, Volume 36, Issue 9, pp 937-944

First online:

Polyunsaturated fatty acids and cerebral function: Focus on monoaminergic neurotransmission

  • Sylvie ChalonAffiliated withINSERM U316, Laboratoire de Biophysique Médicale et Pharmaceutique, UFR Pharmacie Email author 
  • , Sylvie VancasselAffiliated withLaboratoire Nutrition et Sécurité Alimentaire, INRA
  • , Luc ZimmerAffiliated withINSERM U316, Laboratoire de Biophysique Médicale et Pharmaceutique, UFR Pharmacie
  • , Denis GuilloteauAffiliated withINSERM U316, Laboratoire de Biophysique Médicale et Pharmaceutique, UFR Pharmacie
  • , Georges DurandAffiliated withLaboratoire Nutrition et Sécurité Alimentaire, INRA

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More and more reports in recent years have shown that the intake of polyunsaturated fatty acids (PUFA) constitutes an environmental factor able to act on the central nervous system (CNS) function. We recently demonstrated that the effects of PUFA on behavior can be mediated through effects on the monoaminergic neurotransmission processes. Supporting this proposal, we showed that chronic dietary deficiency in α-linolenic acid in rats induces abnormalities in several parameters of the mesocortical and mesolimbic dopaminergic systems. In both systems, the pool of dopamine stored in presynaptic vesicles is strongly decreased. This may be due to a decrease in the number of vesicles. In addition, several other factors of dopaminergic neurotransmission are modified according to the system affected. The mesocortical system seems to be hypofunctional overall [e.g., decreased basal release of dopamine (DA) and reduced levels of dopamine D2 (DAD2) receptors]. In contrast, the mesolimbic system seems to be hyperfunctional overall (e.g., increased basal release of DA and increased levels of DAD2 receptors). These neurochemical changes are in agreement with modifications of behavior already described with this deficiency. The precise mechanisms explaining the effects of PUFA on neurotransmission remain to be clarified. For example, modifications of physical properties of the neuronal membrane, effects on proteins (receptors, transporters) enclosed in the membrane, and effects on gene expression and/or transcription might occur. Whatever the mechanism, it is therefore assumed that interactions exist among PUFA, neurotransmission, and behavior. This might be related to clinical findings. Indeed, deficits in the peripheral amounts of PUFA have been described in subjects suffering from neurological and psychiatric disorders. Involvement of the monoaminergic neurotransmission function has been demonstrated or hypothesized in several of these diseases. It can therefore be proposed that functional links exist among PUFA status, neurotransmission processes, and behavioural disorders in humans. Animal models are tools of choice for the understanding of such links. Improved prevention and complementary treatment of neurological and psychiatric diseases can be expected from these studies.