Recovery of afferent function and synaptic strength in hippocampal CA1 following traumatic brain injury.
Recovery of afferent function and synaptic strength in hippocampal CA1 following traumatic brain injury.
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DOI：
10.1089/neu.2009.1029
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发表时间：
2009-12
影响因子：
4.2
通讯作者：
Scheff SW
中科院分区：
文献类型：
--
作者：
Norris CM;Scheff SW
脑挫裂伤48 h内可导致同侧海马CA 3区神经元部分缺失，导致向CA 1区放射层传入纤维数量成比例减少。虽然损失的传入输入CA 1表现出显着的，虽然不完全，恢复在接下来的几周内，很少有人知道突触前传入损伤后的耗尽和恢复阶段的功能状态。在这里，我们准备了海马切片从成年Sprague道利大鼠在2，7，和14天后，外侧皮质挫伤和测量纤维凌空（FV）的振幅在CA 1放射层细胞外。还测量了场兴奋性突触后电位（EPSP），并将其绘制为FV振幅的函数，以评估残留和/或再生突触接触的相对突触强度。损伤后2天，与对侧海马相比，同侧海马的FV振幅和突触强度显著降低。在同侧CA 1的FV振幅显示了7天的完全恢复，表明损伤后发芽反应。同侧CA 1的突触强度在这段时间内也显示出显著的恢复;然而，在7天和14天的时间点，EPSP-至-FV曲线仍然受到轻微抑制。尽管存在这些缺陷，同侧脑片保留了表达长时程增强的能力，表明至少有一些突触可塑性机制保持完整，或得到补偿。这些结果与解剖学证据相一致，表明在创伤性脑损伤后的最初几周内，同侧CA 1出现了深刻的传入神经阻滞，随后出现了显著的神经再支配。虽然可塑性机制似乎保持完整，在CA 1的突触强度赤字可能会限制在海马的信息吞吐量，导致持久的记忆功能障碍。
Cortical contusion injury can result in the partial loss of ipsilateral CA3 neurons within 48h, leading to a proportional reduction in the number of afferent fibers to CA1 stratum radiatum. While the loss of afferent input to CA1 exhibits a remarkable, albeit incomplete, recovery over the next few weeks, little is known about the functional status of presynaptic afferents during the depletion and recovery phases following injury. Here, we prepared hippocampal slices from adult Sprague Dawley rats at 2, 7, and 14 days after lateral cortical contusion injury and measured fiber volley (FV) amplitudes extracellularly in CA1 stratum radiatum. Field excitatory post-synaptic potentials (EPSPs) were also measured and plotted as a function of FV amplitude to assess relative synaptic strength of residual and/or regenerated synaptic contacts. At 2 days post-injury, FV amplitude and synaptic strength were markedly reduced in the ipsilateral, relative to the contralateral, hippocampus. FV amplitude in ipsilateral CA1 showed a complete recovery by 7 days, indicative of a post-injury sprouting response. Synaptic strength in ipsilateral CA1 also showed a dramatic recovery over this time; however, EPSP-to-FV curves remained slightly suppressed at both the 7 and 14 day time points. Despite these deficits, ipsilateral slices retained the capacity to express long-term potentiation, indicating that at least some mechanisms for synaptic plasticity remain intact, or are compensated for. These results are in agreement with anatomical evidence showing a profound deafferentation, followed by a remarkable re-enervation, of ipsilateral CA1 in the first few weeks after traumatic brain injury. Although plasticity mechanisms appear to remain intact, synaptic strength deficits in CA1 could limit information throughput in the hippocampus, leading to persistent memory dysfunction.
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影响因子：
3.5
作者：
Schwarzbach, E.;Bonislawski, D. P.;Cohen, A. S.
通讯作者：
Cohen, A. S.
影响因子：
4.2
作者：
Singh, Indrapal N.;Sullivan, Patrick G.;Hall, Edward D.
通讯作者：
Hall, Edward D.
影响因子：
5.3
作者：
Albensi, BC;Sullivan, PG;Mattson, MP
通讯作者：
Mattson, MP
DOI：
10.1523/jneurosci.2036-08.2008
发表时间：
2008-08-06
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Boric K;Muñoz P;Gallagher M;Kirkwood A
通讯作者：
Kirkwood A
影响因子：
6.3
作者：
Atkins, Coleen M.;Chen, Shaoyi;Hu, Bing-Ren
通讯作者：
Hu, Bing-Ren