Interleukin-1β depolarizes paraventricular nucleus parvocellular neurones
Interleukin-1β depolarizes paraventricular nucleus parvocellular neurones
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DOI：
10.1046/j.1365-2826.2003.00870.x
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发表时间：
2003-02-01
影响因子：
3.2
通讯作者：
Ferguson, AV
中科院分区：
文献类型：
--
作者：
Ferri, CC;Ferguson, AV
白细胞介素-1 β（IL-1 β）参与下丘脑促肾上腺皮质激素释放激素（CRH）分泌的调节以及随后的神经免疫应答的下游调节。在这项研究中，全细胞膜片钳记录大鼠下丘脑室旁核（PVN）的切片制备的小细胞神经元，检查IL-1 β的细胞效应。响应于1 nm IL-1 β，65%的小细胞神经元测试表现出明确的去极化，这是在河豚毒素（TTX）的存在下被废除。这种去极化部分依赖于一氧化氮的形成，如在N -ω-硝基-L-精氨酸甲酯（一氧化氮合酶抑制剂）存在下反应的衰减所证明的。IL-1 β对反应性小细胞神经元的作用与抑制性突触后电位（IPSPs）频率的降低有关。荷包牡丹碱给药阻断了IL-1 β的作用，表明这种细胞因子调节GABA能输出，导致抑制性输入（IPSPs）减少和随后的去极化。这些数据支持的结论是，IL-1 β影响PVN的小细胞神经元的兴奋性，作为一氧化氮的产生和GABA能抑制输入这些细胞的调制的次要后果。他们阐明了下丘脑室旁核中IL-1 β的神经免疫作用的细胞相关性。
Interleukin-1beta (IL-1beta ) is involved in hypothalamic regulation of corticotropin releasing hormone (CRH) secretion and consequent downstream modulation of the neuroimmune response. In this study, whole-cell patch clamp recordings of rat parvocellular neurones in a slice preparation of the paraventricular nucleus (PVN) of the hypothalamus were performed to examine the cellular effects of IL-1beta . In response to 1 nm IL-1beta , 65% of parvocellular neurones tested exhibited a clear depolarization, which was abolished in the presence of tetrodotoxin (TTX). This depolarization was partially dependent on nitric oxide formation, as demonstrated by attenuation of the response in the presence of N -omega-nitro-l-arginine methylester, a nitric oxide synthase inhibitor. The effects of IL-1beta on responsive parvocellular neurones were associated with a decrease in the frequency of inhibitory post synaptic potentials (IPSPs). Bicuculline administration blocked the effects of IL-1beta , suggesting that this cytokine modulates GABA-ergic output, resulting in a decrease in inhibitory input (IPSPs) and consequent depolarization. These data support the conclusion that IL-1beta influences the excitability of parvocellular neurones in the PVN, as a secondary consequence of nitric oxide generation and modulation of GABAergic inhibitory input to these cells. They elucidate cellular correlates underlying the well-established neuroimmune roles of IL-1beta in the paraventricular nucleus of the hypothalamus.