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首页> 美国卫生研究院文献>The Journal of Neuroscience >Histaminergic Neurons Protect the Developing Hippocampus from Kainic Acid-Induced Neuronal Damage in an Organotypic Coculture System
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Histaminergic Neurons Protect the Developing Hippocampus from Kainic Acid-Induced Neuronal Damage in an Organotypic Coculture System

机译：组胺能神经元在器官型共培养系统中保护海马发育免受海藻酸诱导的神经元损害

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The central histaminergic neuron system inhibits epileptic seizures, which is suggested to occur mainly through histamine 1 (H1) and histamine 3 (H3) receptors. However, the importance of histaminergic neurons in seizure-induced cell damage is poorly known. In this study, we used an organotypic coculture system and confocal microscopy to examine whether histaminergic neurons, which were verified by immunohistochemistry, have any protective effect on kainic acid (KA)-induced neuronal damage in the developing hippocampus. Fluoro-Jade B, a specific marker for degenerating neurons, indicated that, after the 12 h KA (5 μm) treatment, neuronal damage was significantly attenuated in the hippocampus cultured together with the posterior hypothalamic slice containing histaminergic neurons [HI plus HY (POST)] when compared with the hippocampus cultured alone (HI) or with the anterior hypothalamus devoid of histaminergic neurons. Moreover, α-fluoromethylhistidine, an inhibitor of histamine synthesis, eliminated the neuroprotective effect in KA-treated HI plus HY (POST), and extracellularly applied histamine (1 nm to 100 μm) significantly attenuated neuronal damage only at 1 nm concentration in HI. After the 6 h KA treatment, spontaneous electrical activity registered in the CA1 subregion contained significantly less burst activity in HI plus HY (POST) than in HI. Finally, in KA-treated slices, the H3 receptor antagonist thioperamide enhanced the neuroprotective effect of histaminergic neurons, whereas the H1 receptor antagonists triprolidine and mepyramine dose-dependently decreased the neuroprotection in HI plus HY (POST). Our results suggest that histaminergic neurons protect the developing hippocampus from KA-induced neuronal damage, with regulation of neuronal survival being at least partly mediated through H1 and H3 receptors.
机译：中枢组胺能神经元系统抑制癫痫发作，这主要通过组胺1（H1）和组胺3（H3）受体发生。然而，人们对组胺能神经元在癫痫发作诱导的细胞损伤中的重要性知之甚少。在这项研究中，我们使用器官型共培养系统和共聚焦显微镜检查了经免疫组织化学验证的组胺能神经元是否对海藻酸（KA）引起的海马神经元损伤具有任何保护作用。 Fluoro-Jade B是使神经元退化的特异性标志物，它表明，在12 h KA（5μm）处理后，与含有组胺能神经元的下丘脑后片一起培养的海马中，神经元损伤显着减弱[HI + HY（POST ）]与单独培养的海马（HI）或下丘脑前部无组胺能神经元相比。而且，α-氟甲基组氨酸，一种组胺合成抑制剂，消除了在KA处理的HI加HY（POST）中的神经保护作用，并且细胞外施用的组胺（1 nm至100μm）仅在HI中浓度为1 nm时才显着减轻神经元损伤。 KA处理6小时后，在HI加HY（POST）中，在CA1子区域中记录的自发电活动比在HI中具有明显更少的爆发活动。最后，在KA处理过的切片中，H3受体拮抗剂硫代过酰胺增强了组胺能神经元的神经保护作用，而H1受体拮抗剂曲普立定和美吡拉明剂量依赖性地降低了HI加HY（POST）的神经保护作用。我们的结果表明，组胺能神经元可以保护发育中的海马免受KA诱导的神经元损害，并通过H1和H3受体至少部分介导神经元存活的调节。

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