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首页> 外文期刊>Neuron >Follistatin-like 1 Suppresses Sensory Afferent Transmission by Activating Na(+),K(+)-ATPase.
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Follistatin-like 1 Suppresses Sensory Afferent Transmission by Activating Na(+),K(+)-ATPase.

机译：卵泡抑素样1通过激活Na（+），K（+）-ATPase抑制感觉传入传递。

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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 alpha1 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.
机译：兴奋性突触传递受到抑制性神经递质和神经调节剂的调节。我们发现，突触传递的躯体感觉传入可以通过突触前分泌的蛋白质，卵泡抑素样1（FSTL1），其作为Na（+），K（+）-ATPase（NKA）的直接激活剂而快速调节。 FSTL1蛋白在背根神经节（DRG）的小直径神经元中高度表达。它通过小的半透明囊泡运输到轴突末端，并以自发和去极化的方式分泌。生化分析表明，FSTL1与NKA的alpha1亚基结合并提高NKA活性。胞外FSTL1通过激活NKA诱导培养细胞的膜超极化并抑制脊髓切片中传入突触传递。小鼠小DRG神经元中FSTL1的基因缺失导致传入突触传递和感觉超敏性增强，这可以通过鞘内施用FSTL1蛋白来减少。因此，依赖FSTL1的NKA激活可调节体感阈值。

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