Interleukin-1beta release in the supraoptic nucleus area during osmotic stimulation requires neural function.

Interleukin-1beta release in the supraoptic nucleus area during osmotic stimulation requires neural function.
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DOI:
10.1111/j.1365-2826.2008.01783.x
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发表时间:
2008-11
影响因子:
3.2
通讯作者:
Phillips TM
Phillips TM
中科院分区:
医学3区
文献类型:
--
作者:
Summy-Long JY;Hu S;Long A;Phillips TM

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白细胞介素-1 β(IL-1β)存在于整个大细胞神经内分泌系统中,并在盐负荷期间与来自神经叶的催产素和加压素共同消耗。为了检测在渗透刺激过程中大细胞神经元的树突/索马是否释放IL-1β,将清醒大鼠视上核(SON)附近的微透析与免疫毛细管电泳和激光诱导荧光检测相结合,以定量在皮下注射高渗盐水之前(0-180 min;基础)和之后(180-240 min)收集的5 min透析液中的细胞因子。(1.5 M NaCl)。在抑制Na+(河豚毒素; TTX)和Ca 2+(镉和镍)的局部电压门控通道或通过减少细胞内Ca 2+储存(毒胡萝卜素)后,比较了IL-1β的渗透释放。免疫组化结合微透析技术定位细胞因子(IL-1β+)和小胶质细胞(OX-42+)。在微透析条件下,SON区IL-1β+的基础释放是可测量的和稳定的0-60 min(pg/ml;平均值± SEM)(2.2 ± 0.06),60-120 min(2.32 ± 0.05)和120-180 min(2.33 ± 0.06),可能局部来源于活化的小胶质细胞(OX 42 +; IL-1β+;阿米巴样,肥大)和表达IL-1β的大细胞神经元。在对渗透刺激的反应中,IL-1β在SON区域的透析液中通过依赖于对毒胡萝卜素敏感的细胞内Ca 2+储存的机制进行性增加,并且与催产素和加压素的树突分泌类似,需要局部电压门控Na+和Ca 2+通道通过前脑的神经调节途径激活。在渗透刺激过程中,SON区域中IL-1β的神经依赖性释放可能上调大细胞神经元上的神经敏感性阳离子电流(由其他人在体外观察到),以促进神经垂体激素的树突释放。
Interleukin-1β (IL-1β) is present throughout the magnocellular neuroendocrine system and co-depletes with oxytocin and vasopressin from the neural lobe during salt-loading. To examine if IL-1β is released from the dendrites/soma of magnocellular neurons during osmotic stimulation, microdialysis adjacent to the supraoptic nucleus (SON) in conscious rats was combined with immunocapillary electrophoresis and laser-induced fluorescence detection to quantify cytokine in 5 min dialysates collected before (0-180 min; basal), and after (180-240 min), hypertonic saline injected s.c. (1.5 M NaCl). Osmotic release of IL-1β was compared after inhibiting local voltage-gated channels for Na+ (tetrodotoxin; TTX) and Ca2+ (cadmium and nickel) or by reducing intracellular Ca2+ stores (thapsigargin). Immunohistochemistry combined with microdialysis was used to localize cytokine sources (IL-1β+) and microglia (OX-42+). Under conditions of microdialysis, basal release of IL-1β+ in the SON area was measurable and stable (pg/ml; mean ± SEM) from 0-60 min (2.2 ± 0.06), 60-120 min (2.32 ± 0.05) and 120-180 min (2.33 ± 0.06), likely originating locally from activated microglia (OX42+; IL-1β+; ameboid, hypertrophied) and magnocellular neurons expressing IL-1β. In response to osmotic stimulation, IL-1β increased progressively in dialysates of the SON area by a mechanism dependent on intracellular Ca2+ stores sensitive to thapsigargin and, similar to dendritic secretion of oxytocin and vasopressin, required local voltage-gated Na+ and Ca2+ channels for activation by osmoregulatory pathways from the forebrain. During osmotic stimulation, neurally dependent release of IL-1β in the SON area likely upregulates osmosensitive cation currents on magnocellular neurons (observed in vitro by others), to facilitate dendritic release of neurohypophysial hormones.
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