The BDNF Val66Met polymorphism affects HPA-axis reactivity to acute stress.
BACKGROUND
Growing evidence suggests that individual differences in HPA-axis reactivity to psychosocial stress are partly due to heritable influences. However, knowledge about the role of specific genetic variants remains very limited to date. Since brain-derived neurotrophic factor (BDNF) not only exhibits neurotrophic actions but is also involved in the regulation of hypothalamic neuropeptides, we investigated the role of a common functional polymorphism within the BDNF gene (BDNF Val66Met) in the context of endocrine and cardiovascular stress reactivity.


METHODS
Healthy male adults (N=100) were genotyped and exposed to a standardized laboratory stress task (Public Speaking). Saliva cortisol and self-reported mood levels were obtained at 6 time points prior to the stressor and during an extended recovery period. Furthermore, heart rate reactivity as an indicator of sympathetic activation was monitored continuously during the experimental procedure.


RESULTS
We report a small, but significant effect of the BDNF Val66Met polymorphism on stress reactivity. More precisely, carriers of the met-allele showed a significantly attenuated HPA-axis and cardiovascular reactivity to the psychosocial stressor compared to subjects with the val/val genotype. Furthermore, the diminished physiological response in met-allele carriers was also attended by significantly lower self-reported ratings of perceived stress and nervousness.


CONCLUSIONS
Our findings of a diminished endocrine and cardiovascular stress response in healthy male adults is consistent with a previously published study and adds further evidence for a crucial role of the BDNF Val66Met polymorphism in the modulation of stress reactivity.
Alexander
Nina
N
Center for Psychobiology and Behavioral Medicine, University of Giessen, Department of Psychology, Otto-Behaghel-Str. 10, D-35394 Giessen, Germany. nina.alexander@psychol.uni-giessen.de
Osinsky
Roman
R
Schmitz
Anja
A
Mueller
Eva
E
Kuepper
Yvonne
Y
Hennig
Juergen
J
D000328:Adult; D000339:Affect / Q000502:physiology; D000483:Alleles; D019208:Brain-Derived Neurotrophic Factor / Q000235:genetics*; D005838:Genotype; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism; D007030:Hypothalamo-Hypophyseal System / Q000378:metabolism*; D008297:Male; D010913:Pituitary-Adrenal System / Q000378:metabolism*; D011110:Polymorphism, Genetic; D012463:Saliva / Q000378:metabolism; D013315:Stress, Psychological / Q000235:genetics* / Q000503:physiopathology
D019208:Brain-Derived Neurotrophic Factor; D006854:Hydrocortisone