Key result
5-HTTLPR l homozygotes are linked to a strong inverse relationship between QTc and brain 5-HTT binding.
Why the study?
It is less known how 5-HTTLPR polymorphism influences the coupling between brain serotonin transporter binding and neuronal cardiovascular control as reflected by QTc interval.
Does the 5-HTTLPR polymorphism influence the relationship between brain 5-HTT binding and QTc interval in healthy young adults?
Cross-Sectional (n=30)
No
Does the 5-HTTLPR polymorphism influence the relationship between brain 5-HTT binding and QTc interval in healthy young adults?
Answers are grounded in this paper and cite their sources.
The 5-HTTLPR polymorphism appears to dictate the functional coupling between brain serotonergic activity and cardiac repolarization, with a significant inverse correlation between QTc interval and brain 5-HTT binding present only in l homozygotes.
OBJECTIVE: Serotonin transporter gene polymorphism (5-HTTLPR polymorphism) predicts the degree of structural and functional connectivity in the brain, and less consistently the degree of vulnerability for anxiety and depressive disorders. It is less known how 5-HTTLPR polymorphism influences on the coupling between brain and neuronal cardiovascular control. The present study demonstrates the impact of 5-HTTLPR polymorphism on the relations between heart rate (HR) corrected cardiac repolarization interval (QTc interval) and the brain 5-HTT binding. MATERIAL AND METHODS: Thirty healthy young adults (fifteen monozygotic twin pairs) (mean age 26±1.3 years, 16 females) were imagined with single-photon emission computed tomography (SPECT) using iodine-123 labeled 2β-carbomethoxy-3β-(4-iodophenyl) nortropane (nor-β-CIT). Continuous ECG recording was obtained from each participant at supine rest. Signal averaged QTc interval on continuous ECG was calculated and compared with the brain imaging results. RESULTS: In the two groups [l homozygotes (n = 16, 10 females), s carriers (n = 14, 8 female)] HR and the length of QTc interval were not influenced by 5-HTTLPR polymorphism. There were no significant relations between HR and 5-HTT binding in the brain. There were significant associations between QTc interval and nor-β-CIT binding in the brain in l homozygotes, but not in s carriers (correlations for QTc interval and nor-β-CIT binding of striatum, thalamus and right temporal region were -0.8--0.9, (p<0.0005), respectively). CONCLUSION: The finding of longer QTc interval with less 5-HTT binding availability in major serotonergic binding sites in l homozygotes, but not in s carriers, implicate to differentiated control of QTc interval by 5-HTTLPR polymorphism.
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Kauppila et al. (2013) conducted a cross-sectional in Healthy (n=30). 5-HTTLPR polymorphism (l homozygotes) vs. s allele carriers was evaluated on Correlation between heart rate corrected cardiac repolarization interval (QTc) and brain 5-HTT binding (r = -0.82 to -0.87, p=<0.0005). The 5-HTTLPR l homozygote genotype was associated with a significant inverse correlation between QTc interval and brain 5-HTT binding (r = -0.82 to -0.87, p<0.0005), which was absent in s allele carriers.
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