Wu Long-Jun, Xu Hui, Ren Ming, Zhuo Min
Department of Physiology, Faculty of Medicine, University of Toronto, Medical Science Building, Toronto, Ontario, Canada M5S 1A8.
Dev Neurobiol. 2007 Feb 1;67(2):146-57. doi: 10.1002/dneu.20331.
In the anterior cingulate cortex (ACC), GluR5-containing kainate receptor mediated the small portion of excitatory postsynaptic current. However, little is known about its role in modulation of neurotransmitter release in this brain region. In the present study, we address this question by using selective GluR5 agonist and antagonist, as well as GluR5(-/-) mice. Our results showed that activation of GluR5 induced action potential-dependent GABA release, which is also required for the activation of voltage-dependent calcium channel and Ca(2+) influx. The effect of GluR5 activation is selective to the GABAergic, but not glutamatergic synaptic transmission. Endogenous activation of GluR5 also enhanced GABA release to ACC pyramidal neurons and the corresponding postsynaptic tonic GABA current. Our results suggest the somatodendritic, but not presynaptic GluR5, in modulation of GABA release. The endogenous GluR5 activation and the subsequent tonic GABA current may play an inhibitory role in ACC-related brain functions.
在前扣带皮层（ACC）中，含GluR5的海人藻酸受体介导了一小部分兴奋性突触后电流。然而，关于其在该脑区神经递质释放调节中的作用却知之甚少。在本研究中，我们通过使用选择性GluR5激动剂和拮抗剂以及GluR5基因敲除小鼠来解决这个问题。我们的结果表明，GluR5的激活诱导了依赖动作电位的GABA释放，这也是电压依赖性钙通道激活和Ca²⁺内流所必需的。GluR5激活的作用对GABA能突触传递具有选择性，而对谷氨酸能突触传递无选择性。GluR5的内源性激活也增强了向ACC锥体神经元的GABA释放以及相应的突触后紧张性GABA电流。我们的结果表明，在调节GABA释放方面，是树突体而非突触前的GluR5起作用。内源性GluR5激活及随后的紧张性GABA电流可能在与ACC相关的脑功能中发挥抑制作用。
