相关实验视频

Updated: Jul 6, 2025

Partial Sciatic Nerve Ligation: A Mouse Model of Chronic Neuropathic Pain to Study the Antinociceptive Effect of Novel Therapies

Partial Sciatic Nerve Ligation: A Mouse Model of Chronic Neuropathic Pain to Study the Antinociceptive Effect of Novel Therapies

Published on: October 6, 2022

激活LXRs可通过通过PI3K/AKT通路调节微质极化和突触可塑性来缓解神经病痛诱导的认知功能障碍

Siyi Han¹, Xiaoman Yuan¹, Fengtian Zhao¹

¹Department of Anesthesiology, Hubei Key Laboratory of Geriatric Anesthesia and Perioperative Brain Health, and Wuhan Clinical Research Center for Geriatric Anesthesia, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1095 Jiefang Avenue, Wuhan, Hubei Province, China.

Inflammation research : official journal of the European Histamine Research Society ... [et al.]

|January 6, 2024

概括

激活肝X受体 (LXRs) 通过减少神经炎症和增强突触可塑性来改善神经病痛相关的认知缺陷. 这表明LXRs是与慢性疼痛相关的认知障碍的潜在治疗点.

科学领域:

神经科学是一个神经科学.
药理学药理学是指药理学的学科.
免疫学免疫学免疫学

背景情况:

认知功能障碍经常与慢性疼痛同时发生.
肝X受体 (LXRs) 在治疗中枢神经系统疾病中的认知障碍方面具有潜力.

研究的目的:

研究LXRs在神经病痛引起的认知缺陷中的作用.
探索LXR激活对于与疼痛相关的认知障碍的治疗潜力.

主要方法:

建立了节省神经损伤 (SNI) 模型,以诱导神经病痛和认知缺陷.
使用药理剂来激活 (T0901317) 或抑制 (GSK2033) LXRs.
用PI3K抑制剂 (LY294002) 来阐明潜在的机制.
使用生物化学方法评估神经炎症,微质偏振和突触可塑性.

主要成果:

SNI诱导的认知障碍,M1微质两极分化和突触蛋白减少,与减少LXRβ表达和PI3K/AKT通路抑制有关.
用T0901317激活LXR改善了认知缺陷,促进了M2微质极化,减少了炎症,并恢复了突触蛋白.
抑制LXRs或PI3K/AKT通路可以抵消T0901317的有益作用.

结论:

激活LXR可以缓解神经病痛引起的认知障碍.
该机制涉及调节微质极化,神经炎症和突触可塑性,部分通过PI3K/AKT通路.
LXRs代表了与慢性疼痛相关的认知缺陷的有希望的治疗点.

关键词:

认知功能障碍认知功能障碍肝脏X受体肝脏X受体微质质的两极分化神经炎症是一种神经炎症.神经病变性疼痛神经病变性疼痛突触性可塑性突触性可塑性

更多相关视频

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Published on: March 23, 2011

Intracranial Pharmacotherapy and Pain Assays in Rodents

Intracranial Pharmacotherapy and Pain Assays in Rodents

Published on: April 9, 2019

相关概念视频

Long-term Potentiation

Long-term Potentiation

Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.

Long-term Depression

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...