Two independent forms of activity-dependent potentiation regulate electrical transmission at mixed synapses on the Mauthner cell.
Two independent forms of activity-dependent potentiation regulate electrical transmission at mixed synapses on the Mauthner cell.
复制标题
两种独立形式的活动依赖性增强调节毛特纳细胞混合突触的电传输。
DOI：
10.1016/j.brainres.2012.05.059
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发表时间：
2012-12-03
期刊：
影响因子：
2.9
通讯作者：
Pereda AE
中科院分区：
文献类型：
--
作者：
Cachope R;Pereda AE
Mauthner细胞上的混合（电和化学）突触接触，被称为俱乐部末梢，构成了研究脊椎动物电传输的有价值的模型。虽然电突触仍然被许多人认为是被动的细胞间通道，缺乏modifiability，丰富的实验证据表明，在俱乐部的末端缝隙连接受到两个独立的活动依赖性机制，导致增强电传输的动态监管控制。这些机制之一依赖于NMDA受体和突触后CaMKII的激活。第二种机制依赖于mGluR激活和内源性大麻素产生，并通过附近静脉曲张释放多巴胺间接介导，这反过来又通过PKA介导的突触后机制增强突触反应。在这里，我们回顾这两种形式的增强和它们的信号传导机制，其中包括激活两种激酶，作为突触强度的调节器，以及这两种形式的增强的功能意义。
Mixed (electrical and chemical) synaptic contacts on the Mauthner cells, known as Club endings, constitute a valuable model for the study of vertebrate electrical transmission. While electrical synapses are still perceived by many as passive intercellular channels that lack modifiability, a wealth of experimental evidence shows that gap junctions at Club endings are subject to dynamic regulatory control by two independent activity-dependent mechanisms that lead to potentiation of electrical transmission. One of those mechanisms relies on activation of NMDA receptors and postsynaptic CaMKII. A second mechanism relies on mGluR activation and endocannabinoid production and is indirectly mediated via the release of dopamine from nearby varicosities, which in turn leads to potentiation of the synaptic response via a PKA-mediated postsynaptic mechanism. We review here these two forms of potentiation and their signaling mechanisms, which include the activation of two kinases with well-established roles as regulators of synaptic strength, as well as the functional implications of these two forms of potentiation.
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DOI：
10.1073/pnas.0804793105
发表时间：
2008-08-26
影响因子：
11.1
作者：
Flores, Carmen E.;Li, Xinbo;Pereda, Alberto E.
通讯作者：
Pereda, Alberto E.
DOI：
10.1073/pnas.0805408105
发表时间：
2008-12-30
影响因子：
11.1
作者：
Alev, Cantas;Urschel, Stephanie;Dermietzel, Rolf
通讯作者：
Dermietzel, Rolf
影响因子：
3.8
作者：
FUKAMI, Y;FURUKAWA, T;ASADA, Y
通讯作者：
ASADA, Y
影响因子：
--
作者：
Curti, Sebastian;Pereda, Alberto E.
通讯作者：
Pereda, Alberto E.
影响因子：
56.9
作者：
FURSHPAN, EJ
通讯作者：
FURSHPAN, EJ