Effects of the endogenous PPAR‐α agonist, oleoylethanolamide on MDMA‐induced cognitive deficits in mice
Synapse December 22, 2009 Ainhoa Plaza‐zabala, Fernando Berrendero, Juan Suárez et al. 3 citations
Repeated high doses of MDMA impaired mice's ability to learn and recall an active avoidance task. Pretreatment with a low dose (5 mg/kg) of the endogenous PPAR-α agonist oleoylethanolamide (OEA) partially protected against these deficits, while a higher dose (25 mg/kg) worsened them. MDMA also reduced dopamine transporter (DAT)-binding sites in the brain four days after the last dose, an effect prevented by both OEA doses. Coexpression of tyrosine-hydroxylase and PPAR-α receptors was observed in the striatum and substantia nigra pars compacta, suggesting OEA modulates MDMA-induced cognitive deficits through a DAT-independent mechanism.