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钠欲发生中的分子神经生物学标记物。

Molecular neurobiological markers in the onset of sodium appetite.

机构信息

Instituto de Investigación Médica Mercedes y Martín Ferreyra (INIMEC-CONICET-Universidad Nacional de Córdoba), Friuli 2434, Barrio Parque Vélez Sarsfield, Casilla de Correo, 389-5000, 5016, Córdoba, Provincia de Córdoba, Argentina.

Departamento de Biología Bucal, Facultad de Odontología, Universidad Nacional de Córdoba, Córdoba, Argentina.

出版信息

Sci Rep. 2022 Aug 20;12(1):14224. doi: 10.1038/s41598-022-18220-w.

DOI:10.1038/s41598-022-18220-w
PMID:35987984
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9392805/
Abstract

Sodium appetite is a motivational state involving homeostatic behavior, seeking the ingest of salty substances after sodium loss. There is a temporal dissociation between sodium depletion (SD) and the appearance of sodium appetite. However, the responsible mechanisms for this delay remain poorly elucidated. In the present study, we measured the temporal changes at two and 24 h after SD in the gene expression of key elements within excitatory, inhibitory, and sensory areas implicated in the signaling pathways involved in the onset of sodium appetite. In SD rats, we observed that the expression of critical components within the brain control circuit of sodium appetite, including Angiotensin-type-1 receptor (Agtr1a), Oxytocin-(OXT-NP)-neurophysin-I, and serotonergic-(5HT)-type-2c receptor (Htr2c) were modulated by SD, regardless of time. However, we observed reduced phosphorylation of mitogen-activated protein kinases (MAPK) at the paraventricular nucleus (PVN) and increased oxytocin receptor (Oxtr) mRNA expression at the anteroventral of the third ventricle area (AV3V), at two hours after SD, when sodium appetite is inapparent. At twenty-four hours after SD, when sodium appetite is released, we observed a reduction in the mRNA expression of the transient receptor potential channel 1gene (Trpv1) and Oxtr in the AV3V and the dorsal raphe nucleus, respectively. The results indicate that SD exerts a coordinated timing effect, promoting the appearance of sodium appetite through changes in MAPK activity and lower Trpv1 channel and Oxtr expression that trigger sodium consumption to reestablish the hydroelectrolytic homeostasis.

摘要

钠欲是一种涉及体内平衡行为的动机状态，即在钠丢失后寻求摄入咸物质。钠耗竭（SD）和钠欲出现之间存在时间分离。然而，这种延迟的负责机制仍未得到充分阐明。在本研究中，我们测量了 SD 后 2 和 24 小时关键元素的基因表达的时间变化，这些元素涉及到参与钠欲发作的信号通路中的兴奋性、抑制性和感觉区域。在 SD 大鼠中，我们观察到，包括血管紧张素 1 型受体（Agtr1a）、催产素（OXT-NP）-神经垂体 I 和 5-羟色胺（5HT）-2c 型受体（Htr2c）在内的钠欲大脑控制回路的关键组成部分的表达，都受到 SD 的调节，无论时间如何。然而，我们观察到，在 SD 后两小时，当钠欲不明显时，室旁核（PVN）的丝裂原激活蛋白激酶（MAPK）磷酸化减少，前脑室下第三脑室区（AV3V）的催产素受体（Oxtr）mRNA 表达增加。在 SD 后 24 小时，当钠欲释放时，我们观察到 AV3V 和背侧中缝核中瞬时受体电位通道 1 基因（Trpv1）和 Oxtr 的 mRNA 表达分别减少。结果表明，SD 产生了协调的定时效应，通过改变 MAPK 活性和降低触发钠消耗以恢复水电解质平衡的 Trpv1 通道和 Oxtr 表达，促进钠欲的出现。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af86/9392805/befdc40fd438/41598_2022_18220_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af86/9392805/0cc8717fcc8e/41598_2022_18220_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af86/9392805/b5b9b126ef99/41598_2022_18220_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af86/9392805/3ead29b947bc/41598_2022_18220_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af86/9392805/4ea46c47d0bb/41598_2022_18220_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af86/9392805/5b145bac78fc/41598_2022_18220_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af86/9392805/befdc40fd438/41598_2022_18220_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af86/9392805/0cc8717fcc8e/41598_2022_18220_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af86/9392805/b5b9b126ef99/41598_2022_18220_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af86/9392805/3ead29b947bc/41598_2022_18220_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af86/9392805/4ea46c47d0bb/41598_2022_18220_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af86/9392805/5b145bac78fc/41598_2022_18220_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af86/9392805/befdc40fd438/41598_2022_18220_Fig7_HTML.jpg

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