Regulation of a neuronal form of focal adhesion kinase by anandamide
Regulation of a neuronal form of focal adhesion kinase by anandamide
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DOI：
10.1126/science.273.5282.1719
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发表时间：
1996-09-20
期刊：
影响因子：
56.9
通讯作者：
Girault, JA
中科院分区：
文献类型：
--
作者：
Derkinderen, P;Toutant, M;Girault, JA
大麻素是中枢大麻素受体的内源性配体，在神经元去极化后释放。大麻素增加大鼠海马脑片和培养神经元中蛋白酪氨酸磷酸化。大麻素的作用是通过抑制腺苷酸环化酶和环腺苷3 '，5'-磷酸依赖性蛋白激酶实现的。响应于花生四烯酸的磷酸化的蛋白质之一是pp 125-粘着斑激酶（FAK+）的亚型，优先在神经元中表达。粘着斑激酶是一种酪氨酸激酶，参与整合素与肌动蛋白细胞骨架之间的相互作用。因此，大麻素可能发挥神经营养作用，并在突触可塑性中发挥作用。
Anandamide is an endogenous ligand for central cannabinoid receptors and is released after neuronal depolarization. Anandamide increased protein tyrosine phosphorylation in rat hippocampal slices and neurons in culture. The action of anandamide resulted from the inhibition of adenylyl cyclase and cyclic adenosine 3',5'-monophosphate-dependent protein kinase. One of the proteins phosphorylated in response to anandamide was an isoform of pp125-focal adhesion kinase (FAK+) expressed preferentially in neurons. Focal adhesion kinase is a tyrosine kinase involved in the interactions between the integrins and actin-based cytoskeleton. Thus, anandamide may exert neurotrophic effects and play a role in synaptic plasticity.