The intriguing effects of ecstasy (MDMA) on cognitive function in mice subjected to a minimal traumatic brain injury (mTBI).
Shahaf Edut, Vardit Rubovitch, Shaul Schreiber, Chaim G Pick
Psychopharmacology April 1, 2011 DOI: 10.1007/s00213-010-2098-y via PubMed
Summary
AI-generated from the abstractA single dose of MDMA given to mice before a mild traumatic brain injury did not worsen cognitive deficits and instead appeared to improve visual and spatial memory. Mice that received MDMA before injury performed better on cognitive tests than injured mice without the drug. The drug reversed injury-related decreases in tyrosine hydroxylase, an enzyme important for dopamine production, which may explain the cognitive improvements. The IGF-1R signaling pathway was activated but was not the main cause of the benefit.
Study at a glance
| Characteristics | Controlled experiment Peer reviewed |
|---|---|
| Population | Mice |
| Intervention | MDMA |
| Dose | 10 mg/kg |
| Duration | 7 and 30 days post-injury |
| Citations | 36 |
| Key finding | MDMA administered before mild traumatic brain injury in mice reversed injury-induced decreases in tyrosine hydroxylase and improved cognitive performance. |
Abstract
The use of ecstasy (MDMA) among young adults has dramatically increased over the years. Since MDMA may impair the users' driving ability, the risk of being involved in a motor vehicle accident (MVA) is notably increased. Minimal traumatic brain injury (mTBI) a common consequence of MVAs-produces short- and long-term physical, cognitive, and emotional impairments. To investigate the effects of an acute dose of MDMA in mice subjected to closed head mTBI. Mice received 10 mg/kg MDMA 1 h prior to the induction of mTBI. Behavioral tests were conducted 7 and 30 days post-injury. In addition to the behavioral tests, phosphorylation of IGF-1R, ERK, and levels of tyrosine hydroxylase (TH) were measured. mTBI mice showed major cognitive impairments in all cognitive tests conducted. No additional impairments were seen if mTBI was preceded by one dose of MDMA. On the contrary, a beneficial effect was seen in these mice. The western blot analysis of TH revealed a significant decrease in the mTBI mice. These decreases were reversed in mice that were subjected to MDMA prior to the trauma. The presence of MDMA at the time of mTBI minimizes the alteration of visual and spatial memory of the injured mice. The IGF-1R pathway was activated due to mTBI and MDMA but was not the main contributor to the cognitive improvements. MDMA administration inverted the TH decreases seen after injury. We believe this may be the major cause of the cognitive improvements seen in these mice.