippocampal region. Glutamate, kainate or ATPA, a selective agonist of GluR5-containing receptors, generates an inward current in inhibitory interneurons and cause repetitive action potential firing. This results in a massive increase of tonic GABAergic inhibition in the somata and apical dendrites of pyramidal neurons. These effects are prevented by the GluR5 antagonist LY 293558. Electrical stimulation of excitatory afferents generates kainate receptor-mediated excitatory postsynaptic currents (EPSCs) and action potentials in identified interneurons that project to the dendrites and somata of pyramidal neurons. Therefore glutamate acting on kainate receptors containing the GluR5 subunit may provide a protective mechanism against hyperexcitability.