Increased anxiety-like behavior and enhanced synaptic efficacy in the amygdala of GluR5 knockout mice.
Increased anxiety-like behavior and enhanced synaptic efficacy in the amygdala of GluR5 knockout mice.
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DOI：
10.1371/journal.pone.0000167
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发表时间：
2007-01-24
期刊：
影响因子：
3.7
通讯作者：
Zhuo M
中科院分区：
文献类型：
--
作者：
Wu LJ;Ko SW;Toyoda H;Zhao MG;Xu H;Vadakkan KI;Ren M;Knifed E;Shum F;Quan J;Zhang XH;Zhuo M
杏仁核中的GABA能传递调节焦虑的表达。因此，了解GABA能传递和杏仁核兴奋回路之间的相互作用对于理解焦虑的神经生物学基础至关重要。在这里，我们使用了多学科的方法来证明，GluR 5-含有红藻氨酸受体调节局部抑制电路，调制从基底外侧杏仁核中央杏仁核的兴奋性传输，并控制行为焦虑。GluR 5基因缺失或基底外侧杏仁核局部注射GluR 5拮抗剂可增加焦虑样行为。GluR 5的激活选择性地使抑制性神经元去极化，从而增加GABA的释放并有助于基底外侧杏仁核中的紧张性GABA电流。增强的GABA能传递导致中央杏仁核中的兴奋性输入减少。我们的研究结果表明，GluR 5是杏仁核中抑制回路的关键调节器，并强调了GluR 5特异性药物在治疗病理性焦虑中的潜在用途。
GABAergic transmission in the amygdala modulates the expression of anxiety. Understanding the interplay between GABAergic transmission and excitatory circuits in the amygdala is, therefore, critical for understanding the neurobiological basis of anxiety. Here, we used a multi-disciplinary approach to demonstrate that GluR5-containing kainate receptors regulate local inhibitory circuits, modulate the excitatory transmission from the basolateral amygdala to the central amygdala, and control behavioral anxiety. Genetic deletion of GluR5 or local injection of a GluR5 antagonist into the basolateral amygdala increases anxiety-like behavior. Activation of GluR5 selectively depolarized inhibitory neurons, thereby increasing GABA release and contributing to tonic GABA current in the basolateral amygdala. The enhanced GABAergic transmission leads to reduced excitatory inputs in the central amygdala. Our results suggest that GluR5 is a key regulator of inhibitory circuits in the amygdala and highlight the potential use of GluR5-specific drugs in the treatment of pathological anxiety.
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影响因子：
25
作者：
Li, H;Chen, AQ;Rogawski, MA
通讯作者：
Rogawski, MA
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5.3
作者：
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通讯作者：
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