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Titre du document / Document title

Exercise reverses the harmful effects of consumption of a high-fat diet on synaptic and behavioral plasticity associated to the action of brain-derived neurotrophic factor

Auteur(s) / Author(s)

MOLTENI R. (1) ; WU A. (1) ; VAYNMAN S. (1) ; YING Z. (1) ; BARNARD R. J. (1) ; GOMEZ-PINILLA F. (1 2) ;

Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)

(1) Department of Physiological Science, Brain Injury Research Center, University of California at Los Angeles, 621 Charles E. Young Drive, Los Angeles, CA 90095, ETATS-UNIS
(2) Division of Neurosurgery, Brain Injury Research Center, University of California at Los Angeles, Los Angeles, CA 90095, ETATS-UNIS

Résumé / Abstract

A diet high in total fat (HF) reduces hippocampal levels of brain-derived neurotrophic factor (BDNF), a crucial modulator of synaptic plasticity, and a predictor of learning efficacy. We have evaluated the capacity of voluntary exercise to interact with the effects of diet at the molecular level. Animal groups were exposed to the HF diet for 2 months with and without access to voluntary wheel running. Exercise reversed the decrease in BDNF and its downstream effectors on plasticity such as synapsin I, a molecule with a key role in the modulation of neurotransmitter release by BDNF, and the transcription factor cyclic AMP response element binding protein (CREB), important for learning and memory. Furthermore, we found that exercise influenced the activational state of synapsin as well as of CREB, by increasing the phosphorylation of these molecules. In addition, exercise prevented the deficit in spatial learning induced by the diet, tested in the Morris water maze. Furthermore, levels of reactive oxygen species increased by the effects of the diet were decreased by exercise. Results indicate that exercise interacts with the same molecular systems disrupted by the HF diet, reversing their effects on neural function. Reactive oxygen species, and BDNF in conjunction with its downstream effectors on synaptic and neuronal plasticity, are common molecular targets for the action of the diet and exercise. Results unveil a possible molecular mechanism by which lifestyle factors can interact at a molecular level, and provide information for potential therapeutic applications to decrease the risk imposed by certain lifestyles.

Revue / Journal Title

Neuroscience    ISSN  0306-4522   CODEN NRSCDN 

Source / Source

2004, vol. 123, no2, pp. 429-440 [12 page(s) (article)] (1 p.1/4)

Langue / Language

Anglais

Editeur / Publisher

Elsevier, Amsterdam, PAYS-BAS  (1976) (Revue)

Mots-clés anglais / English Keywords

Central nervous system

;

Encephalon

;

Feeding

;

Hippocampus

;

Transcription factor CREB

;

Brain derived neurotrophic factor

;

Behavior

;

Synaptic plasticity

;

Diet

;

Fat

;

Physical exercise

;

Mots-clés français / French Keywords

Système nerveux central

;

Encéphale

;

Alimentation

;

Synapsine I

;

Hippocampe

;

Facteur transcription CREB

;

Facteur BDNF

;

Comportement

;

Plasticité synaptique

;

Régime alimentaire

;

Matière grasse

;

Exercice physique

;

Mots-clés espagnols / Spanish Keywords

Sistema nervioso central

;

Encéfalo

;

Alimentación

;

Hipocampo

;

Factor transcripción CREB

;

Factor BDNF

;

Conducta

;

Plasticidad sináptica

;

Régimen alimentario

;

Materia grasa

;

Ejercicio físico

;

Mots-clés d'auteur / Author Keywords

synapsin I

;

CREB

;

neuronal plasticity

;

cognitive function

;

hippocampus

;

water maze

;

Localisation / Location

INIST-CNRS, Cote INIST : 17194, 35400011637197.0110

Nº notice refdoc (ud4) : 15410434



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