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首页> 外文期刊>The European Journal of Neuroscience >Binding partners L1 cell adhesion molecule and the ezrin-radixin-moesin (ERM) proteins are involved in development and the regenerative response to injury of hippocampal and cortical neurons.
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Binding partners L1 cell adhesion molecule and the ezrin-radixin-moesin (ERM) proteins are involved in development and the regenerative response to injury of hippocampal and cortical neurons.

机译：结合伴侣L1细胞粘附分子和ezrin-radixin-moesin（ERM）蛋白参与海马和皮层神经元损伤的发育和再生反应。

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Abstract Regeneration of the adult central nervous system may require recapitulation of developmental events and therefore involve the re-expression of developmentally significant proteins. We have investigated whether the L1 cell adhesion molecule, and its binding partner, the ezrin-radixin-moesin (ERM) proteins are involved in the neuronal regenerative response to injury. Hippocampal and cortical neurons were cultured in vitro on either an L1 substrate or poly-L-lysine, and ERM and other neuronal proteins were localized immunocytochemically both developmentally and following neurite transection of neurons maintained in long-term culture. Activated ERM was localized to growth cones up to 7 days in vitro but relatively mature cultures (21 days in vitro) were devoid of active ERM proteins. However, ERM proteins were localized to the growth cones of sprouting neuronal processes that formed several hours after neurite transection. In addition, the L1 substrate, relative to poly-L-lysine, resulted in significantly longer regenerative neurites, as well as larger growth cones with more filopodia. Furthermore, neurons derived from the cortex formed significantly longer post-injury neurite sprouts at 6 h post-injury than hippocampal derived neurons grown on both substrates. We have demonstrated that L1 and the ERM proteins are involved in the neuronal response to injury, and that neurons derived from the hippocampus and cortex may have different post-injury regenerative neurite sprouting abilities.
机译：摘要成年中枢神经系统的再生可能需要概括发育事件，因此涉及发育重要蛋白的重新表达。我们研究了L1细胞粘附分子及其结合伴侣ezrin-radixin-moesin（ERM）蛋白是否参与了损伤的神经元再生反应。将海马和皮层神经元在L1底物或聚L-赖氨酸上进行体外培养，并将ERM和其他神经元蛋白在发育过程中和长期培养的神经元神经突横切后进行免疫细胞化学定位。激活的ERM在体外最多7天就定位在生长锥上，但是相对成熟的培养物（体外21天）没有活性ERM蛋白。然而，ERM蛋白位于神经突横切数小时后形成的发芽神经元过程的生长锥。此外，相对于聚-L-赖氨酸，L1底物可导致更长的再生神经突，以及更大的生长锥和更多的丝状伪足。此外，与在两种基质上生长的海马源神经元相比，在损伤后6 h，来自皮质的神经元形成的损伤后神经突芽明显更长。我们已经证明，L1和ERM蛋白参与了对损伤的神经元反应，并且源自海马和皮层的神经元可能具有不同的损伤后再生神经突发芽能力。

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