Disruption of Transient SERT Expression in Thalamic Glutamatergic Neurons Alters Trajectory of Postnatal Interneuron Development in the Mouse Cortex.

Disruption of Transient SERT Expression in Thalamic Glutamatergic Neurons Alters Trajectory of Postnatal Interneuron Development in the Mouse Cortex.
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丘脑谷氨酸能神经元瞬时 SERT 表达的破坏会改变小鼠皮层出生后中间神经元发育的轨迹。

DOI:
10.1093/cercor/bhz191
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发表时间:
2020
期刊:
Cerebral cortex (New York, N.Y. : 1991)
影响因子:
--
通讯作者:
Sze,JiYing
Sze,JiYing
中科院分区:
--
文献类型:
--
作者:
DeGregorio,Roberto;Chen,Xiaoning;Petit,EmilieI;Dobrenis,Kostantin;Sze,JiYing

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在小鼠中,中间神经元亚群的终末分化发生在出生后的晚期,与成年皮质结构的出现平行。在这里,我们研究了改变的初始皮质结构对后来的中间神经元发育的影响。我们发现一类表达生长抑素(SOM)的 GABA 能中间神经元在出生后第 2 周和第 3 周之间在小鼠体感桶状皮层中经历终末分化,并在神经突生长过程中上调 Reelin 表达。我们之前的工作表明,丘脑皮质投射神经元中血清素摄取转运蛋白(SERT)的瞬时表达(E15-P10)在皮质图建立过程中调节桶状精细化。我们在此表明​​,在丘脑神经元 SERT 敲除小鼠中,这些表达 SOM 的中间神经元在正确的时间发育,到达正确的位置并表达正确的神经化学标记物,但只有 70% 的神经元保留在成年桶状皮层中。此外,那些留下来的神经元表现出改变的树突模式。我们的数据表明,皮质目的地的精确架构对于指定晚期发育的中间神经元身份、它们的皮质沉积和空间组织并不重要,但决定了它们最终整合到皮质中的数量和树突结构。我们的研究阐明了皮质图建立过程中时间特异性 SERT 功能和相关关键调节因子的破坏如何改变成人中枢神经系统持续存在的中间神经元发育轨迹。
In mice, terminal differentiation of subpopulations of interneurons occurs in late postnatal stages, paralleling the emergence of the adult cortical architecture. Here, we investigated the effects of altered initial cortical architecture on later interneuron development. We identified that a class of somatostatin (SOM)-expressing GABAergic interneurons undergoes terminal differentiation between 2nd and 3rd postnatal week in the mouse somatosensory barrel cortex and upregulates Reelin expression during neurite outgrowth. Our previous work demonstrated that transient expression (E15-P10) of serotonin uptake transporter (SERT) in thalamocortical projection neurons regulates barrel elaboration during cortical map establishment. We show here that in thalamic neuron SERT knockout mice, these SOM-expressing interneurons develop at the right time, reach correct positions and express correct neurochemical markers, but only 70% of the neurons remain in the adult barrel cortex. Moreover, those neurons that remain display altered dendritic patterning. Our data indicate that a precise architecture at the cortical destination is not essential for specifying late-developing interneuron identities, their cortical deposition, and spatial organization, but dictates their number and dendritic structure ultimately integrated into the cortex. Our study illuminates how disruption of temporal-specific SERT function and related key regulators during cortical map establishment can alter interneuron development trajectory that persists to adult central nervous system.
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