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长期恢复的双侧膈下迷走神经切断大鼠下丘脑神经化学变化

Hypothalamic Neurochemical Changes in Long-Term Recovered Bilateral Subdiaphragmatic Vagotomized Rats.

作者信息

Kobrzycka Anna Teresa, Stankiewicz Adrian Mateusz, Goscik Joanna, Gora Monika, Burzynska Beata, Iwanicka-Nowicka Roksana, Pierzchala-Koziec Krystyna, Wieczorek Marek

机构信息

Department of Neurobiology, Faculty of Biology and Environmental Protection, University of Łodz, Łodz, Poland.

Department of Molecular Biology, Institute of Genetics and Animal Biotechnology, Polish Academy of Sciences, Jastrzebiec, Poland.

出版信息

Front Behav Neurosci. 2022 Jul 8;16:869526. doi: 10.3389/fnbeh.2022.869526. eCollection 2022.

DOI:10.3389/fnbeh.2022.869526
PMID:35874650
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9304976/
Abstract

BACKGROUND

Vagus nerve is one of the crucial routes in communication between the immune and central nervous systems. The impaired vagal nerve function may intensify peripheral inflammatory processes. This effect subsides along with prolonged recovery after permanent nerve injury. One of the results of such compensation is a normalized plasma concentration of stress hormone corticosterone - a marker of hypothalamic-pituitary-adrenal (HPA) axis activity. In this work, we strive to explain this corticosterone normalization by studying the mechanisms responsible for compensation-related neurochemical alterations in the hypothalamus.

MATERIALS AND METHODS

Using microarrays and high performance liquid chromatography (HPLC), we measured genome-wide gene expression and major amino acid neurotransmitters content in the hypothalamus of bilaterally vagotomized rats, 1 month after surgery.

RESULTS

Our results show that, in the long term, vagotomy affects hypothalamic amino acids concentration but not mRNA expression of tested genes.

DISCUSSION

We propose an alternative pathway of immune to CNS communication after vagotomy, leading to activation of the HPA axis, by influencing central amino acids and subsequent monoaminergic neurotransmission.

摘要

背景

迷走神经是免疫与中枢神经系统之间通讯的关键途径之一。迷走神经功能受损可能会加剧外周炎症过程。这种影响会随着永久性神经损伤后的长时间恢复而消退。这种代偿的结果之一是应激激素皮质酮的血浆浓度恢复正常,皮质酮是下丘脑 - 垂体 - 肾上腺(HPA)轴活动的标志物。在这项研究中,我们试图通过研究下丘脑与代偿相关的神经化学改变的机制来解释这种皮质酮的正常化。

材料与方法

利用微阵列和高效液相色谱法(HPLC),我们在双侧迷走神经切断术后1个月测量了大鼠下丘脑的全基因组基因表达和主要氨基酸神经递质含量。

结果

我们的结果表明从长期来看,迷走神经切断术会影响下丘脑氨基酸浓度,但不影响所测基因的mRNA表达。

讨论

我们提出了迷走神经切断术后免疫与中枢神经系统通讯的另一条途径,即通过影响中枢氨基酸及随后的单胺能神经传递来激活HPA轴。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc86/9304976/7ec2d41397e4/fnbeh-16-869526-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc86/9304976/07314a5f9016/fnbeh-16-869526-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc86/9304976/e825b64f2aba/fnbeh-16-869526-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc86/9304976/7ec2d41397e4/fnbeh-16-869526-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc86/9304976/07314a5f9016/fnbeh-16-869526-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc86/9304976/e825b64f2aba/fnbeh-16-869526-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc86/9304976/7ec2d41397e4/fnbeh-16-869526-g003.jpg

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