ArticleJournal of molecular neuroscience : MN2014
A study on the mechanism by which MDMA protects against dopaminergic dysfunction after minimal traumatic brain injury (mTBI) in mice.
Article in Journal of molecular neuroscience : MN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 2 of them syntheses that pooled it.
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Who cites it
8 citing papers in PubMed, 2 syntheses or guidelines pooled it, 18 citations in OpenAlex.
- A Systematic Review of the MDMA Model to Address Social Impairment in Autism.Current neuropharmacology · 2021Pooled it
- A Systematic Review of Closed Head Injury Models of Mild Traumatic Brain Injury in Mice and Rats.Journal of neurotrauma · 2019Pooled it
- Dysregulation of the dopaminergic system secondary to traumatic brain injury: implications for mood and anxiety disorders.Frontiers in neuroscience · 2024Review
- The Role of BDNF in Experimental and Clinical Traumatic Brain Injury.International journal of molecular sciences · 2021Review
- Serotonin 2A receptors are a stress response system: implications for post-traumatic stress disorder.Behavioural pharmacology · 2019Review
- Thrombin as Key Mediator of Seizure Development Following Traumatic Brain Injury.Frontiers in pharmacology · 2019Article
- Factors affecting increased risk for substance use disorders following traumatic brain injury: What we can learn from animal models.Neuroscience and biobehavioral reviews · 2017Review
- Adolescent Traumatic Brain Injury Induces Chronic Mesolimbic Neuroinflammation with Concurrent Enhancement in the Rewarding Effects of Cocaine in Mice during Adulthood.Journal of neurotrauma · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Driving under methylenedioxymethamphetamine (MDMA) influence increases the risk of being involved in a car accident, which in turn can lead to traumatic brain injury. The behavioral deficits after traumatic brain injury (TBI) are closely connected to dopamine pathway dysregulation. We have previously demonstrated in mice that low MDMA doses prior to mTBI can lead to better performances in cognitive tests. The purpose of this study was to assess in mice the changes in the dopamine system that occurs after both MDMA and minimal traumatic brain injury (mTBI). Experimental mTBI was induced using a concussive head trauma device. One hour before injury, animals were subjected to MDMA. Administration of MDMA before injury normalized the alterations in tyrosine hydroxylase (TH) levels that were observed in mTBI mice. This normalization was also able to lower the elevated dopamine receptor type 2 (D2) levels observed after mTBI. Brain-derived neurotrophic factor (BDNF) levels did not change following injury alone, but in mice subjected to MDMA and mTBI, significant elevations were observed. In the behavioral tests, haloperidol reversed the neuroprotection seen when MDMA was administered prior to injury. Altered catecholamine synthesis and high D2 receptor levels contribute to cognitive dysfunction, and strategies to normalize TH signaling and D2 levels may provide relief for the deficits observed after injury. Pretreatment with MDMA kept TH and D2 receptor at normal levels, allowing regular dopamine system activity. While the beneficial effect we observe was due to a dangerous recreational drug, understanding the alterations in dopamine and the mechanism of dysfunction at a cellular level can lead to legal therapies and potential candidates for clinical use.
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Registered trials
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