Traumatic brain injury to primary visual cortex produces long-lasting circuit dysfunction.

Traumatic brain injury to primary visual cortex produces long-lasting circuit dysfunction.
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DOI:
10.1038/s42003-021-02808-5
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发表时间:
2021-11-17
影响因子:
5.9
通讯作者:
Hunt RF
Hunt RF
中科院分区:
生物学2区
文献类型:
--
作者:
Frankowski JC;Foik AT;Tierno A;Machhor JR;Lyon DC;Hunt RF

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哺乳动物新皮层的初级感觉区具有显著的可塑性,使神经回路能够适应动态环境。然而,外伤性脑损伤对视觉回路功能的影响尚不清楚。在本研究中,我们使用解剖和体内电生理记录来量化在初级视觉皮层(V1)轻度控制性皮质撞击损伤两周和三个月后,成年小鼠神经元对视觉刺激的反应。我们发现,尽管脑损伤小鼠的V1基本保持完整,但与兴奋性神经元相比,更广泛影响抑制性细胞的神经元数量减少了约35%。V1神经元活性显著降低,对视觉刺激的反应受损,尺寸选择性和定向调节能力减弱。我们的研究结果表明,单一的轻度挫伤会对V1神经元编码视觉输入的方式产生深刻而持久的损害。这些发现提供了中枢视觉系统神经损伤后皮层回路功能障碍的初步见解。Jan Frankowski和Andrzej Foik等人描述了创伤性脑损伤(TBI)后小鼠初级视觉皮层的神经解剖、电生理和功能缺陷。他们的研究结果表明,创伤性脑损伤对V1神经元产生了持久的损伤,并为视觉皮层损伤后的电路功能障碍提供了进一步的见解。
Primary sensory areas of the mammalian neocortex have a remarkable degree of plasticity, allowing neural circuits to adapt to dynamic environments. However, little is known about the effects of traumatic brain injury on visual circuit function. Here we used anatomy and in vivo electrophysiological recordings in adult mice to quantify neuron responses to visual stimuli two weeks and three months after mild controlled cortical impact injury to primary visual cortex (V1). We found that, although V1 remained largely intact in brain-injured mice, there was ~35% reduction in the number of neurons that affected inhibitory cells more broadly than excitatory neurons. V1 neurons showed dramatically reduced activity, impaired responses to visual stimuli and weaker size selectivity and orientation tuning in vivo. Our results show a single, mild contusion injury produces profound and long-lasting impairments in the way V1 neurons encode visual input. These findings provide initial insight into cortical circuit dysfunction following central visual system neurotrauma. Jan Frankowski and Andrzej Foik et al. characterized neuroanatomical, electrophysiological, and functional deficits in the primary visual cortex of mice after traumatic brain injury (TBI). Their results suggest that TBI produces long-lasting impairments to V1 neurons, and provide further insight into circuit dysfunction following injury of the visual cortex.
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