神经传递
背根神经节
抑制性突触后电位
兴奋性突触后电位
去极化
细胞生物学
超极化(物理学)
化学
细胞外
神经科学
轴突
激活剂(遗传学)
生物
感觉系统
生物物理学
生物化学
受体
有机化学
核磁共振波谱
作者
Kaicheng Li,Fang-Xiong Zhang,Changlin Li,Wenran Feng,Mingyan Yu,Yan-Qing Zhong,Kaihua Zhang,Yao Lu,Qiong Wang,Xiaoli Ma,Jun-Ru Yao,Jin‐Yuan Wang,Li-Bo Lin,Mei Han,Yu‐Qiu Zhang,Rohini Kuner,Huasheng Xiao,Bao Liu,Xiang Gao,Zhen Xu
出处
期刊:Neuron
[Elsevier]
日期:2011-03-01
卷期号:69 (5): 974-987
被引量:84
标识
DOI:10.1016/j.neuron.2011.01.022
摘要
Excitatory synaptic transmission is modulated by inhibitory neurotransmitters and neuromodulators. We found that the synaptic transmission of somatic sensory afferents can be rapidly regulated by a presynaptically secreted protein, follistatin-like 1 (FSTL1), which serves as a direct activator of Na(+),K(+)-ATPase (NKA). The FSTL1 protein is highly expressed in small-diameter neurons of the dorsal root ganglion (DRG). It is transported to axon terminals via small translucent vesicles and secreted in both spontaneous and depolarization-induced manners. Biochemical assays showed that FSTL1 binds to the α1 subunit of NKA and elevates NKA activity. Extracellular FSTL1 induced membrane hyperpolarization in cultured cells and inhibited afferent synaptic transmission in spinal cord slices by activating NKA. Genetic deletion of FSTL1 in small DRG neurons of mice resulted in enhanced afferent synaptic transmission and sensory hypersensitivity, which could be reduced by intrathecally applied FSTL1 protein. Thus, FSTL1-dependent activation of NKA regulates the threshold of somatic sensation.
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