PDF(Pubmed)
Abstract：
Major burdens for patients suffering from stroke are cognitive co-morbidities and epileptogenesis. Neural network disinhibition and deficient inhibitive pulses for fast network activities may result from impaired presynaptic release of the inhibitory neurotransmitter GABA. To test this hypothesis, a cortical photothrombotic stroke was induced in Sprague Dawley rats, and inhibitory currents were recorded seven days later in the peri-infarct blood-brain barrier disrupted (BBBd) hippocampus via patch-clamp electrophysiology in CA1 pyramidal cells (PC). Miniature inhibitory postsynaptic current (mIPSC) frequency was reduced to about half, and mIPSCs decayed faster in the BBBd hippocampus. Furthermore, the paired-pulse ratio of evoked GABA release was increased at 100 Hz, and train stimulations with 100 Hz revealed that the readily releasable pool (RRP), usually assumed to correspond to the number of tightly docked presynaptic vesicles, is reduced by about half in the BBBd hippocampus. These pathophysiologic changes are likely to contribute significantly to disturbed fast oscillatory activity, like cognition-associated gamma oscillations or sharp wave ripples and epileptogenesis in the BBBd hippocampus.
摘要：
中风患者的主要负担是认知共病和癫痫发生。用于快速网络活动的神经网络去抑制和抑制脉冲不足可能是由于抑制性神经递质GABA的突触前释放受损所致。为了检验这个假设，在SpragueDawley大鼠中诱发皮质光血栓性中风，7天后通过膜片钳电生理学在CA1锥体细胞（PC）中记录梗死周围血脑屏障破坏（BBBd）海马的抑制电流。微型抑制性突触后电流（mIPSC）频率降低到大约一半，mIPSCs在BBBd海马中衰减更快。此外，诱发GABA释放的成对脉冲比在100Hz时增加，和训练刺激与100赫兹显示，容易释放池（RRP），通常假定与紧密对接的突触前囊泡的数量相对应，在BBBd海马中减少了大约一半。这些病理生理变化可能会显著导致快速振荡活动受到干扰，例如与认知相关的伽马振荡或尖锐的波波纹和BBBd海马中的癫痫发生。
