...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Neurophysiology >Mu opioid receptor activation inhibits GABAergic inputs to basolateral amygdala neurons through Kv1.1/1.2 channels.
【24h】

Mu opioid receptor activation inhibits GABAergic inputs to basolateral amygdala neurons through Kv1.1/1.2 channels.

机译：Mu阿片受体激活通过Kv1.1 / 1.2通道抑制基底外侧杏仁核神经元的GABA能输入。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The basolateral amygdala (BLA) is the major amygdaloid nucleus distributed with mu opioid receptors. The afferent input from the BLA to the central nucleus of the amygdala (CeA) is considered important for opioid analgesia. However, little is known about the effect of mu opioids on synaptic transmission in the BLA. In this study, we examined the effect of mu opioid receptor stimulation on the inhibitory and excitatory synaptic inputs to CeA-projecting BLA neurons. BLA neurons were retrogradely labeled with a fluorescent tracer injected into the CeA of rats. Whole cell voltage-clamp recordings were performed on labeled BLA neurons in brain slices. The specific mu opioid receptor agonist, (D-Ala2,N-Me-Phe4,Gly5-ol)-enkephalin (DAMGO, 1 microM), significantly reduced the frequency of miniature inhibitory postsynaptic currents (mIPSCs) in 77% of cells tested. DAMGO also significantly decreased the peak amplitude of evoked IPSCs in 75% of cells examined. However, DAMGO did not significantly alter the frequency of mEPSCs or the peak amplitude of evoked EPSCs in 90% and 75% of labeled cells, respectively. Bath application of the Kv channel blockers, 4-AP (Kv1.1, 1.2, 1.3, 1.5, 1.6, 3.1, 3.2), alpha-dendrotoxin (Kv1.1, 1.2, 1.6), dendrotoxin-K (Kv1.1), or tityustoxin-Kalpha (Kv1.2) each blocked the inhibitory effect of DAMGO on mIPSCs. Double immunofluorescence labeling showed that some of the immunoreactivities of Kv1.1 and Kv1.2 were colocalized with synaptophysin in the BLA. This study provides new information that activation of presynaptic mu opioid receptors primarily attenuates GABAergic synaptic inputs to CeA-projecting neurons in the BLA through a signaling mechanism involving Kv1.1 and Kv1.2 channels.
机译：基底外侧杏仁核（BLA）是主要的杏仁核，分布有μ阿片受体。从BLA到杏仁核中央核（CeA）的传入输入被认为对阿片类镇痛很重要。然而，关于μ阿片类药物对BLA中突触传递的影响知之甚少。在这项研究中，我们检查了μ阿片受体刺激对CeA投射BLA神经元的抑制性和兴奋性突触输入的影响。用注射到大鼠CeA中的荧光示踪剂逆行标记BLA神经元。对脑切片中标记的BLA神经元进行全细胞电压钳记录。特定的μ阿片样物质受体激动剂（D-Ala2，N-Me-Phe4，Gly5-ol）-脑啡肽（DAMGO，1 microM）显着降低了77％受测细胞中微型抑制突触后电流（mIPSC）的频率。 DAMGO还显着降低了75％的细胞中诱发的IPSC的峰值幅度。但是，DAMGO并没有显着改变分别在90％和75％的标记细胞中mEPSC的频率或诱发的EPSC的峰值幅度。 Kv通道阻滞剂在浴中的应用，4-AP（Kv1.1、1.2、1.3、1.5、1.6、3.1、3.2），α-树毒素（Kv1.1、1.2、1.6），树毒素-K（Kv1.1）或tityustoxin-Kalpha（Kv1.2）各自阻断DAMGO对mIPSC的抑制作用。双重免疫荧光标记显示，Kv1.1和Kv1.2的某些免疫反应性与BLA中的突触素共定位。这项研究提供了新的信息，即突触前μ阿片受体的激活主要通过涉及Kv1.1和Kv1.2通道的信号传导机制减弱BLA中CeA投射神经元的GABA能突触输入。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号