TrkB kinase is required for recovery, but not loss, of cortical responses following monocular deprivation
TrkB kinase is required for recovery, but not loss, of cortical responses following monocular deprivation
复制标题
DOI：
10.1038/nn2068
复制
发表时间：
2008-04-01
影响因子：
25
通讯作者：
Stryker, Michael P.
中科院分区：
文献类型：
--
作者：
Kaneko, Megumi;Hanover, Jessica L.;Stryker, Michael P.
由单眼视觉剥夺引起的视觉皮层反应的变化是竞争性、经验依赖性神经可塑性的一个广泛研究的例子。人们一直认为，剥夺眼通路无法与睁眼通路竞争有限数量的脑源性神经营养因子，而脑源性神经营养因子作用于TrkB，是维持有效突触连接所必需的。我们通过化学遗传学方法在小鼠体内测试了该模型，以快速特异性地抑制TrkB激酶活性，并在体内诱导皮质可塑性。与模型相反，TrkB激酶活性不需要单眼剥夺的任何影响。当被剥夺的眼睛在关键时期重新打开时，皮层对它的反应恢复了。这种恢复被TrkB抑制所阻断。这些发现表明，TrkB信号在增强反应或新连接的生长中发挥更传统的营养作用，而不是在竞争中发挥作用。
Changes in visual cortical responses that are induced by monocular visual deprivation are a widely studied example of competitive, experience-dependent neural plasticity. It has been thought that the deprived-eye pathway will fail to compete against the open-eye pathway for limited amounts of brain-derived neurotrophic factor, which acts on TrkB and is needed to sustain effective synaptic connections. We tested this model by using a chemical-genetic approach in mice to inhibit TrkB kinase activity rapidly and specifically during the induction of cortical plasticity in vivo. Contrary to the model, TrkB kinase activity was not required for any of the effects of monocular deprivation. When the deprived eye was re-opened during the critical period, cortical responses to it recovered. This recovery was blocked by TrkB inhibition. These findings suggest a more conventional trophic role for TrkB signaling in the enhancement of responses or growth of new connections, rather than a role in competition.