Analysis of NMDA receptor mediated synaptic plasticity using gene targeting: Roles of Fyn and FAK non-receptor tyrosine kinases
Analysis of NMDA receptor mediated synaptic plasticity using gene targeting: Roles of Fyn and FAK non-receptor tyrosine kinases
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DOI：
10.1016/s0928-4257(97)87914-4
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发表时间：
1996-01-01
影响因子：
--
通讯作者：
Grant, SGN
中科院分区：
文献类型：
--
作者：
Grant, SGN
NMDA 受体激活调节突触强度长期变化的生化途径。药理学和基因敲除方法的结合表明，NMDA 受体启动的突触后信号级联涉及 Fyn 酪氨酸激酶。我们发现 Fyn 磷酸化 NMDA 受体以及与受体相关的蛋白质和与受体相关的蛋白质。 NMDA 受体与突触后信号蛋白的相互作用可能会引发突触强度的变化，从而有助于学习和记忆。
The NMDA receptor activates a biochemical pathway that regulates long-term changes in synaptic strength. A combination of pharmacological and gene-knockout approaches shows that the postsynaptic signalling cascade initiated by the NMDA receptor involves Fyn tyrosine kinase. We found that Fyn phosphorylates the NMDA receptor and proteins associated with the receptor and proteins associated with the receptor. The interaction of the NMDA receptor with postsynaptic signalling proteins is likely to initiate changes in synaptic strength that contribute to learning and memory.