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首页> 外文期刊>Journal of pineal research >Melatonin improves neuroplasticity by upregulating the growth-associated protein-43 (GAP-43) and NMDAR postsynaptic density-95 (PSD-95) proteins in cultured neurons exposed to glutamate excitotoxicity and in rats subjected to transient focal cerebral ischemia even during a long-term recovery period
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Melatonin improves neuroplasticity by upregulating the growth-associated protein-43 (GAP-43) and NMDAR postsynaptic density-95 (PSD-95) proteins in cultured neurons exposed to glutamate excitotoxicity and in rats subjected to transient focal cerebral ischemia even during a long-term recovery period

机译：褪黑素通过上调暴露于谷氨酸兴奋性毒性的培养神经元以及即使在长期脑缺血期间遭受短暂性局灶性脑缺血的大鼠中，也通过上调生长相关蛋白43（GAP-43）和NMDAR突触后密度95（PSD-95）蛋白来改善神经可塑性。恢复期

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Recent evidence shows that the NMDAR postsynaptic density-95 (PSD-95), growth-associated protein-43 (GAP-43), and matrix metalloproteinase-9 (MMP-9) protein enhance neuroplasticity at the subacute stage of stroke. Here, we evaluated whether melatonin would modulate the PSD-95, GAP-43, and MMP-9 proteins in cultured neurons exposed to glutamate excitotoxicity and in rats subjected to experimental stroke. Adult male Sprague-Dawley rats were treated with melatonin (5 mg/kg) or vehicle at reperfusion onset after transient occlusion of the right middle cerebral artery (tMCAO) for 90 min. Animals were euthanized for Western immunoblot analyses for the PSD-95 and GAP-43 proteins and gelatin zymography for the MMP-9 activity at 7 days postinsult. Another set of animals was sacrificed for histologic and Golgi-Cox-impregnated sections at 28 days postinsult. In cultured neurons exposed to glutamate excitotoxicity, melatonin significantly upregulated the GAP-43 and PSD-95 expressions and improved dendritic aborizations (P < 0.05, respectively). Relative to controls, melatonin-treated stroke animals caused a significant improvement in GAP-43 and PSD-95 expressions as well as the MMP-9 activity in the ischemic brain (P < 0.05). Consequently, melatonin also significantly promoted the dendritic spine density and reduced infarction in the ischemic brain, and improved neurobehaviors as well at 28 days postinsult (P < 0.05, respectively). Together, melatonin upregulates GAP-43, PSD-95, and MMP-9 proteins, which likely accounts for its actions to improve neuroplasticity in cultured neurons exposed to glutamate excitotoxicity and to enhance long-term neuroprotection, neuroplasticity, and brain remodeling in stroke rats.
机译：最近的证据表明，NMDAR突触后密度95（PSD-95），生长相关蛋白43（GAP-43）和基质金属蛋白酶9（MMP-9）蛋白可在中风亚急性期增强神经可塑性。在这里，我们评估了褪黑激素是否会调节暴露于谷氨酸兴奋性毒性的培养神经元和实验性中风大鼠的PSD-95，GAP-43和MMP-9蛋白。成年雄性Sprague-Dawley大鼠在短暂性阻塞右脑中动脉（tMCAO）90分钟后，于再灌注开始时用褪黑激素（5 mg / kg）或媒介物治疗。对动物进行安乐死以进行7天后的PSD-95和GAP-43蛋白的Western免疫印迹分析，以及明胶酶谱分析的MMP-9活性。在受伤后28天，将另一组动物处死以进行组织学和高尔基-科克斯浸渍的切片。在暴露于谷氨酸兴奋性毒性的培养神经元中，褪黑激素显着​​上调了GAP-43和PSD-95的表达，并改善了树突状的无精化（分别为P <0.05）。相对于对照，褪黑素治疗的中风动物在缺血性脑中引起了GAP-43和PSD-95表达以及MMP-9活性的显着改善（P <0.05）。因此，褪黑素还可以在缺血后28天显着提高缺血性脑的树突棘密度并减少梗塞，并改善神经行为（分别为P <0.05）。褪黑素共同上调GAP-43，PSD-95和MMP-9蛋白，这可能是其改善暴露于谷氨酸兴奋性毒性的培养神经元中的神经可塑性以及增强中风大鼠长期神经保护，神经可塑性和脑重构的作用。 。

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