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Journal of Lipid Research, Vol. 43, 1209-1219, August 2002
Copyright © 2002 by Lipid Research, Inc.

Reversibility of n-3 fatty acid deficiency-induced changes in dopaminergic neurotransmission in rats

Ercem Kodas^*, Sylvie Vancassel, Bernard Lejeune, Denis Guilloteau^* and Sylvie Chalon^1,*

^* INSERM U316, UFR des Sciences Pharmaceutiques, 37200 Tours, France
Laboratoire de Biophysique Médicale et Pharmaceutique, Université François Rabelais, and Laboratoire de Biophysique et Mathématiques, UFR des Sciences Pharmaceutiques, 37200 Tours, France
INRA, Laboratoire de Nutrition et Sécurité Alimentaire, Jouy-en-Josas, France

¹ To whom correspondence should be addressed. e-mail: chalon{at}univ-tours.fr

Previous investigations have shown that the lipid composition of cerebral membranes and dopaminergic neurotransmission are changed under chronic -linolenic acid diet deficiency in the rat. This study investigated whether these changes could be reversed and if the stage of brain maturation might play a role in the recovery process. The effects of reversion on the fatty acid (FA) composition and dopaminergic neurotransmission were studied in brain regions known to be affected by such deficiency (i.e., the prefrontal cortex and nucleus accumbens) in 2-month-old animals. Dopamine release under pharmacological stimulation was studied using a dual-probe microdialysis method. Vesicular monoamine transporters were studied using quantitative autoradiography. The reversal diet, with adequate levels of n-6 and n-3 polyunsaturated fatty acids (PUFAs), was given to deficient rats at different stages of development (0, 7, 14, or 21 days of age). The results showed that when given during the lactating period, this diet was able to restore both the FA composition of brain membranes and the parameters of dopaminergic neurotransmission studied. However, when given from weaning, it allowed partial recovery of biochemical parameters but no recovery of neurochemical factors.

The occurrence of profound n-3 PUFA deficiency during the lactating period could therefore be an environmental insult leading to irreversible damage to specific brain functions.

Abbreviations: AA, arachidonic acid; DA, dopamine; DHA, docosahexaenoic acid; FA, fatty acid; LC-PUFA, long chain polyunsaturated fatty acid; MUFA, monounsaturated fatty acid; NAcc, nucleus accumbens; PC, phosphatidylcholine; PE, phosphatidylethanolamine; PFCx, prefrontal cortex; PS, phosphatidylserine; PUFA, polyunsaturated fatty acid; SFA, saturated fatty acid; VMAT₂, vesicular monoamine transporter

Supplementary key words -linolenic acid diet deficiency • -linolenic acid diet supplementation • brain development • dopamine • docosahexaenoic acid • microdialysis • phospholipids

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