Chronic Dietary Alpha-Linoleic Acid Deficiency Alters Dopaminergic and Serotoninergic Neurotransmission in Rats.

January 1, 1994 Human Health and Nutrition Data 0 Comments

Chronic Dietary Alpha-Linoleic Acid Deficiency Alters Dopaminergic and Serotoninergic Neurotransmission in Rats.

Year: 1994
Authors: S Delion, S Chalon, J Herault, D Guilloteau, J C Besnard, G Durand.
Publication Name: J. Nutr.
Publication Details: Volume 124; Number 12; 2466.


Previous research has shown that diets deficient in ALA affect the FA composition of membrane PLs in the CNS resulting in alterations in membrane fluidity, enzyme activities and the binding of neurotransmitters and hormones to membrane receptors. Diets deficient in ALA impair brain functions such as learning and memory, cognitive functions and reinforcement processes. These same activities are also compromised when dopaminergic neurons are damaged. The authors speculated that the similarities in the two effects suggests that ALA deficiency may impair the dopaminergic system. The aim of the present study was to examine the effects of dietary ALA deficiency on dopaminergic and serotoninergic neurotransmission systems in male Wistar rats. The research focussed on the dopaminergic D2 and serotoninergic 5-HT2 receptors because of their involvement in several physiological functions. Levels of endogenous monoamines were also measured. These factors were assessed in 3 cerebral regions: the frontal cortex, the striatum and the cerebellum. Rats were fed semipurified diets containing peanut oil as the (n-3)- deficient group or peanut oil plus canola oil (200 mg/100 g diet of ALA – control group) from weaning to 60 days of age. Long-term feeding of the (n-3)- deficient diet induced a significantly higher 5-HT2 receptor density in the frontal cortex compared with the control rats. No differences were noted between the dietary groups in regard to endogenous serotonin concentrations. The serotoninergic systems are involved in memory and learning processes. Modifications in dopaminergic neurotransmission, specifically in the frontal cortex, were noted in rats fed the diet deficient in ALA. A significantly lower density of D2 receptors and a significantly lower concentration of endogenous dopamine were also found in these rats in comparison to control rats. The dopaminergic systems are involved in the regulation of behavioral processes such as motor activity, emotion and spatial orientation. In rats fed the ALA diet, DHA was the predominant PUFA found in all 3 brain regions. Lower levels of the n-3 PUFAs in all brain regions studied were noted in the deficient rats. DHA levels were 68%, 75% and 71% lower in the frontal cortex, the striatum and the cerebellum, respectively when ALA deficient rats were compared to controls. Levels of n-6 PUFAs were significantly higher in the animals fed the diet deficient in ALA. The authors speculated that the changes noted in 5 HT2 and the D2 site densities may be associated with variations in the lipid composition of cortical membranes in the deficient animals. It was concluded that chronic consumption of an ALA deficient diet could induce modifications in neurotransmission pathways in the brain which may be responsible for behavioral disturbances previously described in ALA-deficient animals. The authors noted that it is often difficult to define the effect of ALA deficiency on learning as other performance factors are affected at the same time.

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