The upstream V ariable N umber T andem R epeat polymorphism of the monoamine oxidase type A gene influences trigeminal pain‐related evoked responses

Monoamines have an important role in neural plasticity, a key factor in cortical pain processing that promotes changes in neuronal network connectivity. Monoamine oxidase type A ( MAOA ) is an enzyme that, due to its modulating role in monoaminergic activity, could play a role in cortical pain processing. The X ‐linked MAOA gene is characterized by an allelic variant of length, the MAOA upstream V ariable N umber T andem R epeat ( MAOA ‐u VNTR ) region polymorphism. Two allelic variants of this gene are known, the high‐activity MAOA ( HAM ) and low‐activity MAOA ( LAM ). We investigated the role of MAOA ‐u VNTR in cortical pain processing in a group of healthy individuals measured by the trigeminal electric pain‐related evoked potential (t PREP ) elicited by repeated painful stimulation. A group of healthy volunteers was genotyped to detect MAOA ‐u VNTR polymorphism. Electrical t PREP s were recorded by stimulating the right supraorbital nerve with a concentric electrode. The N 2 and P 2 component amplitude and latency as well as the N 2– P 2 inter‐peak amplitude were measured. The recording was divided into three blocks, each containing 10 consecutive stimuli and the N 2– P 2 amplitude was compared between blocks. Of the 67 volunteers, 37 were HAM and 30 were LAM . HAM subjects differed from LAM subjects in terms of amplitude of the grand‐averaged and first‐block N 2– P 2 responses ( HAM > LAM ). The N 2– P 2 amplitude decreased between the first and third block in HAM subjects but not LAM subjects. The MAOA ‐u VNTR polymorphism seemed to influence the brain response in a repeated t PREP paradigm and suggested a role of the MAOA as a modulator of neural plasticity related to cortical pain processing.