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10-05 Genotypes and neural binding in negative affect: the contribution of genetic polymorphisms to 40 Hz gamma phase synchrony

Published online by Cambridge University Press:  24 June 2014

JM Gatt
Affiliation:
The Brain Dynamics Centre, Westmead Millennium Institute, Westmead Hospital and Western Clinical School, University of Sydney, Australia
S Kuan
Affiliation:
The Brain Dynamics Centre, Westmead Millennium Institute, Westmead Hospital and Western Clinical School, University of Sydney, Australia
C Dobson-Stone
Affiliation:
Prince of Wales Medical Research and Garvan Institutes, Australia
RH Paul
Affiliation:
Brown Medical School, Rhode Island, USA
PR Schofield
Affiliation:
Prince of Wales Medical Research and Garvan Institutes, Australia
E Gordon
Affiliation:
The Brain Resource International Database (The Brain Resource Company), Australia
LM Williams
Affiliation:
The Brain Dynamics Centre, Westmead Millennium Institute, Westmead Hospital and Western Clinical School, University of Sydney, Australia
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Abstract

Type
Abstracts from ‘Brainwaves’— The Australasian Society for Psychiatric Research Annual Meeting 2006, 6–8 December, Sydney, Australia
Copyright
Copyright © 2006 Blackwell Munksgaard

Objective:

Binding of diverse neural activity is essential for complex cognitive and emotional functions. There is increasing evidence for the contribution of genetic polymorphisms to these functions, but their role in neural binding is unknown. We explored differences in 40 Hz gamma synchrony (an index of high-frequency binding) according to COMT Val108/158Met, BDNF Val66Met, MAOA and 5HTT-LPR genotypes, and their combined role in negative mood.

Methods:

About 155 healthy subjects from the Brain Resource International Database provided cheek swabs (for genotyping) and were assessed for level of depressed mood and anxiety and early life stress. Gamma phase synchrony was extracted from EEG recordings during perception of facial emotion stimuli, pertinent to eliciting biases in negative affect states.

Results:

Reduced synchrony to emotional expressions was related to higher depression, and enhanced synchrony to higher anxiety, suggesting distinct biases in binding with these aspects of mood. Consistent with this pattern, the 5HTT-LPR SS allele was linked to reduced frontal and parieto-occipital synchrony to fear with higher stress. The COMT Met allele was linked to similarly reduced frontotemporal synchrony to fear and happiness. By contrast, the BDNF Met allele was related to enhanced synchrony to both fear and happiness with higher stress, suggesting heightened sensitivity to emotion. Synchrony was also enhanced, right parietally and frontotemporally, for the MAO-A low-activity allele, particularly later in the time course.

Conclusion:

Polymorphisms that influence brain function may have distinct effects on neural binding associated with processing salient signals of emotion, and may contribute to behavioural states of depressed mood and anxiety.