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Methamphetamine is, worldwide, one of the most consumed drugs of abuse. One important side effect is neurodegeneration leading to a decrease in life expectancy. The aim of this paper was to check whether the drug affects one of the receptors involved in neurodegeneration/neuroprotection events, namely the adenosine A 2A receptor (A 2A R). First, we noticed that methamphetamine does not affect A 2A functionality if the receptor is expressed in a heterologous system. However, A 2A R becomes sensitive to the drug upon complexes formation with the cannabinoid CB 1 receptor (CB 1 R) and the sigma 1 receptor (σ 1 R). Signaling via both adenosine A 2A R and cannabinoid CB 1 R was affected by methamphetamine in cells co-expressing the two receptors. In striatal primary cultures, the A 2A R-CB 1 R heteromer complex was detected and methamphetamine not only altered its expression but completely blocked the A 2A R- and the CB 1 R-mediated activation of the mitogen activated protein kinase (MAPK) pathway. In conclusion, methamphetamine, with the participation of σ 1 R, alters the expression and function of two interacting receptors, A 2A R, which is a therapeutic target for neuroprotection, and CB 1 R, which is the most abundant G protein-coupled receptor (GPCR) in the brain.

Methamphetamine Blocks Adenosine A2A Receptor Activation via Sigma 1 and Cannabinoid CB1 Receptors