Acupuncture alleviates CSDS-induced depressive-like behaviors by modulating synaptic plasticity in vCA1.
Study Goal
The researchers aimed to determine the mechanism by which acupuncture at the LR3 point alleviates depressive-like behaviors in mice subjected to chronic social defeat stress (CSDS), focusing on synaptic function in the ventral CA1 (vCA1) region.
Results Summary
Acupuncture treatment significantly improved emotional deficits, restored pyramidal neuron activity, enhanced glutamatergic transmission, and improved synaptic plasticity in the vCA1 region. These effects were linked to increased AMPAR trafficking and BDNF expression, though the study was conducted in mice and may not fully translate to humans.
Population
Mice subjected to chronic social defeat stress (CSDS).
Effective Dosage
Not specified (acupuncture at LR3 point).
Duration
Duration of intervention not explicitly stated in the abstract.
Interactions
None mentioned.
| Intervention | Direction | Endpoint | Population | Dosage | Impact | Claim # |
|---|---|---|---|---|---|---|
Acupuncture (Acu) treatment at the LR3 point | decrease | emotional deficits | mice subjected to chronic social defeat stress (CSDS) | - | significantly alleviated | #1 |
Acupuncture (Acu) treatment at the LR3 point | increase | activity of pyramidal neurons | mice subjected to chronic social defeat stress (CSDS) | - | restored | #2 |
Acupuncture (Acu) treatment at the LR3 point | increase | spontaneous excitatory postsynaptic currents (sEPSCs) | mice subjected to chronic social defeat stress (CSDS) | - | reversed the decrease in | #3 |
Acupuncture (Acu) treatment at the LR3 point | increase | glutamatergic transmission | mice subjected to chronic social defeat stress (CSDS) | - | enhancing | #4 |
Acupuncture (Acu) treatment at the LR3 point | increase | synaptic plasticity | mice subjected to chronic social defeat stress (CSDS) | - | improved | #5 |
Acupuncture (Acu) treatment at the LR3 point | increase | dendritic spine density | mice subjected to chronic social defeat stress (CSDS) | - | increased | #6 |
Acupuncture (Acu) treatment at the LR3 point | increase | phosphorylated CaMKIIα | mice subjected to chronic social defeat stress (CSDS) | - | restored expression levels of | #7 |
Acupuncture (Acu) treatment at the LR3 point | increase | GluA1 | mice subjected to chronic social defeat stress (CSDS) | - | restored expression levels of | #8 |
Acupuncture (Acu) treatment at the LR3 point | increase | GluA2 | mice subjected to chronic social defeat stress (CSDS) | - | restored expression levels of | #9 |
Acupuncture (Acu) treatment at the LR3 point | increase | BDNF | mice subjected to chronic social defeat stress (CSDS) | - | restored expression levels of | #10 |
Acupuncture (Acu) treatment at the LR3 point | decrease | depressive-like behaviors | mice subjected to chronic social defeat stress (CSDS) | - | alleviates | #11 |
Acupuncture (Acu) treatment at the LR3 point | increase | synaptic function in the vCA1 region | mice subjected to chronic social defeat stress (CSDS) | - | enhances | #12 |
Acupuncture (Acu) has been clinically validated as an effective treatment for depression. However, the underlying mechanism of Acu treatment's antidepressant effect remains unclear. Methods: We investigate the antidepressant effects of Acu treatment at the LR3 point in mice subjected to chronic social defeat stress (CSDS). GCaMP6m-based fiber-optic photometry was employed in the ventral CA1 (vCA1) regions for the first time to monitor Ca2+ transients in vivo during behavioral testing. Electrophysiological recordings were used to detect the activity and synaptic function of pyramidal neurons. Golgi staining was performed to measure the density of dendritic spines in the vCA1. Western blot analysis was conducted to quantify the expression levels of phosphorylated CaMKIIα, AMPA receptor protein (GluA1, GluA2), and brain-derived neurotrophic factor (BDNF) in the hippocampus. Results: Our findings indicated that Acu treatment significantly alleviated emotional deficits and restored the activity of pyramidal neurons, which were suppressed by CSDS. Acu treatment also reversed the decrease in spontaneous excitatory postsynaptic currents (sEPSCs), thereby enhancing glutamatergic transmission. Moreover, Acu treatment improved synaptic plasticity, as evidenced by increased dendritic spine density and restored expression levels of phosphorylated CaMKIIα, GluA1, GluA2 and BDNF. Conclusion: Collectively, these findings suggest that Acu treatment alleviates depressive-like behaviors induced by CSDS and enhances synaptic function in the vCA1 region, potentially through mechanisms involving increased AMPAR trafficking and BDNF expression.