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探讨慢性弓形体病和 NMDAR 功能障碍的相互作用：精神分裂样行为及治疗潜力的新见解。

Exploring the interplay of chronic toxoplasmosis and NMDAR dysfunction: Insights into schizophrenia-like behaviors and therapeutic potential.

机构信息

Department of Veterinary Parasitology, Karaj Branch, Islamic Azad University, Karaj, Iran.

Department of Veterinary Parasitology, Babol Branch, Islamic Azad University, Karaj, Iran.

出版信息

Open Vet J. 2024 Jul;14(7):1634-1643. doi: 10.5455/OVJ.2024.v14.i7.13. Epub 2024 Jul 31.

DOI:10.5455/OVJ.2024.v14.i7.13
PMID:39175964
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11338605/
Abstract

BACKGROUND

Chronic toxoplasmosis has been strongly implicated in the development of psychosis and schizophrenia. Additionally, the understanding of schizophrenia has been significantly reshaped by insights into N-methyl-D-aspartate receptor (NMDAR) hypofunction.

AIM

This study aimed to compare the behavioral, antioxidant, and NMDAR changes in mice subjected to infection and those treated with ketamine to induce schizophrenia-like symptoms.

METHODS

Sixty male BALB/c mice were divided into six groups: toxoplasmosis (TOXO) (infected), ketamine-induced schizophrenia (KET), TOXO+KET, TOXO+sulfadiazine-trimethoprim treatment (SDT), TOXO+KET+SDT, and control (CON) (uninfected). After 10 weeks post-infection, behavioral tests were conducted, brain antioxidant status and lipid peroxidation were analyzed, and NMDA-NR1/NR2A expressions were assessed. TOXO and KET induced distinct behaviors: hyperlocomotion, anxiety, and memory impairment.

RESULTS

Antioxidant enzyme levels decreased, and lipid peroxidation increased in TOXO and schizophrenic mice brains. NMDAR downregulation, especially NR-1 and NR2A, was evident due to and ketamine. Sulfadiazine-trimethoprim ameliorated NMDAR downregulation, but not all of the behavioral alterations.

CONCLUSION

Further studies are needed to elucidate specific NMDAR subunit roles in toxoplasmosis-induced pathophysiology, offering potential therapeutic insights. This investigation highlights the intricate relationship between chronic toxoplasmosis, NMDAR dysfunction, and schizophrenia-like behaviors. Insights gained could pave the way for innovative interventions targeting both cognitive and neurological impairments associated with these conditions.

摘要

背景

慢性弓形虫感染与精神分裂症的发生发展密切相关。此外，对 N-甲基-D-天冬氨酸受体（NMDAR）功能低下的认识极大地改变了人们对精神分裂症的理解。

目的

本研究旨在比较弓形虫感染小鼠和氯胺酮诱导的精神分裂症样症状模型小鼠的行为、抗氧化和 NMDAR 变化。

方法

将 60 只雄性 BALB/c 小鼠分为 6 组：弓形虫感染组（TOXO）、氯胺酮诱导的精神分裂症组（KET）、TOXO+KET 组、TOXO+磺胺嘧啶-三甲氧苄啶治疗组（SDT）、TOXO+KET+SDT 组和对照组（CON）（未感染）。感染后 10 周进行行为学测试，分析大脑抗氧化状态和脂质过氧化，评估 NMDA-NR1/NR2A 表达。TOXO 和 KET 诱导了不同的行为：过度活跃、焦虑和记忆障碍。

结果

TOXO 和精神分裂症小鼠大脑中的抗氧化酶水平降低，脂质过氧化增加。NMDAR 下调，特别是 NR-1 和 NR2A，由于 和氯胺酮。磺胺嘧啶-三甲氧苄啶改善了 NMDAR 的下调，但不能改善所有的行为改变。

结论

需要进一步研究以阐明弓形虫感染诱导的病理生理学中特定的 NMDAR 亚基作用，为提供潜在的治疗见解。本研究强调了慢性弓形虫感染、NMDAR 功能障碍与精神分裂症样行为之间的复杂关系。获得的见解可能为针对这些疾病相关的认知和神经损伤的创新干预措施铺平道路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd0a/11338605/8d5d48d6956d/OpenVetJ-14-1634-g006.jpg
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