Dietary low linolenic acid compared with docosahexaenoic acid alter synaptic plasma membrane phospholipid fatty acid composition and sodium–potassium ATPase kinetics in developing rats

Abstract

The objective of this study was to investigate if maternal dietary 20:4n-6 arachidonic acid (AA) and 22:6n-3 compared with adequate or low levels of 18:3n-3 linolenic acid (LNA) increases synaptic plasma membrane (SPM) cholesterol and phospholipid content, phospholipid 20:4n-6 and 22:6n-3 content, and Na,K-ATPase kinetics in rat pups at two and five weeks of age. At parturition, Sprague-Dawley rats were fed semi-purified diets containing either AA + docosahexaenoic acid (DHA), adequate LNA (control; 18:2n-6 : 18:3n-3 ratio of 7.1 : 1) or low LNA (18:2n-6 : 18:3n-39 ratio of 835 : 1). During the first two weeks of life, the rat pups received only their dams' milk. After weaning, pups received the same diet as their respective dams to five weeks of age. No significant difference was observed among rat pups fed the diet treatments for SPM cholesterol or total and individual phospholipid content at two and five weeks of age. Fatty acid analysis revealed that maternal dietary AA + DHA, compared with feeding the dams the control diet or the low LNA diet, increased 20:4n-6 in phosphatidylserine and 22:6n-3 content of SPM phospholipids. Rats fed dietary AA + DHA or the control diet exhibited a significantly increased V max for SPM Na,K-ATPase. Diet treatment did not alter the K m (affinity) of SPM Na,K-ATPase in rat pups at two and five weeks of age. It is concluded that dietary AA + DHA does not alter SPM cholesterol and phospholipid content but increases the 22:6n-3 content of SPM phospholipids modulating activity of Na,K-ATPase.

Dietary cholesterol, fats and risk of Parkinson's disease in the Singapore Chinese Health Study

“…537 MUFA have been shown to have anti-inflammatory and immune-modulating properties 538 and might protect against oxidative stress. 245 In addition, it has been suggested that low MUFA in the brain cell membranes may result in greater degeneration in PD.…”

Dietary fat intake and risk of Parkinson's disease: A case-control study in Japan

“…On the other hand, because of the high concentration of polyunsaturated fatty acids in the brain, reactive products of lipid peroxidation are likely contributors to neurodegeneration [15]. Laboratory studies in rats showed that the brain content of fatty acids such as polyunsaturated fatty acids depends on dietary intake [16][17][18].…”

Fatty Aspirin: A New Perspective in the Prevention of Dementia of Alzheimers Type?

“…At the cellular level, DHA can protect neuronal cells from apoptotic death [58], induce synaptic growth cones during neuronal development [91], enhance synaptic function [19,92], stimulate neurite outgrowth cells [18], regulate nerve growth factors and influence neuronal size [93]. DHA also plays a crucial role at the membrane level as it can alter membrane receptors [94], can regulate the activity of membrane-bound enzymes [95], ionic channels [96] neurotransmitters [97] and induce BDNF protein expression (hence the ability of DHA to regulate BDNF, an enhancer of synaptic plasticity, may contribute to its therapeutic efficacy) [14]. Moreover, it is known that BDNF facilitates the synapse by modulating synapsin I and cyclic AMP-response element-binding protein (CREB), which have been implicated in synaptic plasticity associated to learning and memory [98].…”