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由BDNF驱动的突触可塑性需要自克林矩阵金属蛋白酶-9活性

Diana Legutko^1,2, Lukasz Bijoch¹, Grzegorz Olszak¹

¹BRAINCITY, Laboratory of Neurobiology, The Nencki Institute, Pasteura 3, 02-093 Warsaw, Poland.

Science advances

|September 24, 2025

概括

矩阵金属蛋白酶-9 (MMP-9) 直接将亲脑衍生神经营养因子 (proBDNF) 分割成成熟的BDNF. 这一过程对于激活TrkB受体和使树突脊柱具有结构性可塑性至关重要,这对学习和记忆至关重要.

科学领域:

神经科学是一个神经科学.
分子生物学分子生物学
细胞可塑性细胞可塑性

背景情况:

树突脊柱的结构可塑性是学习和记忆的基础.
这种可塑性取决于来自大脑的神经营养因子 (BDNF) 和它的受体TrkB.
成熟的BDNF需要从其前体,proBDNF的蛋白质分解裂变来结合TrkB.

研究的目的:

研究矩阵金属蛋白酶-9 (MMP-9) 在BDNF成熟和TrkB激活中的作用.
为了确定MMP-9是否参与树突的结构可塑性.

主要方法:

利用双光子显微镜进行实时观测.
通过谷氨酸脱而使用单个脊柱刺激.
在刺激后评估MMP-9释放和蛋白质分解活性.
研究了MMP-9对proBDNF的直接切割.

主要成果:

在突触刺激时,MMP-9迅速释放,活性在2分钟内局部化到激活的棘中.
MMP-9活性对于托罗普米奥辛受体激酶B (TrkB) 的激活至关重要.
MMP-9直接将亲脑衍生神经营养因子 (proBDNF) 分割成成熟的BDNF.
MMP-9对于树突脊柱的活动依赖性结构可塑性是必需的.

结论:

矩阵金属蛋白酶-9 (MMP-9) 在处理来自大脑的神经营养因子 (BDNF) 中起着至关重要的作用.
MMP-9直接促进了BDNF的成熟,使TrkB受体的激活成为可能.
这种MMP-9-BDNF相互作用对于调节树突脊柱结构可塑性至关重要,影响学习和记忆机制.

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