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首页> 外文期刊>The European Journal of Neuroscience >Synaptic and non-synaptic mechanisms of amygdala recruitment into temporolimbic epileptiform activities.
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Synaptic and non-synaptic mechanisms of amygdala recruitment into temporolimbic epileptiform activities.

机译：杏仁核募集进入颞下肢癫痫样活动的突触和非突触机制。

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Lateral amygdala (LA) activity during synchronized-epileptiform discharges in temporolimbic circuits was investigated in rat horizontal slices containing the amygdala, hippocampus (Hip), perirhinal (Prh) and lateral entorhinal (LEnt) cortex, through multiple-site extra- and intracellular recording techniques and measurement of the extracellular K+ concentration. Application of 4-aminopyridine (50 micro m) induced epileptiform discharges in all regions under study. Slow interictal-like burst discharges persisted in the Prh/LEnt/LA after disconnection of the Hip, seemed to originate in the Prh as shown from time delay analyses, and often preceded the onset of ictal-like activity. Disconnection of the amygdala resulted in de-synchronization of epileptiform discharges in the LA from those in the Prh/LEnt. Interictal-like activity was intracellularly reflected in LA projection neurons as gamma-aminobutyric acid (GABA)A/B receptor-mediated synaptic responses, and depolarizing electrogenic events (spikelets) residing on the initial phase of the GABA response. Spikelets were considered antidromically conducted ectopic action potentials generated at axon terminals, as they were graded in amplitude, were not abolished through hyperpolarizing membrane responses (which effectively blocked evoked orthodromic action potentials), lacked a clear prepotential or synaptic potential, were not affected through blockers of gap junctions, and were blocked through remote application of tetrodotoxin at putative target areas of LA projection neurons. Remote application of a GABAB receptor antagonist facilitated spikelet generation. A transient elevation in the extracellular K+ level averaging 3 mm above baseline occurred in conjunction with interictal-like activity in all areas under study. We conclude that interictal-like discharges in the LA/LEnt/Prh spread in a predictable manner through the synaptic network with the Prh playing a leading role. The rise in extracellular K+ may provide a depolarizing mechanism for recruitment ofinterneurons and generation of ectopic action potentials at axon terminals of LA projection neurons. Antidromically conducted ectopic action potentials may provide a spreading mechanism of seizure activity mediated by diffuse axonal projections of LA neurons.
机译：通过多位细胞外和细胞内记录，在包含杏仁核，海马（Hip），皮层（Prh）和外侧内啡肽（LEnt）皮质的大鼠水平切片中，研究了颞睑回路同步癫痫样放电过程中的外侧杏仁核（LA）活动技术和细胞外K +浓度的测量。在研究的所有区域中应用4-氨基吡啶（50微米）引起的癫痫样放电。 Hip断开后，Prh / LEnt / LA中缓慢的发作期样爆裂放电持续存在，如时间延迟分析所示，似乎起源于Prh，通常早于发作样样活动。杏仁核的断开导致LA中的癫痫样放电与Prh / LEnt中的癫痫样放电不同步。间隔间样活性在细胞内反映为γ-氨基丁酸（GABA）A / B受体介导的突触反应，并在GABA反应的初始阶段消退电事件（小尖峰）。小穗被认为是抗轴突传导的在轴突末端产生的异位动作电位，因为它们的幅度是分级的，不会通过超极化膜反应而被消除（有效地阻断了诱发的正畸动作电位），缺乏明确的电位或突触电位，不会受到阻断剂的影响间隙连接，并通过远程应用河豚毒素在洛杉矶投射神经元的假定目标区域被阻止。 GABA B受体拮抗剂的远程应用促进了小穗的产生。在研究的所有区域中，细胞外K +的平均水平平均升高了3 mm以上，并伴有发作间期样的活动。我们得出的结论是，LA / LEnt / Prh中的间隙样放电通过可突触网络以可预测的方式传播，其中Prh起主导作用。细胞外K +的增加可能为去中间神经元募集和在LA投射神经元轴突末端产生异位作用电位提供了去极化机制。对抗性地传导的异位动作电位可提供由LA神经元弥漫性轴突投射介导的癫痫发作活动的传播机制。

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