ArticleBiological psychiatry2013
Scopolamine rapidly increases mammalian target of rapamycin complex 1 signaling, synaptogenesis, and antidepressant behavioral responses.
Article in Biological psychiatry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers.
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Who cites it
145 citing papers in PubMed, 260 citations in OpenAlex.
- Group-Based Symptom Trajectory of Intramuscular Administration of Scopolamine Augmentation in Moderate to Severe Major Depressive Disorder: A Post-Hoc Analysis.Neuropsychiatric disease and treatment · 2023Trial
- Neurophysiological Changes Associated with Antidepressant Response to Ketamine Not Observed in a Negative Trial of Scopolamine in Major Depressive Disorder.The international journal of neuropsychopharmacology · 2019Trial
- Exploring the Evolving Role of Scopolamine in Pharmacotherapy: From Cognitive Impairment to Neuroplasticity?-A Narrative Review.Molecules (Basel, Switzerland) · 2026Review
- The synaptic triad in depression: how stress-related pathways converge on BDNF, NMDA receptor, and MMP-9.Pharmacological reports : PR · 2026Review
- Mouse neuronal dendritic complexity and resilience to stress-induced depression in Drosophila melanogaster are enhanced by Withania somnifera alkaloids.Journal of ethnopharmacology · 2026Article
- Scopolamine exerted antidepressant-like behavioral effects via restoring the synaptic plasticity in CRS-treated mice.Metabolic brain disease · 2025Article
- Optimizing predictive biomarkers for alzheimer's disease: muscarinic M1 antagonist-induced synaptic signaling disruptions and bee venom intervention through cholinergic modulation and multiregression dose selection.Metabolic brain disease · 2025Article
- L-type calcium channel blockade attenuates the anxiogenic-like effects of cocaine abstinence in female and male rats.Neuroscience · 2025Article
- The synergistic extract ofFrontiers in aging neuroscience · 2025Article
- Sinisan ameliorates early-life stress-induced depressive-like behaviors by repairing DRN synaptic damage through CaSR.Frontiers in pharmacology · 2025Article
- Danshensu Interventions Mediate Rapid Antidepressant Effects by Activating the Mammalian Target of Rapamycin Signaling and Brain-Derived Neurotrophic Factor Release.Psychiatry investigation · 2024Article
- Ketamine metabolism via hepatic CYP450 isoforms contributes to its sustained antidepressant actions.Neuropharmacology · 2024Article
- L-type calcium channel regulation of depression, anxiety and anhedonia-related behavioral phenotypes following chronic stress exposure.Neuropharmacology · 2024Article
- Article
- Exploring Novel Antidepressants Targeting G Protein-Coupled Receptors and Key Membrane Receptors Based on Molecular Structures.Molecules (Basel, Switzerland) · 2024Review
- Depression and the Glutamate/GABA-Glutamine Cycle.Current neuropharmacology · 2024Review
- Rapid Synthesis of Psychoplastogenic Tropane Alkaloids.JACS Au · 2023Article
- The Potential of Scopolamine as an Antidepressant in Major Depressive Disorder: A Systematic Review of Randomized Controlled Trials.Biomedicines · 2023Review
- HCN channel inhibitor induces ketamine-like rapid and sustained antidepressant effects in chronic social defeat stress model.Neurobiology of stress · 2023Article
- M1 acetylcholine receptors in somatostatin interneurons contribute to GABAergic and glutamatergic plasticity in the mPFC and antidepressant-like responses.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
85 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
backgroundClinical studies report that scopolamine, an acetylcholine muscarinic receptor antagonist, produces rapid antidepressant effects in depressed patients, but the mechanisms underlying the therapeutic response have not been determined. The present study examines the role of the mammalian target of rapamycin complex 1 (mTORC1) and synaptogenesis, which have been implicated in the rapid actions of N-methyl-D-aspartate receptor antagonists.
methodsThe influence of scopolamine on mTORC1 signaling was determined by analysis of the phosphorylated and activated forms of mTORC1 signaling proteins in the prefrontal cortex (PFC). The numbers and function of spine synapses were analyzed by whole cell patch clamp recording and two-photon image analysis of PFC neurons. The actions of scopolamine were examined in the forced swim test in the absence or presence of selective mTORC1 and glutamate receptor inhibitors.
resultsThe results demonstrate that a single, low dose of scopolamine rapidly increases mTORC1 signaling and the number and function of spine synapses in layer V pyramidal neurons in the PFC. Scopolamine administration also produces an antidepressant response in the forced swim test that is blocked by pretreatment with the mTORC1 inhibitor or by a glutamate alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor antagonist.
conclusionsTaken together, the results demonstrate that the antidepressant actions of scopolamine require mTORC1 signaling and are associated with increased glutamate transmission, and synaptogenesis, similar to N-methyl-D-aspartate receptor antagonists. These findings provide novel targets for safer and more efficacious rapid-acting antidepressant agents.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.