MDMA Increases Glutamate Release and Reduces Parvalbumin-Positive GABAergic Cells in the Dorsal Hippocampus of the Rat: Role of Cyclooxygenase
Journal of Neuroimmune Pharmacology November 17, 2012 John H. Anneken, Jacobi I. Cunningham, Stuart A. Collins et al. 52 citations
Repeated doses of MDMA (Ecstasy) cause a delayed and sustained increase in glutamate release in the rat hippocampus. Blocking cyclooxygenase (COX) enzymes, particularly COX-2, with drugs like ketoprofen or nimesulide reduces this glutamate rise, while a COX-1 inhibitor does not. Direct application of prostaglandin E2, a COX product, also raises glutamate levels. Repeated MDMA treatment reduces the number of parvalbumin-positive GABA interneurons in the dentate gyrus, an effect lessened by ketoprofen. However, COX inhibition does not prevent long-term serotonin depletion in the hippocampus. These findings suggest COX activity contributes to MDMA-induced glutamate release and GABA neuron loss but not to serotonin depletion.