Myelinated and unmyelinated axons of the corpus callosum differ in vulnerability and functional recovery following traumatic brain injury
Myelinated and unmyelinated axons of the corpus callosum differ in vulnerability and functional recovery following traumatic brain injury
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DOI：
10.1016/j.expneurol.2005.07.014
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发表时间：
2005-11-01
影响因子：
5.3
通讯作者：
Povlishock, JT
中科院分区：
文献类型：
--
作者：
Reeves, TM;Phillips, LL;Povlishock, JT
创伤性轴索损伤（TAI）是创伤性脑损伤的一个常见特征，与损伤后发病率和死亡率相关。然而，TAI 并非在所有轴突群体中均一表达，纤维口径和解剖位置影响特定的 TAI 病理。为了研究不同的轴突对脑损伤的脆弱性，对大鼠流体冲击损伤后胼胝体的轴突兴奋性和完整性进行了评估。在脑切片电生理记录中，在胼胝体中诱发复合动作电位（CAP），并分别量化有髓轴突（N-2波）和无髓轴突（N-2波）产生的CAP波形分量的损伤效应。还对 TAI 诱导的这些轴突群体的形态变化进行了超微结构分析。在受伤后第一周内，这两个轴突群对脑损伤的反应以及功能恢复有所不同。 N-1和N-2的振幅在3小时、1天和3天存活时显着降低。受伤后 7 天，N-1 振幅恢复至控制水平。相比之下，N-2 振幅在受伤后 7 天持续受到抑制。诱发 CAP 的强度-持续时间特性进一步区分了这些轴突群体中损伤的影响，N-2 在损伤后表现出升高的强度-持续时间时间常数。超微结构观察揭示了有髓轴突的变性，与弥漫性损伤后遗症以及之前未记录的无髓纤维群内的病理学一致。总的来说，这些发现证明了轴突对脑损伤的不同脆弱性，并表明无髓鞘纤维的损伤可能在与脑损伤相关的发病中发挥重要作用。 (c) 2005 Elsevier Inc. 保留所有权利。
Traumatic axonal injury (TAI), a corm-non feature of traumatic brain injury, is associated with postinjury morbidity and mortality. However, TAI is not uniformly expressed in all axonal populations, with fiber caliber and anatomical location influencing specific TAI pathology. To study differential axonal vulnerability to brain injury, axonal excitability and integrity were assessed in the corpus callosurn following fluid percussion injury in the rat. In brain slice electrophysiological recordings, compound action potentials (CAPs) were evoked in the corpus callosum, and injury effects were quantified separately for CAP waveform components generated by myelinated axons (N-2 wave) and by unmyelinated axons (N-2 wave). Ultrastructural analyses were also conducted of TAI-induced morphological changes in these axonal populations. The two populations of axons differed in response to brain injury, and in their functional recovery, during the first week postinjury. Amplitudes of N-1 and N-2 were significantly depressed at 3 h, 1 day, and 3 days survival. N-1 amplitudes exhibited a recovery to control levels by 7 days postinjury. In contrast, N-2 amplitudes were persistently suppressed through 7 days postinjury. Strength-duration properties of evoked CAPs further differentiated the effects of injury in these axonal populations, with N-2 exhibiting an elevated strength-duration time constant postinjury. Ultrastructural observations revealed degeneration of myelinated axons consistent with diffuse injury sequelae, as well as previously undocumented pathology within the unmyelinated fiber population. Collectively, these findings demonstrate differential vulnerabilities of axons to brain injury and suggest that damage to unmyelinated fibers may play a significant role in morbidity associated with brain injury. (c) 2005 Elsevier Inc. All rights reserved.