ArticleTranslational psychiatry2015
BDNF-TrkB signaling in the nucleus accumbens shell of mice has key role in methamphetamine withdrawal symptoms.
Article in Translational psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Association Between Brain-Derived Neurotrophic Factor Val66Met Polymorphism and Methamphetamine Use Disorder: A Meta-Analysis.Frontiers in psychiatry · 2020Pooled it
- Trial
- Molecular architects of memory: BDNF/TrkB signaling and trafficking in neuronal plasticity and memory.Molecular psychiatry · 2026Review
- Disruption of Dopamine Homeostasis by Psychostimulants.Molecular neurobiology · 2026Review
- The impact of endurance training on reducing inflammatory markers in the cardiac tissue of methamphetamine-exposed rats.PloS one · 2026Article
- Article
- AAV-Mediated Expression of Methamphetamine Monoclonal Antibody Attenuates Methamphetamine Behaviour Sensitization in Mice.Addiction biology · 2025Article
- Luteolin Potentially Alleviates Methamphetamine Withdrawal-Induced Negative Emotions and Cognitive Deficits Through the AKT/FOXO1/HO-1 Signaling Pathway in the Prefrontal Cortex and Caudate Putamen.International journal of molecular sciences · 2025Article
- Environmental enrichment as a therapeutic strategy against methamphetamine induces depressive behaviors in mice.PloS one · 2025Article
- Knockdown and overexpression of basolateral amygdala SIRT1 via AAV bidirectionally alter morphine-induced conditioned place preference extinction in mice.Frontiers in cellular neuroscience · 2025Article
- Ketamine attenuates kidney damage and depression-like behaviors in mice with cisplatin-induced acute kidney injury.Translational psychiatry · 2024Article
- The Effectiveness of Mindfulness in the Treatment of Methamphetamine Addiction Symptoms: Does Neuroplasticity Play a Role?Brain sciences · 2024Review
- Repeated intermittent administration of (R)-ketamine during juvenile and adolescent stages prevents schizophrenia-relevant phenotypes in adult offspring after maternal immune activation: a role of TrkB signaling.European archives of psychiatry and clinical neuroscience · 2022Article
- Cannabidiol inhibits methamphetamine-induced dopamine release via modulation of the DRD1-MeCP2-BDNF-TrkB signaling pathway.Psychopharmacology · 2022Article
- Microglial ERK-NRBP1-CREB-BDNF signaling in sustained antidepressant actions of (R)-ketamine.Molecular psychiatry · 2022Article
- 7,8-Dihydroxyflavone and Neuropsychiatric Disorders: A Translational Perspective from the Mechanism to Drug Development.Current neuropharmacology · 2022Review
- RhANP attenuates endotoxin-derived cognitive dysfunction through subdiaphragmatic vagus nerve-mediated gut microbiota-brain axis.Journal of neuroinflammation · 2021Article
- Olfactory learning and memory in the greater short-nosed fruit bat Cynopterus sphinx: the influence of conspecifics distress calls.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2021Article
- Rapid-acting and long-lasting antidepressant-like action of (R)-ketamine in Nrf2 knock-out mice: a role of TrkB signaling.European archives of psychiatry and clinical neuroscience · 2021Article
- Nutritional Ketosis as a Potential Treatment for Alcohol Use Disorder.Frontiers in psychiatry · 2021Review
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6 authors.
Funding
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Abstract
Depression is a core symptom of methamphetamine (METH) withdrawal during the first several weeks of abstinence. However, the precise mechanisms underlying METH withdrawal symptoms remain unknown. Brain-derived neurotrophic factor (BDNF) and its specific receptor, tropomyosin-related kinase (TrkB), have a role the in pathophysiology of depression. In this study, we examined the role of BDNF-TrkB signaling in different brain regions of male mice with METH withdrawal symptoms. Repeated METH (3 mg kg(-1) per day for 5 days) administration to mice caused a long-lasting depression-like behavior including anhedonia. Western blot analysis showed that BDNF levels in the nucleus accumbens (NAc) of METH-treated mice were significantly higher than those of control mice whereas BDNF levels in other regions, including the prefrontal cortex and hippocampus, were not altered. METH-induced depression-like behavior, behavioral sensitization and dendritic changes in the NAc shell were improved by subsequent subchronic administration of TrkB antagonist ANA-12 (0.5 mg kg(-1) per day for 14 days), but not TrkB agonist 7,8-dihydroxyflavone (10 mg kg(-1) per day for 14 days). In vivo microdialysis showed that METH (1 mg kg(-1))-induced dopamine release in NAc shell of METH-treated mice was attenuated after subsequent subchronic ANA-12 administration. Interestingly, a single bilateral infusion of ANA-12 into the NAc shell, but not NAc core, showed a rapid and long-lasting therapeutic effect. However, ketamine and paroxetine had no effect. These findings suggest that increased BDNF-TrkB signaling in the NAc shell has an important role in the behavioral abnormalities after withdrawal from repeated METH administration, and that TrkB antagonists are potential therapeutic drugs for withdrawal symptoms in METH abusers.
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