Effects of Stress and MDMA on Hippocampal Gene Expression
Georg F. Weber, Bethann N. Johnson, Bryan K. Yamamoto, Gary A. Gudelsky
BioMed Research International 2014 DOI: 10.1155/2014/141396 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Animal study Peer reviewed |
|---|---|
| Population | Control rats and rats exposed to chronic stress |
| Intervention | MDMA |
| Topics | MDMA Serotonin |
| Keywords | Neurotoxicity Hippocampus Pharmacology Endocrinology |
| Citations | 19 |
| Key points | MDMA altered hippocampal gene expression related to protein folding and neuropeptide signaling, and reversed stress-induced downregulation of circadian rhythm genes. |
Abstract
MDMA (3,4-methylenedioxymethamphetamine) is a substituted amphetamine and popular drug of abuse. Its mood-enhancing short-term effects may prompt its consumption under stress. Clinical studies indicate that MDMA treatment may mitigate the symptoms of stress disorders such as posttraumatic stress syndrome (PTSD). On the other hand, repeated administration of MDMA results in persistent deficits in markers of serotonergic (5-HT) nerve terminals that have been viewed as indicative of 5-HT neurotoxicity. Exposure to chronic stress has been shown to augment MDMA-induced 5-HT neurotoxicity. Here, we examine the transcriptional responses in the hippocampus to MDMA treatment of control rats and rats exposed to chronic stress. MDMA altered the expression of genes that regulate unfolded protein binding, protein folding, calmodulin-dependent protein kinase activity, and neuropeptide signaling. In stressed rats, the gene expression profile in response to MDMA was altered to affect sensory processing and responses to tissue damage in nerve sheaths. Subsequent treatment with MDMA also markedly altered the genetic responses to stress such that the stress-induced downregulation of genes related to the circadian rhythm was reversed. The data support the view that MDMA-induced transcriptional responses accompany the persistent effects of this drug on neuronal structure/function. In addition, MDMA treatment alters the stress-induced transcriptional signature.
Comparable studies
Other preclinical and animal studies on MDMA, most cited first.
Citations in the library
Cited by 4
- 3,4-Methylenedioxymethamphetamine (MDMA) - Assisted psychotherapy for treatment of posttraumatic stress disorder: Literature review Romanian Journal of Psychiatry & Psychotherapy March 31, 2020
- MDMA decreases glutamic acid decarboxylase (GAD) 67-immunoreactive neurons in the hippocampus and increases seizure susceptibility: Role for glutamate. Neurotoxicology December 2016
- Chronic MDMA induces neurochemical changes in the hippocampus of adolescent and young adult rats: Down-regulation of apoptotic markers. Neurotoxicology July 2015
- Reduced Contextual Discrimination following Alcohol Consumption or MDMA Administration in Mice. PLoS One 2015
Cites 23
- Durability of improvement in post-traumatic stress disorder symptoms and absence of harmful effects or drug dependency after 3,4-methylenedioxymethamphetamine-assisted psychotherapy: a prospective long-term follow-up study. Journal of Psychopharmacology 2013
- Memory impairment in abstinent MDMA ("Ecstasy") users Neurology December 1, 1998
- (±)3,4-Methylenedioxymethamphetamine (‘Ecstasy’)-Induced Serotonin Neurotoxicity: Clinical Studies Neuropsychobiology 2000
- Decreased cerebral cortical serotonin transporter binding in ecstasy users: a positron emission tomography/[11C]DASB and structural brain imaging study Brain May 17, 2010
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and 18 more in the library