Cossart R, Esclapez M, Hirsch J C, Bernard C, Ben-Ari Y
Epilepsie et Ischémie Cérébrale, INSERM U29, Hôpital de Port Royal, Paris, France.
Nat Neurosci. 1998 Oct;1(6):470-8. doi: 10.1038/2185.
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.
我们研究了谷氨酸和海人酸作用于海马CA1区含GluR5的海人酸受体时对GABA能抑制的调节作用。谷氨酸、海人酸或ATPA（一种含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发放。这导致锥体神经元胞体和顶端树突中紧张性GABA能抑制大量增加。这些效应可被GluR5拮抗剂LY 293558阻断。对兴奋性传入纤维的电刺激在投射到锥体神经元树突和胞体的特定中间神经元中产生海人酸受体介导的兴奋性突触后电流（EPSCs）和动作电位。因此，作用于含GluR5亚基的海人酸受体的谷氨酸可能提供一种对抗过度兴奋的保护机制。
