A novel postsynaptic mechanism for heterosynaptic sharing of short-term plasticity.
A novel postsynaptic mechanism for heterosynaptic sharing of short-term plasticity.
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DOI：
10.1523/jneurosci.4767-09.2010
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发表时间：
2010-06-30
期刊：
影响因子：
--
通讯作者：
Carew TJ
中科院分区：
文献类型：
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作者：
Reissner KJ;Pu L;Schaffhausen JH;Boyle HD;Smith IF;Parker I;Carew TJ
胞内储存的钙离子突触后释放是细胞信号传导的重要手段，介导多种形式的突触可塑性。先前的研究已经确定了一种短期可塑性的突触后细胞内Ca2+需求，即感觉-运动神经元（SN-MN）突触的破伤风后增强（PTP）。在这里，我们发现突触后ip3介导的Ca2+释放对突触前破伤风的反应，诱导PTP，可以将短暂的可塑性赋予接受阈下激活的相邻SN突触。这种异突触共享的可塑性代表了一种动态的、短期的突触增强，突触输入到一个共同的突触后目标。异突触共享被Ca2+和IP3介导的信号的突触后破坏所阻断，相反，它可以通过突触后注射不可水解的IP3和MN中笼子IP3的光解来模拟。异突触共享的分子机制涉及mGluR和Homer-dependent相互作用，这表明Homer可以促进Ca2+依赖性可塑性在邻近的突触后位点的整合，并为突触前激活诱导的可塑性传播提供了一种突触后机制。我们的研究结果支持一个模型，在这个模型中，来自阈上和阈下输入的IP3信号的突触后求和导致分子重合检测，从而产生一种新的异突触可塑性形式。
Postsynaptic release of Ca2+ from intracellular stores is an important means of cellular signaling which mediates numerous forms of synaptic plasticity. Previous studies have identified a postsynaptic intracellular Ca2+ requirement for a form of short-term plasticity, post-tetanic potentiation (PTP) at sensory-motor neuron (SN-MN) synapses in Aplysia. Here we show that postsynaptic IP3-mediated Ca2+ release in response to a presynaptic tetanus in a SN that induces PTP can confer transient plasticity onto a neighboring SN synapse receiving subthreshold activation. This heterosynaptic sharing of plasticity represents a dynamic, short-term synaptic enhancement of synaptic inputs onto a common postsynaptic target. Heterosynaptic sharing is blocked by postsynaptic disruption of Ca2+ and IP3-mediated signaling, and conversely, it is mimicked by postsynaptic injection of non-hydrolysable IP3, and by photolysis of caged IP3 in the MN. The molecular mechanism for heterosynaptic sharing involves mGluR and Homer-dependent interactions, indicating that Homer can facilitate the integration of Ca2+-dependent plasticity at neighboring postsynaptic sites and provides a postsynaptic mechanism for spread of plasticity induced by presynaptic activation. Our results support a model in which postsynaptic summation of IP3 signals from suprathreshold and subthreshold inputs results in molecular coincidence detection that gives rise to a novel form of heterosynaptic plasticity.