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首页> 外文期刊>The European Journal of Neuroscience >Electroconvulsive seizure restores neurogenesis and hippocampus-dependent fear memory after disruption by irradiation.
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Electroconvulsive seizure restores neurogenesis and hippocampus-dependent fear memory after disruption by irradiation.

机译：抽搐后惊厥性癫痫发作可恢复神经发生和海马依赖性恐惧记忆。

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摘要

Ongoing neurogenesis in the adult hippocampus is thought to play a role in learning and memory processes, and in response to antidepressant treatments. Low doses of irradiation (IRR) produce a significant long-lasting inhibitory effect on hippocampal neurogenesis that correlates with long-lasting behavioral deficits. Here we report that electroconvulsive seizure (ECS), which robustly increases adult neurogenesis in naive animals, also reverses the disruption of neurogenesis produced by IRR exposure. Moreover, we find that vascular endothelial growth factor (VEGF) is an essential mediator of this effect. Expression of VEGF in the granule cell layer (GCL) of the hippocampus is decreased by IRR, and ECS administration reverses this deficit in VEGF. There is a corresponding alteration in the number of endothelial cells, which express VEGF, in the hippocampal GCL following IRR and ECS. We also find that blockade of VEGF signaling attenuates ECS-induced proliferation, and VEGF infusion partially restores proliferation in irradiated animals. To examine the functional consequences of IRR and ECS on neurogenesis, hippocampus-dependent contextual fear conditioning was assessed. We found that following disruption by IRR, ECS restores contextual learning to baseline levels at time points consistent with its effects on neurogenesis. These findings demonstrate that ECS, in part via induction of VEGF, can reverse long-term neurogenesis deficits resulting from IRR, and that these effects have functional consequences on hippocampus-dependent fear memory.
机译：据认为，成年海马体中正在进行的神经发生在学习和记忆过程以及抗抑郁治疗的反应中发挥着作用。低剂量辐射（IRR）对海马神经发生产生显着的长期抑制作用，这与长期的行为缺陷有关。在这里，我们报道电惊厥性癫痫发作（ECS）可以在幼稚的动物中强有力地增加成年神经发生，还可以逆转IRR暴露所产生的神经发生破坏。此外，我们发现血管内皮生长因子（VEGF）是这种作用的重要介体。 IRR可以降低海马颗粒细胞层（GCL）中VEGF的表达，而ECS的使用可以逆转VEGF的这一缺陷。 IRR和ECS后，海马GCL中表达VEGF的内皮细胞数量发生相应变化。我们还发现，VEGF信号传导的阻滞减弱了ECS诱导的增殖，而VEGF输注可部分恢复受辐照动物的增殖。为了检查IRR和ECS对神经发生的功能影响，评估了海马依赖性情景恐惧条件。我们发现，受IRR干扰后，ECS在与其对神经发生的影响一致的时间点将上下文学习恢复到基线水平。这些发现表明，ECS部分地通过诱导VEGF可以逆转由IRR引起的长期神经发生缺陷，并且这些作用对海马依赖性恐惧记忆具有功能性影响。

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