Homeostatic increase in excitability in area CA1 after Schaffer collateral transection in vivo.
Homeostatic increase in excitability in area CA1 after Schaffer collateral transection in vivo.
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DOI：
10.1111/j.1528-1167.2011.03113.x
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发表时间：
2011-09
期刊：
影响因子：
5.6
通讯作者：
Thompson SM
中科院分区：
文献类型：
--
作者：
Dinocourt C;Aungst S;Yang K;Thompson SM
癫痫是创伤性脑损伤（TBI）的重要长期后果，可能由多种机制引起。许多形式的TBI的共同特征是去神经支配。我们问是否在体内慢性部分去神经支配将导致一个稳态增加的兴奋性去神经细胞群体。为了回答这个问题，我们利用了海马体的独特解剖结构，其中输入到CA1神经元的Schaffer侧支可以在体内被横切，保留其输出并且只有轻微的细胞死亡。我们观察到神经元兴奋性的延迟增加，明显的细胞外记录从海马脑片制备14天（而不是3天）postlesion。虽然在休息条件下，从控制和病变动物的切片中的人口尖峰是可比的，应用的解决方案，是轻度的惊厥（高K+，低Mg2+，低浓度的荷包牡丹碱）产生的数量增加的人口尖峰从病变大鼠的切片，但不是在切片从unlestered假对照。去神经支配没有引起GABA能突触抑制的几个标志物的变化，包括GABA能神经元的数量、α1 GABAA受体亚单位、囊泡GABA转运体或微型抑制性突触后电流。我们的结论是，慢性部分失神经支配确实会导致神经元兴奋性的延迟稳态增加，因此可能有助于创伤性脑损伤的长期神经学后果。
Epilepsy is a significant long-term consequence of traumatic brain injury (TBI) and is likely to result from multiple mechanisms. One feature that is common to many forms of TBI is denervation. We asked whether chronic partial denervation in vivo would lead to a homeostatic increase in the excitability of a denervated cell population. To answer this question, we took advantage of the unique anatomy of the hippocampus where the input to the CA1 neurons, the Schaffer collaterals, could be transected in vivo with preservation of their outputs and only minor cell death. We observed a delayed increase in neuronal excitability, as apparent in extracellular recordings from hippocampal brain slices prepared 14 days (but not 3 days) postlesion. Although population spikes in slices from control and lesioned animals were comparable under resting conditions, application of solutions that were mildly proconvulsive (high K+, low Mg2+, low concentrations of bicuculline) produced increases in the number of population spikes in slices from lesioned rats, but not in slices from unlesioned sham controls. Denervation did not produce changes in several markers of GABAergic synaptic inhibition, including the number of GABAergic neurons, α1 GABAA receptor subunits, the vesicular GABA transporter, or miniature inhibitory postsynaptic currents. We conclude that chronic partial denervation does lead to a delayed homeostatic increase in neuronal excitability, and may therefore contribute to the long-term neurological consequences of traumatic brain injury.
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影响因子：
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