...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Neurophysiology >Contribution of PKC to the maintenance of 5-HT-induced short-term facilitation at sensorimotor synapses of aplysia
【24h】

Contribution of PKC to the maintenance of 5-HT-induced short-term facilitation at sensorimotor synapses of aplysia

机译：PKC有助于维持感觉觉突触的5-HT的5-HT的短期促进。

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

Aplysia senso-rimotor synapses provide a useful model system for analyzing molecular processes that contribute to heterosynaptic plasticity. For example, previous studies demonstrated that multiple kinase cascades contribute to serotonin (5-HT)-induced short-term synaptic facilitation (STF), including protein kinase A (PKA) and protein kinase C (PKC). Moreover, the contribution of each kinase is believed to depend on the state of the synapse (e.g., depressed or nondepressed) and the time after application of 5-HT. Here, a previously unappreciated role for PKC-dependent processes was revealed to underlie the maintenance of STF at relatively nondepressed synapses. This PKC dependence was revealed when the synapse was stimulated repeatedly after application of 5-HT. The contributions of the PKA and PKC pathways were examined by blocking adenylyl cyclase-coupled 5-HT receptors with methiothepin and by blocking PKC with chelerythrine. STF was assessed 20 s after 5-HT application. The effects of PKC were consistent with enhanced mobilization of transmitter, as assessed by application of hypertonic sucrose solutions to measure the readily releasable pool of vesicles and recovery of the readily releasable pool after depletion. A computational model of transmitter release demonstrated that a PKC-dependent mobilization process was sufficient to explain the maintenance of STF at nondepressed synapses and the facilitation of depressed synapses.
机译：海螺感觉-突触突触提供了有用的模型系统，用于分析有助于异突触可塑性的分子过程。例如，以前的研究表明，多个激酶级联反应有助于血清素（5-HT）诱导的短期突触促进（STF），包括蛋白激酶A（PKA）和蛋白激酶C（PKC）。此外，据信每种激酶的贡献取决于突触的状态（例如，抑制或未抑制）和施加5-HT后的时间。在这里，PKC依赖的过程以前未被认识的作用被揭示为维持STF在相对非抑郁突触的基础。应用5-HT后反复刺激突触可揭示这种PKC依赖性。通过用甲硫基噻吩阻断腺苷酸环化酶偶联的5-HT受体和通过白屈菜红碱阻断PKC来检查PKA和PKC途径的贡献。在应用5-HT 20 s后评估STF。 PKC的作用与增强的递质动员相一致，如通过应用高渗蔗糖溶液测量易释放的囊泡池和耗竭后易释放的池池的恢复来评估。递质释放的计算模型表明，依赖PKC的动员过程足以解释STF在非抑郁突触中的维持和抑郁突触的促进。

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