The 4-aminopyridine in vitro epilepsy model analyzed with a perforated multi-electrode array.

The 4-aminopyridine in vitro epilepsy model analyzed with a perforated multi-electrode array.
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使用穿孔多电极阵列分析 4-氨基吡啶体外癫痫模型。

DOI:
10.1016/j.neuropharm.2010.10.007
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发表时间:
2011-06
期刊:
影响因子:
4.7
通讯作者:
Dzakpasu, Rhonda
Dzakpasu, Rhonda
中科院分区:
医学2区
文献类型:
--
作者:
Gonzalez-Sulser, Alfredo;Wang, Jing;Motamedi, Gholam K.;Avoli, Massimo;Vicini, Stefano;Dzakpasu, Rhonda

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在4-氨基吡啶(4-AP)的体外癫痫模型中记录到的癫痫样放电是由谷氨酸和GABA能信号介导的。使用60通道穿孔多电极阵列(PMEA)在2-3周龄小鼠的皮质海马片上记录发作间期和发作样事件。当谷氨酸能传递被阻断时,发作间样事件不再起始于门区或CA3/CA1锥体层,而是起源于齿状回颗粒和分子层。此外,发作间样事件的频率减少,持续时间在这些区域增加,而皮质放电完全被阻断。GABAA受体阻断后,发作间样事件不再传播到齿状回,但在CA3区的出现频率增加;此外,发作样皮层事件变短,出现频率增加。最后,影响强直和突触GABA能电导的药物调节发作间歇性事件的频率、持续时间、启动和传播。这些发现证实并扩展了先前的研究,这些研究表明多种突触机制有助于前脑结构中神经元网络活动的同步。
Epileptiform discharges recorded in the 4-aminopyridine (4-AP) in vitro epilepsy model are mediated by glutamatergic and GABAergic signaling. Using a 60-channel perforated multi-electrode array (pMEA) on corticohippocampal slices from 2 to 3 week old mice we recorded interictal- and ictal-like events. When glutamatergic transmission was blocked, interictal-like events events no longer initiated in the hilus or CA3/CA1 pyramidal layers but originated from the dentate gyrus granule and molecular layers. Furthermore, frequencies of interictal-like events were reduced and durations were increased in these regions while cortical discharges were completely blocked. Following GABAA receptor blockade interictal-like events no longer propagated to the dentate gyrus while their frequency in CA3 increased; in addition, ictal-like cortical events became shorter while increasing in frequency. Lastly, drugs that affect tonic and synaptic GABAergic conductance modulate the frequency, duration, initiation and propagation of interictal-like events. These findings confirm and expand on previous studies indicating that multiple synaptic mechanisms contribute to synchronize neuronal network activity in forebrain structures.
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