• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >Cellular action of cholecystokinin-8S-mediated excitatory effects in the rat periaqueductal gray.
【24h】

Cellular action of cholecystokinin-8S-mediated excitatory effects in the rat periaqueductal gray.

机译：胆囊收缩素8S介导的大鼠导水管灰色兴奋作用的细胞作用。

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 peptide cholecystokinin (CCK) is one of the major neurotransmitters modulating satiety, nociception, and anxiety behavior. Although many behavioral studies showing anti-analgesic and anxiogenic actions of CCK have been reported, less is known about its cellular action in the central nervous system (CNS). Therefore, we examined the action of CCK in rat dorsolateral periaqueductal gray (PAG) neurons using slice preparations and whole-cell patch-clamp recordings. Application of CCK-8S produced an inward current accompanied by increased spontaneous synaptic activities. The CCK-8S-induced inward current (I(CCK)) was recovered after washout and reproduced by multiple exposures. Current-voltage plots revealed that I(CCK) reversed near the equilibrium potential for K(+) ions with a decreased membrane conductance. When several K(+) channel blockers were used, application of CdCl(2), TEA, or apamin significantly reduced I(CCK). I(CCK) was also significantly reduced by the CCK(2) receptor antagonist, L-365,260, while it was not affected by the CCK(1) receptor antagonist, L-364,718. Furthermore, we examined the effects of CCK-8S on miniature excitatory postsynaptic currents (mEPSCs) in order to determine the mechanism of CCK-mediated increase on synaptic activities. We found that CCK-8S increased the frequency of mEPSCs, but had no effect on mEPSC amplitude. This presynaptic effect persisted in the presence of CdCl(2) or Ca(2+)-free bath solution, but was completely abolished by pre-treatment with BAPTA-AM, thapsigargin or L-365,260. Taken together, our results indicate that CCK can excite PAG neurons at both pre- and postsynaptic loci via the activation of CCK(2) receptors. These effects may be important for the effects of CCK on behavior and autonomic function that are mediated via PAG neurons.
机译：肽胆囊收缩素（CCK）是调节饱腹感，伤害感受和焦虑行为的主要神经递质之一。尽管已经报道了许多显示CCK具有抗镇痛和抗焦虑作用的行为研究，但对CCK在中枢神经系统（CNS）中的细胞作用了解较少。因此，我们使用切片制剂和全细胞膜片钳记录检查了CCK在大鼠背外侧水管周围灰色（PAG）神经元中的作用。应用CCK-8S会产生内向电流，并伴有自发的突触活动增加。冲洗后恢复CCK-8S诱导的内向电流（I（CCK）），并通过多次暴露进行复制。电流-电压图显示，I（CCK）在K（+）离子的平衡电势附近反转，膜电导降低。当使用几种K（+）通道阻滞剂时，应用CdCl（2），TEA或Apapamin可以显着降低I（CCK）。 I（CCK）也受到CCK（2）受体拮抗剂L-365,260的显着降低，而不受CCK（1）受体拮抗剂L-364,718的影响。此外，我们研究了CCK-8S对微型兴奋性突触后突触电流（mEPSCs）的影响，以确定CCK介导的突触活动增加的机制。我们发现CCK-8S增加了mEPSC的频率，但对mEPSC振幅没有影响。这种突触前的效果在没有CdCl（2）或不含Ca（2+）的浴液的情况下持续存在，但是通过用BAPTA-AM，thapsigargin或L-365,260进行预处理而被完全废除。两者合计，我们的结果表明CCK可以通过激活CCK（2）受体在突触前和突触后基因位点激发PAG神经元。这些影响对于CCK对通过PAG神经元介导的行为和自主功能的影响可能很重要。

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