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Cerebral Cortex Advance Access originally published online on June 2, 2006
Cerebral Cortex 2007 17(5):1007-1019; doi:10.1093/cercor/bhl011
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© The Author 2006. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

DRD4 and DAT1 Polymorphisms Modulate Human Gamma Band Responses

Tamer Demiralp1,2, Christoph S. Herrmann2, M. Emin Erdal3, Tolgay Ergenoglu4, Yasemin H. Keskin1, Mehmet Ergen1 and Hüseyin Beydagi4

1 Department of Physiology, Istanbul Faculty of Medicine, Istanbul University, Turkey, 2 Department of Biological Psychology, Otto-von-Guericke University Magdeburg, Germany, 3 Department of Medical Biology and Genetics, Medical Faculty, Mersin University, Turkey, 4 Department of Physiology, Medical Faculty, Mersin University, Turkey

Address correspondence to Prof. Dr Tamer Demiralp, Department of Physiology, Istanbul Medical Faculty, Istanbul University, 34390 Çapa-Istanbul, Turkey. Email: demiralp{at}istanbul.edu.tr.

Gamma oscillations (30–80 Hz) have been demonstrated to be important for perceptual and cognitive processes. Animal and in vitro studies have revealed possible underlying generation mechanisms of the gamma rhythm. However, little is known about the neurochemical modulation of these oscillations during human cognition. Schizophrenia and Attention Deficit Hyperactivity Disorder, which lead to failure of attentional modulation and working memory, introduce significant changes in gamma responses and have significant associations with genetic polymorphisms of dopamine receptor D4 (DRD4), dopamine transporter (DAT), and catechol-O-methyltransferase (COMT). Therefore, the presence of direct relations between these polymorphisms and gamma oscillations was investigated in human subjects using an auditory target detection paradigm. The 7-repeat isoform of the DRD4 polymorphism that produces a subsensitive variant of the D4 receptor enhanced the auditory evoked and induced gamma responses to both standard and target stimuli. The 10/10 genotype of the DAT1 polymorphism, which reduces DAT expression and hence yields an increase in extracellular dopamine, specifically enhanced evoked gamma responses to target stimuli. The COMT polymorphism did not significantly change gamma responses. It seems plausible to assume that the modulation pattern of the evoked gamma response by DRD4 polymorphism relates to reduced inhibition via the D4 receptor, whereas the DAT1 effect is related to the target detection mechanism probably mediated by the D1 receptor.

Key Words: ADHD • COMT • dopamine • gamma band response • schizophrenia


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