Skip Navigation



Cerebral Cortex Advance Access published online on June 2, 2006

Cerebral Cortex, doi:10.1093/cercor/bhl011
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow Supplementary Material
Right arrow All Versions of this Article:
17/5/1007    most recent
bhl011v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Demiralp, T.
Right arrow Articles by Beydagi, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Demiralp, T.
Right arrow Articles by Beydagi, H.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2006. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Article

DRD4 and DAT1 Polymorphisms Modulate Human Gamma Band Responses

Tamer Demiralp 1 *, Christoph S. Herrmann 2, M. Emin Erdal 3, Tolgay Ergenoglu 4, Yasemin H. Keskin 5, Mehmet Ergen 5, and Hüseyin Beydagi 4

1 Department of Physiology, Istanbul Faculty of Medicine, Istanbul University, Turkey; Department of Biological Psychology, Otto-von-Guericke University Magdeburg, Germany
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
5 Department of Physiology, Istanbul Faculty of Medicine, Istanbul University, Turkey

* To whom correspondence should be addressed.
Tamer Demiralp, E-mail: demiralp{at}istanbul.edu.tr


   Abstract

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.

Keywords: ADHD; COMT; dopamine; gamma band response; schizophrenia.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.