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外侧臂旁核传入通路的激活与钠欲调节中的内分泌反应。

Activation of lateral parabrachial afferent pathways and endocrine responses during sodium appetite regulation.

机构信息

Instituto de Investigación Médica Mercedes y Martín Ferreyra (INIMEC-CONICET), Casilla de Correo 389-5000, Córdoba, Argentina.

出版信息

Exp Neurol. 2010 Feb;221(2):275-84. doi: 10.1016/j.expneurol.2009.11.001. Epub 2009 Nov 11.

DOI:10.1016/j.expneurol.2009.11.001
PMID:19913016
Abstract

Modulation of salt appetite involves interactions between the circumventricular organs (CVOs) receptive areas and inhibitory hindbrain serotonergic circuits. Recent studies provide support to the idea that the serotonin action in the lateral parabrachial nucleus (LPBN) plays an important inhibitory role in the modulation of sodium appetite. The aim of the present work was to identify the specific groups of neurons projecting to the LPBN that are activated in the course of sodium appetite regulation, and to analyze the associated endocrine response, specifically oxytocin (OT) and atrial natriuretic peptide (ANP) plasma release, since both hormones have been implicated in the regulatory response to fluid reestablishment. For this purpose we combined the detection of a retrograde transported dye, Fluorogold (FG) injected into the LPBN with the analysis of the Fos immunocytochemistry brain pattern after sodium intake induced by sodium depletion. We analyzed the Fos-FG immunoreactivity after sodium ingestion induced by peritoneal dialysis (PD). We also determined OT and ANP plasma concentration by radioimmunoassay (RIE) before and after sodium intake stimulated by PD. The present study identifies specific groups of neurons along the paraventricular nucleus, central extended amygdala, insular cortex, dorsal raphe nucleus, nucleus of the solitary tract and the CVOs that are activated during the modulation of sodium appetite and have direct connections with the LPBN. It also shows that OT and ANP are released during the course of sodium satiety and fluid reestablishment. The result of this brain network activity may enable appropriate responses that re-establish the body fluid balance after induced sodium consumption.

摘要

盐欲的调节涉及到室周器官(CVOs)感受区域和抑制性脑桥后血清素能回路之间的相互作用。最近的研究支持了这样一种观点,即侧臂旁核(LPBN)中的血清素作用在钠欲调节中发挥重要的抑制作用。本研究的目的是确定在钠欲调节过程中被激活的投射到 LPBN 的特定神经元群,并分析相关的内分泌反应,特别是催产素(OT)和心钠素(ANP)的血浆释放,因为这两种激素都与液体再建立的调节反应有关。为此,我们将 LPBN 中注射的逆行转运染料 Fluorogold(FG)的检测与钠摄入诱导的钠耗竭后 Fos 免疫细胞化学脑图谱的分析结合起来。我们分析了腹膜透析(PD)诱导的钠摄入后 Fos-FG 免疫反应性。我们还通过放射免疫分析(RIE)在 PD 刺激的钠摄入前后测定 OT 和 ANP 的血浆浓度。本研究确定了在钠欲调节过程中被激活的沿室旁核、中央扩展杏仁核、岛叶皮质、中缝背核、孤束核和 CVOs 的特定神经元群,它们与 LPBN 直接相连。它还表明,OT 和 ANP 在钠饱腹感和液体再建立过程中释放。该脑网络活动的结果可能使机体在诱导性钠摄入后能够对重新建立体液平衡做出适当的反应。

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