Dataset Information

HTR3B is associated with alcoholism with antisocial behavior and alpha EEG power--an intermediate phenotype for alcoholism and co-morbid behaviors.

ABSTRACT: Alcohol use disorders (AUD) with co-morbid antisocial personality disorder (ASPD) have been associated with serotonin (5-HT) dysfunction. 5-HT3 receptors are potentiated by ethanol and appear to modulate reward. 5-HT3 receptor antagonists may be useful in the treatment of early-onset alcoholics with co-morbid ASPD. Low-voltage alpha electroencephalogram (EEG) power, a highly heritable trait, has been associated with both AUD and ASPD. A recent whole genome linkage scan in one of our samples, Plains American Indians (PI), has shown a suggestive linkage peak for alpha power at the 5-HT3R locus. We tested whether genetic variation within the HTR3A and HTR3B genes influences vulnerability to AUD with comorbid ASPD (AUD+ASPD) and moderates alpha power. Our study included three samples: 284 criminal alcoholic Finnish Caucasians and 234 controls; two independent community-ascertained samples with resting EEG recordings: a predominantly Caucasian sample of 191 individuals (Bethesda) and 306 PI. In the Finns, an intronic HTR3B SNP rs3782025 was associated with AUD+ASPD (P=.004). In the Bethesda sample, the same allele predicted lower alpha power (P=7.37e(-5)). Associations between alpha power and two other HTR3B SNPs were also observed among PI (P=.03). One haplotype in the haplotype block at the 3' region of the gene that included rs3782025 was associated with AUD+ASPD in the Finns (P=.02) and with reduced alpha power in the Bethesda population (P=.00009). Another haplotype in this block was associated with alpha power among PI (P=.03). No associations were found for HTR3A. Genetic variation within HTR3B may influence vulnerability to develop AUD with comorbid ASPD. 5-HT3R might contribute to the imbalance between excitation and inhibition that characterize the brain of alcoholics.

SUBMITTER: Ducci F

PROVIDER: S-EPMC2754808 | biostudies-literature | 2009 Feb

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

HTR3B is associated with alcoholism with antisocial behavior and alpha EEG power--an intermediate phenotype for alcoholism and co-morbid behaviors.

Ducci Francesca F Enoch Mary-Anne MA Yuan Qiaoping Q Shen Pei-Hong PH White Kenneth V KV Hodgkinson Colin C Albaugh Bernard B Virkkunen Matti M Goldman David D

Alcohol (Fayetteville, N.Y.) 20090201 1

Alcohol use disorders (AUD) with co-morbid antisocial personality disorder (ASPD) have been associated with serotonin (5-HT) dysfunction. 5-HT3 receptors are potentiated by ethanol and appear to modulate reward. 5-HT3 receptor antagonists may be useful in the treatment of early-onset alcoholics with co-morbid ASPD. Low-voltage alpha electroencephalogram (EEG) power, a highly heritable trait, has been associated with both AUD and ASPD. A recent whole genome linkage scan in one of our samples, Pla ...[more]

PMID: 19185213

Similar Datasets

Project description:Transcranial alternating current stimulation (tACS) sees increased use in neurosciences as a tool for the exploration of brain oscillations. It has been shown that tACS stimulation in specific frequency bands can result in aftereffects of modulated oscillatory brain activity that persist after the stimulation has ended. The general relationship between persistency of the effect and duration of stimulation is sparsely investigated but previous research has shown that the occurrence of tACS aftereffects depends on the brain state before and during stimulation. Early alpha neurofeedback research suggests that particularly in the alpha band the responsiveness to a manipulation depends on the ambient illumination during measurement. Therefore, in the present study we assessed the brain's susceptibility to tACS at the individual alpha frequency during darkness compared to ambient illumination. We measured alpha power after 10 min of stimulation in 30 participants while they continuously performed a visual vigilance task. Our results show that immediately after stimulation, the alpha power in the illumination condition for both the stimulated and sham group has increased by only about 7%, compared to about 20% in both groups in the 'dark' condition. For the group that did not receive stimulation, the power in darkness remained stable after stimulation, whereas the power in light increased by an additional 10% during the next 30 min. For the group that did receive stimulation, alpha power during these 30 min increased by another 11% in light and 22% in darkness. Since alpha power already increased by about 10% without stimulation, the effect of illumination does not seem to have interacted with the effect of stimulation. Instead, both effects seem to have added up linearly. Although our findings do not show that illumination-induced differences in oscillatory activity influence the susceptibility toward tACS, they stress the importance of controlling for factors like ambient light that might add an independent increase or decrease to the power of brain oscillations during periods, where possible persistent effects of stimulation are explored.

Project description:IntroductionElectroencephalographic (EEG) data quality is severely compromised when recorded inside the magnetic resonance (MR) environment. Here we characterized the impact of the ballistocardiographic (BCG) artifact on resting-state EEG spectral properties and compared the effectiveness of seven common BCG correction methods to preserve EEG spectral features. We also assessed if these methods retained posterior alpha power reactivity to an eyes closure-opening (EC-EO) task and compared the results from EEG-informed fMRI analysis using different BCG correction approaches.MethodElectroencephalographic data from 20 healthy young adults were recorded outside the MR environment and during simultaneous fMRI acquisition. The gradient artifact was effectively removed from EEG-fMRI acquisitions using Average Artifact Subtraction (AAS). The BCG artifact was corrected with seven methods: AAS, Optimal Basis Set (OBS), Independent Component Analysis (ICA), OBS followed by ICA, AAS followed by ICA, PROJIC-AAS and PROJIC-OBS. EEG signal preservation was assessed by comparing the spectral power of traditional frequency bands from the corrected rs-EEG-fMRI data with the data recorded outside the scanner. We then assessed the preservation of posterior alpha functional reactivity by computing the ratio between the EC and EO conditions during the EC-EO task. EEG-informed fMRI analysis of the EC-EO task was performed using alpha power-derived BOLD signal predictors obtained from the EEG signals corrected with different methods.ResultsThe BCG artifact caused significant distortions (increased absolute power, altered relative power) across all frequency bands. Artifact residuals/signal losses were present after applying all correction methods. The EEG reactivity to the EC-EO task was better preserved with ICA-based correction approaches, particularly when using ICA feature extraction to isolate alpha power fluctuations, which allowed to accurately predict hemodynamic signal fluctuations during the EEG-informed fMRI analysis.DiscussionCurrent software solutions for the BCG artifact problem offer limited efficiency to preserve the EEG spectral power properties using this particular EEG setup. The state-of-the-art approaches tested here can be further refined and should be combined with hardware implementations to better preserve EEG signal properties during simultaneous EEG-fMRI. Existing and novel BCG artifact correction methods should be validated by evaluating signal preservation of both ERPs and spontaneous EEG spectral power.

Dataset Information

HTR3B is associated with alcoholism with antisocial behavior and alpha EEG power--an intermediate phenotype for alcoholism and co-morbid behaviors.

Publications

HTR3B is associated with alcoholism with antisocial behavior and alpha EEG power--an intermediate phenotype for alcoholism and co-morbid behaviors.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets