Regulation of synaptic cur rents by mGluR2 at reciprocal syna pses in the mouse accessory olfact ory bulb
Regulation of synaptic cur rents by mGluR2 at reciprocal syna pses in the mouse accessory olfact ory bulb
复制标题
mGluR2 对小鼠副嗅球互惠突触突触电流的调节
DOI：
10.1111/ejn.12059
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发表时间：
2013
期刊：
影响因子：
--
通讯作者：
Kaba H
中科院分区：
文献类型：
--
作者：
Taniguchi M;Yokoi M;Shinohara Y;Okutani F;Murata Y;Nakanishi S;Kaba H
从副嗅球(AOB)到下游结构的信息吞吐量是由颗粒细胞对二尖瓣细胞的树突相互抑制所控制的。鉴于代谢性谷氨酸受体mGluR2在AOB中的高表达，以及mGluR2的激活允许形成特定的嗅觉记忆，我们推测mGluR2可能在调节树突状细胞抑制中发挥重要作用。为了验证这一假设，我们检测了mGluR2的药理和遗传操作对23至36天的Balb/c小鼠切片中二尖瓣或颗粒细胞突触反应的影响。为了引起树突状抑制，对二尖瓣细胞施加从-70到0 mV的去极化电压阶跃或调节以诱发动作电位的阈值电流刺激(S)，采用制霉菌素穿孔或传统的全细胞配置。我们发现第二组代谢性谷氨酸受体激动剂(mGluR2/mGluR3)抑制[(2S，1′R，2′R，3′R)‐2‐(2，3‐dicarboxycyclopropyl)glycine]，，而mGluR2/mGluR3拮抗剂LY341495[(αS)‐α‐amino‐α‐[(1S，2S)‐2‐carboxycyclopropyl]‐9H‐xanthine‐9‐propanoic酸]则增强树突状细胞的抑制。基因消融mGluR2可明显减弱DCG-IV和LY341495对树突状细胞的抑制作用。DCG-IV降低颗粒细胞记录的自发微小兴奋性突触后电流的频率和幅度。此外，DCG-IV抑制二尖瓣和颗粒细胞的高电压激活的钙电流。这些结果表明，mGluR2通过抑制AOB内二尖瓣细胞和颗粒细胞之间的突触传递来减轻树突状细胞的抑制作用。
The throughput of information from the accessory olfactory bulb (AOB) to downstream structures is controlled by reciprocal dendrodendritic inhibition of mitral cells by granule cells. Given the high expression levels of mGluR2, a metabotropic glutamate receptor, in the AOB and the fact that the activation of mGluR2 permits the formation of a specific olfactory memory, we reasoned that mGluR2 might play an important role in regulating dendrodendritic inhibition. To test this hypothesis, we examined the effects of pharmacological and genetic manipulations of mGluR2 on synaptic responses measured from mitral or granule cells in slice preparations from 23‐ to 36‐day‐old Balb/c mice. To evoke dendrodendritic inhibition, a depolarizing voltage step from –70 to 0 mV or a threshold current stimulus adjusted to elicit action potential(s) was applied to a mitral cell using either a nystatin‐perforated or conventional whole‐cell configuration. We found that an agonist for group II metabotropic glutamate receptors (mGluR2/mGluR3), DCG‐IV [(2S,1′R,2′R,3′R)‐2‐(2,3‐dicarboxycyclopropyl)glycine], suppressed, whereas the mGluR2/mGluR3 antagonist LY341495 [(αS)‐α‐amino‐α‐[(1S,2S)‐2‐carboxycyclopropyl]‐9H‐xanthine‐9‐propanoic acid] enhanced dendrodendritic inhibition. Genetic ablation of mGluR2 markedly impaired the effects of DCG‐IV and LY341495 on dendrodendritic inhibition. DCG‐IV reduced both the frequency and the amplitude of spontaneous miniature excitatory postsynaptic currents recorded from granule cells. Additionally, DCG‐IV inhibited high‐voltage‐activated calcium currents in both mitral and granule cells. These results suggest that mGluR2 reduces dendrodendritic inhibition by inhibiting synaptic transmission between mitral cells and granule cells in the AOB.