Polyunsaturated fatty acids and cerebral function: Focus on monoaminergic neurotransmission

More and more reports in recent years have shown that the intake of polyuns aturated fatty acids (PUFA) constitutes an environmental factor able to act on the central nervous system (CNS) function. We recently demonstrated tha t the effects of PUFA on behavior can be mediated through effects on the mo noaminergic neurotransmission processes. Supporting this proposal, we showe d that chronic dietary deficiency in a-linolenic acid in rats induces abnor malities in several parameters of the mesocortical and mesolimbic dopaminer gic systems. In both systems, the pool of dopamine stored in presynaptic ve sicles is strongly decreased. This may be due to a decrease in the number o f vesicles. In addition, several other factors of dopaminergic neurotransmi ssion are modified according to the system affected. The mesocortical syste m seems to be hypofunctional overall [e.g., decreased basal release of dopa mine (DA) and reduced levels of dopamine D-2 (DAD(2)) receptors]. In contra st, the mesolimbic system seems to be hyperfunctional overall (e.g., increa sed basal release of DA and increased levels of DAD2 receptors). These neur ochemical changes are in agreement with modifications of behavior already d escribed with this deficiency. The precise mechanisms explaining the effect s of PUFA on neurotransmission remain to be clarified. For example, modific ations of physical properties of the neuronal membrane, effects on proteins (receptors, transporters) enclosed in the membrane, and effects on gene ex pression and/or transcription might occur. Whatever the mechanism, it is th erefore assumed that interactions exist among PUFA, neurotransmission, and behavior, This might be related to clinical findings. Indeed, deficits in t he peripheral amounts of PUFA have been described in subjects suffering fro m 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 exis t among PUFA status, neurotransmission processes, and behavioral 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.