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首页> 外文期刊>The European Journal of Neuroscience >A novel form of presynaptic CaMKII-dependent short-term potentiation between Lymnaea neurons.
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A novel form of presynaptic CaMKII-dependent short-term potentiation between Lymnaea neurons.

机译:lymnaea神经元之间的突触前CaMKII依赖性短期增强的一种新型形式。

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摘要

Short-term plasticity is thought to form the basis for working memory, the cellular mechanisms of which are the least understood in the nervous system. In this study, using in vitro reconstructed synapses between the identified Lymnaea neuron visceral dorsal 4 (VD4) and left pedal dorsal 1 (LPeD1), we demonstrate a novel form of short-term potentiation (STP) which is 'use'- but not time-dependent, unlike most previously defined forms of short-term synaptic plasticity. Using a triple-cell configuration we demonstrate for the first time that a single presynaptic neuron can reliably potentiate both inhibitory and excitatory synapses. We further demonstrate that, unlike previously described forms of STP, the synaptic potentiation between Lymnaea neurons does not involve postsynaptic receptor sensitization or presynaptic residual calcium. Finally, we provide evidence that STP at the VD4-LPeD1 synapse requires presynaptic calcium/calmodulin dependent kinase II (CaMKII). Taken together, our study identifies a novel form of STP which may provide the basis for both short- and long-term potentiation, in the absence of any protein synthesis-dependent steps, and involve CaMKII activity exclusively in the presynaptic cell.
机译:短期可塑性被认为是工作记忆的基础,在神经系统中对其细胞机制了解最少。在这项研究中,使用已确定的淋巴神经元内脏背侧4(VD4)和左脚掌背侧1(LPeD1)之间的体外重建突触,我们证明了一种新型的短期增强(STP)形式,即“使用”,但不是与时间有关,与大多数先前定义的短期突触可塑性不同。使用三细胞配置,我们首次证明了单个突触前神经元可以可靠地增强抑制性和兴奋性突触。我们进一步证明,与先前描述的STP形式不同,Lymnaea神经元之间的突触增强不涉及突触后受体致敏或突触前残留钙。最后,我们提供证据表明VD4-LPeD1突触处的STP需要突触前钙/钙调蛋白依赖性激酶II(CaMKII)。综上所述,我们的研究确定了STP的一种新型形式,它可以在缺乏任何蛋白质合成依赖性步骤的情况下为短期和长期增强提供基础,并且仅在突触前细胞中涉及CaMKII活性。

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