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 Peer reviewed DOI: 10.1007/s00213-010-2098-y via PubMed
Summary
An acute dose of MDMA given to mice before experiencing a mild traumatic brain injury (mTBI) resulted in cognitive improvements compared to those who only suffered the injury. Mice that received 10 mg/kg MDMA showed reversed declines in tyrosine hydroxylase levels and minimized alterations in visual and spatial memory. While mTBI caused significant cognitive impairments, the administration of MDMA prior to the injury did not lead to additional deficits, indicating a potential protective effect.
Study at a glance
| Population | mice |
|---|---|
| Key finding | MDMA administration prior to mild traumatic brain injury minimized cognitive impairments and reversed declines in tyrosine hydroxylase levels. |
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.