Reference : Influence of Brain-Derived Neurotrophic Factor val66met human polymorphism on declara...
Scientific congresses and symposiums : Poster
Life sciences : Genetics & genetic processes
Human health sciences : Neurology
Influence of Brain-Derived Neurotrophic Factor val66met human polymorphism on declarative memory consolidation during sleep
Mascetti, Laura mailto [Université de Liège - ULg > > Centre de recherches du cyclotron >]
Foret, Ariane [Université de Liège - ULg > > Centre de recherches du cyclotron >]
Matarazzo, Luca mailto [Université de Liège - ULg > > Centre de recherches du cyclotron > >]
Muto, Vincenzo mailto [Université de Liège - ULg > > Centre de recherches du cyclotron >]
DIDEBERG, Vinciane mailto [Centre Hospitalier Universitaire de Liège - CHU > > Génétique >]
Bours, Vincent mailto [Université de Liège - ULg > Département des sciences biomédicales et précliniques > GIGA-R : Génétique humaine >]
Maquet, Pierre mailto [Université de Liège - ULg > > Centre de recherches du cyclotron >]
European Sleep Research Society
14 - 18 septembre 2010
[en] Objectives
The Brain-Derived Neurotrophic Factor (BDNF) is a neurotrophin which in the adult brain, regulates long-term potentiation and has been involved in the build up of the homeostatic sleep pressure in rodents. In humans, valine (val) to methionine (met) substitution in the 5’ pro-region of the BDNF protein is associated with poorer episodic memory. Neurons transfected with met-BDNF-Green Fluorescence Protein showed lower depolarization-induced secretion, while constitutive secretion is unchanged. Here, we hypothesized that the differences in BDNF release determined by this polymorphism would influence sleep-dependent memory consolidation and that in comparison with the met-carriers (val/met or met/met), val/val individuals would show higher memory performance after one night of sleep rather than an immediate retrieval session.
Participants encoded a series of neutral faces in the afternoon. Retrieval sessions took place one hour after the encoding session, and in the following morning, after a night of polysomnographic-monitored sleep. During retrieval, studied faces and new ones were presented in random order. For each stimulus, the subjects indicated whether they could retrieve the encoding episode with (“Remember” response), or without details (“know” response), or if they thought the item had not been presented during encoding (“New” response).
A repeated-measure ANOVA on discrimination index (d’) showed significant effects of group (F(1, 22)=4.66, p=0.042) and session (F(1, 22)=12.21, df=1, p=0.002). Although the group by session interaction was not significant (F(1, 22)=1.84, p=0.188), exploratory planned comparisons showed that at immediate retrieval, d’ was not significantly different between groups (val/val, d’ = 1.94±0.16; met-carriers, d’= 1.61±0.14; p>0.5). In contrast, during the second retest (the next day) d’ in the val/val group (d’=2.56±0.23) was significantly higher than in the met-carriers group (d’=1.88±0.21; p=0.041). Likewise, a between-session enhancement in d’ was detected only in the val/val population (p=0.003).
Val/val individuals demonstrate higher memory performance than met-carriers after a night of sleep but not at immediate retest. These data suggest that activity-dependent BDNF release promotes memory consolidation during the first post-training hours. Further analysis of the present data set will assess the respective effect of sleep and time on the BDNF-associated delayed memory enhancement.
This study was supported by FNRS-FRIA, the University of Liège, and the QEMF.

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