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首页> 外文期刊>The European Journal of Neuroscience >Synchronous GABA-receptor-dependent potentials in limbic areas of the in-vitro isolated adult guinea pig brain.
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Synchronous GABA-receptor-dependent potentials in limbic areas of the in-vitro isolated adult guinea pig brain.

机译：体外分离的成年豚鼠脑边缘区域的同步GABA受体依赖性电位。

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Epileptiform discharges are known to reflect the hypersynchronous glutamatergic activation of cortical neurons. However, experimental evidence has revealed that epileptiform synchronization is also contributed to by population events mediated by GABA(A) receptors. Here, we analysed the spatial distribution of GABA(A)-receptor-dependent interictal events in the hippocampal/parahippocampal region of the adult guinea pig brain isolated in vitro. We found that arterial perfusion of this preparation with 4-aminopyridine caused the appearance of glutamatergic-independent interictal potentials that were reversibly abolished by GABA(A) receptor antagonism. Laminar profiles and current source density analysis performed in different limbic areas demonstrated that these GABA(A)-receptor-mediated events were independently generated in different areas of the hippocampal/parahippocampal formation (most often in the medial entorhinal cortex) and propagated between interconnected limbic structures of both hemispheres.Finally, intracellular recordings from principal neurons of the medial entorhinal cortex demonstrated that the GABAergic field potential correlated to inhibitory postsynaptic potentials (membrane potential reversal, -68.12 +/- 8.01 mV, n = 5) that were interrupted by ectopic spiking. Our findings demonstrate that, in an acute seizure model developed in the adult guinea pig brain, hypersynchronous GABA(A)-receptor-mediated interictal events are generated from independent sources and propagate within limbic cortices in the absence of excitatory synaptic transmission. As spared or enhanced inhibition was reported in models of epilepsy, our data may support a role of GABA-mediated signaling in ictogenesis and epileptogenesis.
机译：已知癫痫样放电可反映皮质神经元的超同步谷氨酸能激活。但是，实验证据表明，癫痫样同步也归因于GABA（A）受体介导的群体事件。在这里，我们分析了成年豚鼠脑离体分离的海马/海马区GABA（A）受体依赖间质事件的空间分布。我们发现该制剂与4-氨基吡啶的动脉灌注引起了与谷氨酸能无关的发作间期电位的出现，该电位被GABA（A）受体拮抗作用可逆地消除。在不同边缘区域进行的层流剖面和电流源密度分析表明，这些GABA（A）-受体介导的事件是在海马/海马旁形成的不同区域（最常在内侧内嗅皮层）独立产生的，并在相互连接的边缘之间传播最后，内侧内嗅皮层主要神经元的细胞内记录表明，GABA能场电位与抑制性突触后电位（膜电位反转，-68.12 +/- 8.01 mV，n = 5）相关，被异位干扰尖刺。我们的发现表明，在成年豚鼠大脑中形成的急性癫痫发作模型中，超同步GABA（A）受体介导的间质事件是由独立来源产生的，并且在没有兴奋性突触传递的情况下在边缘皮质内传播。由于在癫痫模型中已有关于抑制或增强抑制作用的报道，我们的数据可能支持GABA介导的信号在信息生成和癫痫发生中的作用。

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