ArticleMetabolic brain disease2025
Scopolamine exerted antidepressant-like behavioral effects via restoring the synaptic plasticity in CRS-treated mice.
Article in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Depression stands as a widespread psychiatric illness, yet existing therapeutic approaches are constrained by delayed effectiveness and adverse reactions. Scopolamine, as a M-AChRs antagonist, has shown significant antidepressant-like effects in preclinical studies, but its mechanisms remain unclear. The present study is designed to explore the molecular mechanisms that underpin the antidepressant-like actions of scopolamine. Four-week chronic restraint stress (CRS) was employed to induce depression-like behaviors, while behavioral assessments—including TST (the tail suspension test) and FST (the forced swimming test)—were utilized to evaluate the behavioral effects of scopolamine. Additionally, RT-qPCR (quantitative real-time PCR), Golgi-Cox staining, and electrophysiological recordings were applied to explore the molecular mechanisms underlying these behavioral effects of scopolamine. Our behavioral results revealed that 24 h after drug injection, scopolamine (0.3 mg/kg, i.p.) notably reversed CRS-induced increases in the immobility time in the TST and FST. Notably, further RT-qPCR analyses revealed that CRS led to a significant reduction in the mRNA levels of glutamatergic pyramidal neuron markers in the prefrontal cortex (PFC) and hippocampus, and this downregulation was fully reversed by scopolamine administration. Moreover, our electrophysiological measurements showed that scopolamine notably counteracted the CRS-induced drops in the firing frequencies of glutamatergic pyramidal neurons situated in the medial prefrontal cortex (mPFC); our Golgi-Cox results suggested that scopolamine improved the CRS-induced impairments in the synaptic plasticity in the mPFC and hippocampus. These observations implied that the synaptic plasticity of pyramidal neurons might be involved in regulating the antidepressant-like behavioral effects of scopolamine, providing mechanistic insights for the development of next-generation antidepressant medications.
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