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首页> 外文期刊>Molecular pain >An in vivo mouse model of long-term potentiation at synapses between primary afferent C-fibers and spinal dorsal horn neurons: essential role of EphB1 receptor
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An in vivo mouse model of long-term potentiation at synapses between primary afferent C-fibers and spinal dorsal horn neurons: essential role of EphB1 receptor

机译：初级传入C纤维和脊髓背角神经元之间的突触的长期增强的体内小鼠模型：EphB1受体的基本作用。

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Background Long-term potentiation (LTP), a much studied cellular model of synaptic plasticity, has not been demonstrated at synapses between primary afferent C-fibers and spinal dorsal horn (DH) neurons in mice in vivo. EphrinB-EphB receptor signaling plays important roles in synaptic connection and plasticity in the nervous system, but its role in spinal synaptic plasticity remains unclear. Results This study characterizes properties of LTP at synapses of C-fibers onto neurons in the superficial DH following high-frequency stimulation (HFS) of a peripheral nerve at an intensity that activates C-fibers and examines associated activation of Ca2+/calmodulin-activated protein kinase II (p-CaMKII), extracellular signal-regulated kinase (p-ERK) and the cyclic AMP response element binding protein (p-CREB) and expression of c-Fos, and it investigates further roles for the EphB1 receptor in LTP. HFS induced LTP within 5 min and lasts for 3–8 h during the period of recording and resulted in upregulation of p-CaMKII, p-ERK and p-CREB protein levels in the spinal cord and expression of c-Fos in DH. Intrathecal pretreatment of MK-801 or EphB2-Fc prevented LTP and significantly reduced upregulation of p-CaMKII, p-ERK, p-CREB and c-Fos. Further, targeted mutation of EphB1 receptor prevented induction of LTP and associated increases in phosphorylation of CaMKII, ERK, and CREB. Conclusion This study provides an in vivo mouse model of LTP at synapses of C-fibers onto the superficial DH neurons that will be valuable for studying the DH neuron excitability and their synaptic plasticity and hyperalgesia. It further takes advantage of examining functional implications of a specific gene targeted mice and demonstrates that the EphB1 receptor is essential for development of LTP.
机译：背景技术在小鼠体内初级传入C纤维和脊髓背角（DH）神经元之间的突触中，尚未证实长期增强（LTP），突触可塑性的细胞模型。 EphrinB-EphB受体信号传导在神经系统的突触连接和可塑性中起重要作用，但在脊髓突触可塑性中的作用仍不清楚。结果本研究表征了高频刺激（HFS）激活周围神经后，C纤维突触到浅表DH神经元上C纤维突触的特性，并研究了Ca2 + /钙调蛋白激活蛋白的相关激活激酶II（p-CaMKII），细胞外信号调节激酶（p-ERK）和环状AMP响应元件结合蛋白（p-CREB）和c-Fos的表达，它研究了Lph中EphB1受体的进一步作用。 HFS在5分钟内诱导LTP，并在记录期间持续3–8 h，并导致脊髓中p-CaMKII，p-ERK和p-CREB蛋白水平上调以及DH中c-Fos的表达。鞘内预处理MK-801或EphB2-Fc可防止LTP并显着降低p-CaMKII，p-ERK，p-CREB和c-Fos的上调。此外，EphB1受体的靶向突变阻止了LTP的诱导和CaMKII，ERK和CREB磷酸化的相关增加。结论这项研究提供了在C纤维突触到浅表DH神经元上的LTP的体内小鼠模型，这对于研究DH神经元的兴奋性及其突触可塑性和痛觉过敏具有重要的价值。它进一步利用了检查特定基因靶向小鼠的功能含义的优势，并证明了EphB1受体对于LTP的发展至关重要。

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