Su Xiaorui, Dong Xuetong, Lu Chao-Long, Zhang Minglong, Li Yaping, Xiao Han, Wang Jian, Sun Yufei, Cong Bin, Wang Songjun
Hebei Key Laboratory of Forensic Medicine, Collaborative Innovation Center of Forensic Medical Molecular Identification, Research Unit of Digestive Tract Microecosystem Pharmacology and Toxicology, Chinese Academy of Medical Sciences, College of Forensic Medicine, Hebei Medical University, No. 361 Zhong Shan Road, Shijiazhuang, Hebei, China.
Department of Genetics, College of Basic Medicine, Qiqihar Medical University, No. 333 Bukui South Street, Qiqihar, 161006, Heilongjiang, China.
Sci Rep. 2025 Jul 21;15(1):26424. doi: 10.1038/s41598-025-10130-x.
Modern life's fast-paced and the unexpected conditions contribute to escalating stress levels, often leading to anxiety disorders and posing significant challenges to physical and mental health. In judicial practice, the parties often suffer from anxiety disorder under the great stress. However, the precise mechanisms underlying stress-induced anxiety disorders remain incompletely understood. This study aims to explore the neural mechanisms by which stress-induced imbalances in the basolateral amygdala (BLA) parvalbumin interneurons (PV-INs) and glutamatergic neurons lead to anxiety. This study used behavioral analysis, morphology, patch clamp electrophysiology, and viral interference techniques to detect the number of BLA PV-INs and glutamatergic neurons, as well as the excitability of glutamatergic neurons. Results demonstrated that acute and chronic stress adversely affect PV-INs in the BLA, diminishing their numbers and resulting in glutamatergic neurons disinhibition, thereby enhancing glutamatergic neurons excitability and precipitating anxiety behaviour. The anxiety disorder can be effectively improved by activating PV-INs. This study reveals the mechanism of internal amygdala PV-INs regulation leading to anxiety disorders under acute and chronic stress.
现代生活节奏快且状况多变，导致压力水平不断攀升，常常引发焦虑症，给身心健康带来重大挑战。在司法实践中，当事人在巨大压力下常患有焦虑症。然而，压力诱发焦虑症的确切机制仍未完全明晰。本研究旨在探究压力导致基底外侧杏仁核（BLA）小白蛋白中间神经元（PV-INs）与谷氨酸能神经元失衡进而引发焦虑的神经机制。本研究运用行为分析、形态学、膜片钳电生理学及病毒干扰技术，检测BLA中PV-INs和谷氨酸能神经元的数量，以及谷氨酸能神经元的兴奋性。结果表明，急性和慢性应激会对BLA中的PV-INs产生不利影响，使其数量减少，导致谷氨酸能神经元去抑制，从而增强谷氨酸能神经元的兴奋性并引发焦虑行为。激活PV-INs可有效改善焦虑症。本研究揭示了急性和慢性应激下杏仁核内部PV-INs调节导致焦虑症的机制。
