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首页> 外文期刊>BMC Neuroscience >Causal relationship of CA3 back-projection to the dentate gyrus and its role in CA1 fast ripple generation
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Causal relationship of CA3 back-projection to the dentate gyrus and its role in CA1 fast ripple generation

机译：CA3背部投影对仪式回到的因果关系及其在CA1快速纹波中的作用

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Pathophysiological evidence from temporal lobe epilepsy models highlights the hippocampus as the most affected structure due to its high degree of neuroplasticity and control of the dynamics of limbic structures, which are necessary to encode information, conferring to it an intrinsic epileptogenicity. A loss in this control results in observable oscillatory perturbations called fast ripples, in epileptic rats those events are found in CA1, CA3, and the dentate gyrus (DG), which are the principal regions of the trisynaptic circuit of the hippocampus. The present work used Granger causality to address which relationships among these three regions of the trisynaptic circuit are needed to cause fast ripples in CA1 in an in vivo model. For these purposes, male Wistar rats (210–300?g) were injected with a single dose of pilocarpine hydrochloride (2.4?mg/2?μl) into the right lateral ventricle and video-monitored 24?h/day to detect spontaneous and recurrent seizures. Once detected, rats were implanted with microelectrodes in these regions (fixed-recording tungsten wire electrodes, 60-μm outer diameter) ipsilateral to the pilocarpine injection. A total of 336 fast ripples were recorded and probabilistically characterized, from those fast ripples we made a subset of all the fast ripple events associated with sharp-waves in CA1 region (n?=?40) to analyze them with Granger Causality. Our results support existing evidence in vitro in which fast ripple events in CA1 are initiated by CA3 multiunit activity and describe a general synchronization in the theta band across the three regions analyzed DG, CA3, and CA1, just before the fast ripple event in CA1 have begun. This in vivo study highlights the causal participation of the CA3 back-projection to the DG, a connection commonly overlooked in the trisynaptic circuit, as a facilitator of a closed-loop among these regions that prolongs the excitatory activity of CA3. We speculate that the loss of inhibitory drive of DG and the mechanisms of ripple-related memory consolidation in which also the CA3 back-projection to DG has a fundamental role might be underlying processes of the fast ripples generation in CA1.
机译：来自颞叶癫痫模型的病理生理学证据突出了海马作为受影响最大的结构，由于其高度的神经塑性和肢体结构动态的控制，这是编码信息所必需的，赋予其内在癫痫发作性。该对照中的损失导致可观察到的振荡扰动，称为快速涟漪，在癫痫大鼠中，在Ca1，Ca 3和齿状回收（Dg）中发现这些事件，其是海马触翼电路的主要区域。目前的工作使用了GRANGER因果关系来解决这三个区域之间的这种关系，需要在体内模型中引起CA1中的快速涟漪。对于这些目的，将雄性Wistar大鼠（210-300〜G）用一体剂量的盐酸盐（2.4Ω·mg / 2μl）注射到右侧肠道肠道和视频监测的24℃/天中以检测自发性和经常癫痫发作。一旦检测到，将大鼠植入这些区域中的微电极（固定记录钨丝电极，60μm外径）同侧到汲取燃料喷射。记录了336个快速涟漪和概率的特征，从那些快速涟漪中，我们制造了与CA1区域中的尖锐波相关的所有快速纹波事件的子集（n？=Δ40），以分析它们与格兰杰因果关系。我们的结果支持在体外的现有证据中，CA1中的快速纹波事件由CA3 Multiunit活动启动，并描述在CA1中的快速纹波事件之前的三个区域跨越DG，CA3和CA1的Theta频段中的一般同步开始。这在体内研究中强调了CA3背部投影对DG的因果关系，通常俯视在触翼电路中的连接，作为延长CA3兴奋活性的这些区域中的闭环的辅导器。我们推测DG的抑制驱动的损失和纹波相关的存储器固结机制，其中CA3对DG的CA3背部投影具有基本作用，可能是CA1中的快速涟漪产生的基础过程。

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