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Updated: Jun 28, 2026

Chronic Unpredictable Mild Stress in Rats based on the Mongolian medicine

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Published on: October 27, 2023

Curculigoside Alleviates CSDS-induced Depressive-like Behavior by Modulating Pyramidal Neuron Excitability and

Yuhong Jing^1,2, Tianshu Zhang^1,3, Zihao Wei¹

¹Innovative Institute of Chinese Medicine and Pharmacy, Shandong University of Traditional Chinese Medicine, Jinan, 250355, China.

Neuromolecular Medicine

|June 26, 2026

Summary

This summary is machine-generated.

Curculigoside (CUR), a flavonoid, alleviates depression-like behaviors by restoring neuronal activity in key brain regions. It modulates the cAMP-PKA-GluA1 pathway, improving synaptic function and offering potential as an antidepressant therapy.

Keywords:

CAMP-PKA Curculigoside Depression GluA1 PRKACA Synaptic plasticity

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Area of Science:

Neuroscience
Pharmacology
Molecular Biology

Background:

Depression is a complex mood disorder with unclear underlying mechanisms.
Curculigoside (CUR), a flavonoid from traditional Chinese medicine, shows promise for treating depression.
The precise mechanisms of CUR's antidepressant effects require further investigation.

Purpose of the Study:

To investigate the antidepressant effects of CUR in a chronic social defeat stress (CSDS) mouse model.
To elucidate CUR's mechanism of action on pyramidal neuronal excitability and synaptic transmission in the medial prefrontal cortex (mPFC) and ventral CA1 (vCA1).
To identify CUR's pharmacological targets and signaling pathways involved in its antidepressant activity.

Main Methods:

Administration of CUR (20 mg/kg) intraperitoneally for seven days in CSDS-induced mice.
Electrophysiological recordings to assess pyramidal neuronal activity in the mPFC and vCA1.
Network pharmacology and molecular docking to identify CUR's targets.
Analysis of the cAMP-PKA signaling pathway and GluA1 subunit trafficking.

Main Results:

CUR significantly alleviated depression-like behaviors and emotional deficits in CSDS mice.
CUR restored suppressed pyramidal neuronal activity in the mPFC and vCA1.
CUR modulated the cAMP-PKA signaling pathway and GluA1 trafficking, ameliorating synaptic dysfunction.
CUR's antidepressant effects were partly mediated by the cAMP-PKA-GluA1 signaling pathway.

Conclusions:

CUR alleviates depression-like behaviors by restoring pyramidal neuronal excitability and synaptic transmission in the mPFC and vCA1.
The antidepressant mechanism of CUR involves the activation of the cAMP-PKA-GluA1 signaling pathway.
CUR demonstrates significant potential as a therapeutic agent for depression, warranting further clinical investigation.