针灸可以缓解抑郁样行为。然而,抗抑郁作用背后的神经机制仍然未知。在多种精神疾病中已报道了神经周网络(PNN)异常。本研究探讨了电针(EA)在百会(GV20)和印堂(GV29)点的抗抑郁过程中PNNs的调制和神经机制。通过慢性不可预测的轻度应激(CUMS)诱导大鼠抑郁模型。结果显示,CUMS,申请四周,特别减少小白蛋白(PV)周围的PNN。此外,EA和氟西汀治疗逆转了CUMS后内侧前额叶皮质(mPFC)中PNN细胞密度的降低以及PV和PNN双阳性细胞与PV神经元的比例。此外,EA处理可以逆转由应激引起的mPFC中PNN组分(聚集蛋白聚糖和brevican)的蛋白质表达的降低。EA治疗后,CUMS诱导的mPFC中GAD67,GLuA1和PSD95的表达下降4周也被逆转。mPFC脑区的PNN降解可能会干扰EA在CUMS诱导的抑郁症大鼠中的抗抑郁作用。在大鼠的mPFC脑区中,在PNN降解后,EA处理没有增加PNN+细胞密度以及PV和PNN双阳性细胞与PV+神经元的比率。这一发现表明,针灸抗抑郁作用的机制可能是基于逆转CUMS诱导的PNN表达下降,γ-氨基丁酸(GABA)神经元的功能损害,和兴奋性突触蛋白表达的调节。
Acupuncture can alleviate depression-like behaviors. However, the neural mechanisms behind the anti-depressive effect remain unknown. Perineuronal net (PNN) abnormalities have been reported in multiple psychiatric disorders. This study investigated the modulation and neural mechanism of
PNNs in the anti-depressant process of electroacupuncture (EA) at Baihui (GV20) and Yintang (GV29) points. A rat depression model was induced by chronic unpredicted mild stress (CUMS). The results revealed that CUMS, applied for four weeks, specifically reduces
PNNs around parvalbumin (PV). In addition, EA and fluoxetine treatments reverse the decrease in
PNNs+ cell density and the ratio of PV and PNN double-positive cells to PV+ neurons in the medial prefrontal cortex (mPFC) after CUMS. Furthermore, EA treatment can reverse the decrease in the protein expression of PNN components (aggrecan and brevican) in the mPFC caused by stress. After EA treatment, the decreased expression of GAD67, GLuA1, and PSD95 in the mPFC induced by CUMS for four weeks was also reversed. PNN degradation in mPFC brain areas potentially interferes with the anti-depressant benefits of EA in rats with depression induced by CUMS. EA treatment did not increase
PNNs+ cell density and the ratio of PV and PNN double-positive cells to PV+ neurons after
PNNs degradation in the mPFC brain region of rats. This finding indicated that the mechanism of acupuncture\'s anti-depressant effect may be based on reversing the CUMS-induced decline in PNN expression, the functional impairment of γ-aminobutyric acid (GABA) neurons, and the regulation of excitatory synaptic proteins expression.