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首页> 外文期刊>The European Journal of Neuroscience >Thalamocortical oscillations in a genetic model of absence seizures.
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Thalamocortical oscillations in a genetic model of absence seizures.

机译：失神发作的遗传模型中的丘脑皮质振荡。

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We used field potential recordings in an in vitro thalamocortical slice preparation to compare the rhythmic oscillations generated by reciprocally connected networks of the thalamus and cerebral cortex obtained from epileptic (> 160 days old) WAG/Rij and age-matched, nonepileptic control (NEC) rats. To increase neuronal excitability, and thus to elicit spontaneous field potential activity in vitro, we applied medium containing: (i) zero [Mg2+]; (ii) high [K+] (8.25 mm); or (iii) low concentrations of the K+ channel blocker 4-aminopyridine (4AP, 0.5-1 micro m). Of these procedures, only the last was effective in triggering oscillatory activity that depended on the type of tissue. Thus, during 4AP application: (i) sequences of fast (intraburst frequency 9.5-16.1 Hz) and slower (5-8.9 Hz) field potential oscillations (FPOs) were recorded in WAG/Rij slices (n = 23), but (ii) only fast FPOs were seen in NEC slices (n = 7). Slower FPOs in WAG/Rij slices reflected a larger degree of thalamocortical synchronization than fast FPOs, and disappeared after surgical separation of cortex and thalamus (n = 5); under these conditions fast FPOs continued to occur in thalamus only. In addition, fast and slower FPOs disappeared in all areas of the WAG/Rij slice during thalamic application of the excitatory amino acid receptor antagonist kynurenic acid (n = 3), while fast FPOs continued to occur in thalamus when kynurenic acid was applied to the cortex (n = 4). Bath application of the N-methyl-D-aspartic acid (NMDA) receptor antagonist 3,3-(2-carboxypiperazine-4-yl)-propyl-1-phosphonate (CPP) abolished slower FPOs in WAG/Rij cortex and thalamus (n = 6) without infuencing fast FPOs recorded in WAG/Rij (n = 6) or NEC slices (n = 4). Moreover, cortical application of CPP (n = 6) abated slower FPOs although they persisted following CPP application to the thalamus (n = 7). Our data demonstrate that highly synchronized, slower FPOs can occur during 4AP application in WAG/Rij but not in NEC slices. This activity, which mayrepresent an in vitro hallmark of thalamocortical epileptogenicity, requires the function of reciprocally connected thalamic and cortical networks and depends on cortical NMDA receptor-mediated mechanisms.
机译：我们在体外丘脑皮质切片制备中使用了场电势记录，以比较由癫痫性WAG / Rij（年龄大于160天）和年龄匹配的非癫痫性对照（NEC）获得的丘脑和大脑皮层的相互连接的网络所产生的节律性振荡大鼠。为了增加神经元的兴奋性，从而在体外引起自发的场电位活性，我们使用了含有以下物质的培养基：（i）零[Mg2 +]; （ii）[K +]高（8.25毫米）; （iii）低浓度的K +通道阻滞剂4-氨基吡啶（4AP，0.5-1微米）。在这些程序中，只有最后一个有效触发了取决于组织类型的振荡活动。因此，在4AP应用期间：（i）在WAG / Rij切片（n = 23）中记录了快速（爆发内频率9.5-16.1 Hz）和较慢（5-8.9 Hz）场电势振荡（FPO）的序列，但是（ii ）在NEC切片中仅看到快速的FPO（n = 7）。与快速FPO相比，WAG / Rij切片中较慢的FPO反映了更大程度的丘脑皮层同步性，并且在手术分离皮质和丘脑后消失了（n = 5）。在这些情况下，快速的FPO仅在丘脑中持续发生。此外，在丘脑中应用兴奋性氨基酸受体拮抗剂强尿酸（n = 3）时，WAG / Rij切片的所有区域中的快速FPO和慢速FPO均消失，而当将强尿酸酸应用于丘脑中时，快速FPO在丘脑中继续发生。皮质（n = 4）。 N-甲基-D-天冬氨酸（NMDA）受体拮抗剂3,3-（2-羧基哌嗪-4-基）-丙基-1-膦酸酯（CPP）的沐浴应用消除了WAG / Rij皮质和丘脑中较慢的FPO（ n = 6），而不会影响记录在WAG / Rij（n = 6）或NEC切片（n = 4）中的快速FPO。此外，CPP的皮质应用（n = 6）减轻了较慢的FPO，尽管它们在CPP应用于丘脑后仍然存在（n = 7）。我们的数据表明，在WAG / Rij中4AP应用期间可能发生高度同步，速度较慢的FPO，而在NEC切片中则不会。这种活性可能代表了丘脑皮质癫痫发生的体外特征，它需要相互连接的丘脑和皮质网络的功能，并取决于皮质NMDA受体介导的机制。

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