Dietary Fish Oil Affects Monoaminergic Neurotransmission and Behavior in Rats

Chalon, Sylvie; Delion-Vancassel, Sylvie; Belzung, Catherine; Guilloteau, Denis; Leguisquet, Anne-Marie; Besnard, Jean‐Claude; Durand, Georges

doi:10.1093/jn/128.12.2512

Cited by 238 publications

(152 citation statements)

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“…Furthermore, dopamine levels in the frontal cortex of rats fed a PUFAdeficient diet were also reduced (32)(33)(34). Importantly, the opposite trend (increased dopamine levels) was observed in rats fed a PUFA-rich diet (35). A potential role for ␣S in the formation and/or maintenance of synaptic vesicles has been shown in other studies (36,37).…”

Section: Cell Typementioning

confidence: 80%

Altered Fatty Acid Composition of Dopaminergic Neurons Expressing α-Synuclein and Human Brains with α-Synucleinopathies

Sharon

Bar-Joseph

Mirick

et al. 2003

Journal of Biological Chemistry

167

184

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␣-Synuclein (␣S) is an abundant neuronal protein that accumulates in insoluble inclusions in Parkinson's disease (PD) and the related disorder, dementia with Lewy bodies (DLB).A central question about the role of ␣S in the pathogenesis of PD and DLB concerns how this normally soluble protein assembles into insoluble aggregates associated with neuronal dysfunction. We recently detected highly soluble oligomers of ␣S in normal brain supernatants and observed their augmentation in PD and DLB brains. Further, we found that polyunsaturated fatty acids (PUFAs) enhanced ␣S oligomerization in intact mesencephalic neuronal cells. We now report the presence of elevated PUFA levels in PD and DLB brain soluble fractions. Higher PUFA levels were also detected in the supernatants and high-speed membrane fractions of neuronal cells over-expressing wild-type or PD-causing mutant ␣S. This increased PUFA content in the membrane fraction was accompanied by increased membrane fluidity in the ␣S overexpressing neurons. In accord, membrane fluidity and the levels of certain PUFAs were decreased in the brains of mice genetically deleted of ␣S. Together with our earlier observations, these results suggest that ␣S-PUFA interactions help regulate neuronal PUFA levels as well as the oligomerization state of ␣S, both normally and in human synucleinopathies.␣-Synuclein (␣S), 1 a 140-residue protein implicated in both familial and sporadic Parkinson's disease (PD), occurs principally as a cytoplasmic polypeptide in neurons and is localized in part to presynaptic terminals (1). In general, brain ␣S is highly soluble, and purified recombinant ␣S is reported to have a disordered random coil structure in solution (2). A wide array of factors has been found to induce the aggregation of ␣S under experimental conditions. These include PD-causing missense mutations in ␣S (3-5), mitochondrial inhibitors and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) (6, 7), proteosome inhibitors (8, 9), heavy metals (10, 11), oxidative stress (12, 13), ␣S phosphorylation (14), and fatty acids, whether within phospholipids (15) or as free fatty acids (16). Interestingly, some of the factors that can induce ␣S aggregation experimentally have been found to be associated with PD, e.g. ␣S mutations, mitochondrial complex I dysfunction, proteosomal dysfunction, and oxidative stress. Other factors, including free fatty acid composition, have not been comprehensively studied in the brains of patients with PD and other synucleinopathies.We recently obtained evidence that ␣S can directly bind fatty acids (17) and can form highly soluble oligomers in response to the treatment of cultured neurons with polyunsaturated fatty acids (PUFA) (16). Further, we observed a pool of soluble ␣S oligomers that is detectable only after biochemical treatments that remove fatty acids and other lipids (16, 17). These highly soluble, lipid-associated oligomers were detected in mesencephalic neuronal (MES) cells expressing human ␣S, in the brains of normal and human ␣S transgenic mice, an...

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Section: Cell Typementioning

confidence: 80%

Altered Fatty Acid Composition of Dopaminergic Neurons Expressing α-Synuclein and Human Brains with α-Synucleinopathies

Sharon

Bar-Joseph

Mirick

et al. 2003

Journal of Biological Chemistry

167

184

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“…As for dopamine concentrations, frontal cortex serotonin concentrations were increased in rats fed diets supplemented with n-3 PUFA 85 . In line with this, serotonin in the frontal cortex was reduced in piglets fed n-3 and n-6 PUFA-deficient formula for 18 d from birth compared with piglets fed formula supplemented with linoleic acid and alinolenic acid and/or arachidonic acid and DHA 96 .…”

Section: Findings and Mechanisms In Different Mammalsmentioning

confidence: 96%

“…n-3 PUFA-deficient rats had a lower number of D 2 receptors in the frontal cortex 91,92,94 but higher in the nucleus accumbens 93,94 . Rats fed diets supplemented with EPA and DHA had an increased dopamine concentration and D 2 binding possibly as a result of a reduction in monoamine oxidase activity in the frontal cortex compared with rats fed adequate amounts of PUFA 85 .…”

Section: Findings and Mechanisms In Different Mammalsmentioning

confidence: 98%

“…For example, chronic dietary deficiency in n-3 PUFA resulted in low concentrations of n-3 PUFA in the rat brain 76,77 whereas diets high in EPA and DHA resulted in high concentrations of EPA and DHA in the brain of rats 85,100,101 . In addition, dietary a-linolenic acid deficiency induces a more pronounced reduction in DHA concentrations in the frontal cortex than in the striatum and cerebellum 72,91 .…”

Section: Findings and Mechanisms In Different Mammalsmentioning

confidence: 99%

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Impact of nutrition on canine behaviour: current status and possible mechanisms

et al. 2007

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Each year, millions of dogs worldwide are abandoned by their owners, relinquished to animal shelters, and euthanised because of behaviour problems. Nutrition is rarely considered as one of the possible contributing factors of problem behaviour. This contribution presents an overview of current knowledge on the influence of nutrition on canine behaviour and explores the underlying mechanisms by which diet may affect behaviour in animals. Behaviour is regulated by neurotransmitters and hormones, and changes in the availability of their precursors may influence behaviour. Tryptophan, the precursor of serotonin, may affect the incidence of aggression, selfmutilation and stress resistance. The latter may also be influenced by dietary tyrosine, a precursor to catecholamines. As diet composition, nutrient availability and nutrient interactions affect the availability of these precursors in the brain, behaviour or stress resistance may be affected. PUFA, especially DHA, have an important role as structural constituents in brain development, and dietary supply of n-3 and n-6 PUFA could modify aspects of the dopaminergic and serotonergic system and, consequently, cognitive performance and behaviour. Finally, persistent feeding motivation between meals can increase stereotyped behaviour and aggression and decrease resting time. This feeding motivation may be altered by dietary fibre content and source. At present, few studies have been conducted to evaluate the role of nutrition in canine (problem) behaviour through the above mentioned mechanisms. Studies that explore this relationship may help to improve the welfare of dogs and their owners.

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“…LCn3PUFAs may also increase levels of monoaminergic neurotransmitters in the brain [11], and inhibit inflammation that is associated with depression [9]. The mechanisms underlying depression are complex and, while there is some evidence linking change to cerebrovascular structure and function with depression [12], other evidence suggests that inflammatory changes are central [13].…”

Section: Introductionmentioning

confidence: 99%