Biochemical changes of rat brain membranes with aging

Calderini, G.; Bonetti, A; Battistella, A.; Crews, Fulton T.; Toffano, G.

doi:10.1007/bf00965104

Cited by 72 publications

(27 citation statements)

References 24 publications

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“…These results are in agreement with others (Samson and Quinn 1967;Mishra and Shankar 1980;Tsutsumi et al 1995) showing enhanced Na,K-ATPase activity with age. These findings of increased SPM Na,K-ATPase activity with age differ from those reported by Calderini et al (1983) who showed a decrease ( 35%) in SPM Na,K-ATPase with age. The reason for this discrepancy between studies may be due to the time periods in which Na,K-ATPase activity was measured (weeks vs. months).…”

Section: Discussioncontrasting

confidence: 99%

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

Bowen

Clandinin

2002

Journal of Neurochemistry

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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.

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Section: Discussioncontrasting

confidence: 99%

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

Bowen

Clandinin

2002

Journal of Neurochemistry

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“…Like tCho, phosphorylethanolamine levels continued their developmental trend for decrease during adulthood and aging. The inverse trajectory in the evolution of tCho and phosphorylethanolamine levels in the aging brain may be related to modifications in cell membrane fluidity (Calderini et al, 1983). In line with this, a 31 P MRS study showed that the glycerylated forms of such phospholipids increase with age in the human brain (Blüml et al, 1999).…”

Section: Discussionmentioning

confidence: 73%

Longitudinal neurochemical modifications in the aging mouse brain measured in vivo by 1H magnetic resonance spectroscopy

Duarte

Gruetter

2014

Neurobiology of Aging

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H MRS Brain Metabolism a b s t r a c tAlterations to brain homeostasis during development are reflected in the neurochemical profile determined noninvasively by 1 H magnetic resonance spectroscopy. We determined longitudinal biochemical modifications in the cortex, hippocampus, and striatum of C57BL/6 mice aged between 3 and 24 months . The regional neurochemical profile evolution indicated that aging induces general modifications of neurotransmission processes (reduced GABA and glutamate), primary energy metabolism (altered glucose, alanine, and lactate) and turnover of lipid membranes (modification of choline-containing compounds and phosphorylethanolamine), which are all probably involved in the frequently observed age-related cognitive decline. Interestingly, the neurochemical profile was different in male and female mice, particularly in the levels of taurine that may be under the control of estrogen receptors. These neurochemical profiles constitute the basal concentrations in cortex, hippocampus, and striatum of healthy aging male and female mice.

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“…A number of reports have indicated that aging is associated with changes in membrane composition (15,42,43), and, although the underlying cause remains unclear, it has been accepted that lipid peroxidation, apparently triggered by reactive oxygen species, can lead to a decrease in membrane polyunsaturated fatty acids (23), which contributes to membrane rigidity (22,44). We have found that lipid peroxidation is increased, whereas membrane arachidonic acid concentration is decreased, in hippocampal tissue prepared from aged rats 2 ; these data, albeit obtained in separate experiments, suggested that arachidonic acid may be one target molecule for lipid peroxidation.…”

Section: Fig 3 the Age-related Increases In Il-1␤ Concentration (A)mentioning

confidence: 99%

“…Previous observations have indicated changes in membrane composition, particularly in arachidonic acid concentration, with age (3,19,42,43). Arachidonic acid modulates synaptic function (3,5), and its membrane concentration correlates with ability of aged rats to sustain LTP (3); therefore, it was predicted that the age-related changes in arachidonic acid may underlie some of the impairments in neuronal function that accompany aging (e.g.…”

Section: Fig 3 the Age-related Increases In Il-1␤ Concentration (A)mentioning

confidence: 99%

Dietary Supplementation with Vitamin E Reverses the Age-related Deficit in Long Term Potentiation in Dentate Gyrus

Murray

Lynch

1998

Journal of Biological Chemistry

145

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Long term potentiation (LTP) in dentate gyrus is impaired in aged rats, and this has been associated with an age-related decrease in membrane arachidonic acid concentration. In this study, we considered whether the trigger for this age-related decrease in arachidonic acid might be increased lipid peroxidation stimulated by the proinflammatory cytokine, interleukin-1␤. Groups of aged and young rats were fed on a control diet or a diet supplemented with ␣-tocopherol and assessed for their ability to sustain LTP. Aged rats fed on the control diet exhibited an impaired ability to sustain LTP and analysis of tissue prepared from these rats exhibited increased interleukin-1␤, increased lipid peroxidation, and decreased membrane arachidonic acid concentration compared with young rats fed on either diet. Aged rats fed on the supplemented diet sustained LTP in a manner indistinguishable from young rats, and the agerelated increases in interleukin-1␤ and lipid peroxidation and the decrease in membrane arachidonic acid concentration were all reversed. We propose that interleukin-1␤ may be the trigger that induces these agerelated changes and may therefore be responsible for the deficit in long term potentiation in aged rats. The observation that ␣-tocopherol reverses these changes is consistent with the hypothesis that some age-related changes in hippocampus might derive from oxidative stress.Aging is associated with compromised neuronal activity, perhaps typified by a deficit in cognitive function. One particular age-related impairment in neuronal function in the rat is a decrease in ability to sustain long term potentiation (LTP 1 ; Refs. 1-5), which is a putative biological substrate for cognitive function and a model for learning and/or memory. Evidence suggests that a cascade of biochemical changes, initiated by activation of the N-methyl-D-aspartate subtype of glutamate receptor is required to support this form of synaptic plasticity in the dentate gyrus (6). Although the underlying cause of the age-related impairment in ability to sustain LTP is not known, down-regulation of several components of the biochemical cascade has been identified in aged rats. Thus, N-methyl-D-aspartate receptor activity is compromised with age (e.g. Ref. 7), whereas down-regulation of other factors that play a role in induction of LTP, like calcium handling by cells (1) and activation of enzymes such as phospholipase A 2 (3) and protein kinases (8), has been reported. Similarly, factors that play a role in maintenance of LTP, like increased glutamate release, have also been shown to be compromised in hippocampus of aged rats (3,5,9). In addition, the more persistent aspects of LTP, which rely on increased synthesis of new proteins (10 -12) and morphological changes (13), are also impaired in the hippocampus of aged rats (12,14). Despite this immense body of data, the underlying cause of the impairment in ability of aged rats to sustain LTP is not known.One unifying cause of the age-related changes in biochemical parameters might be a chan...

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Biochemical changes of rat brain membranes with aging

Cited by 72 publications

References 24 publications

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

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

Longitudinal neurochemical modifications in the aging mouse brain measured in vivo by 1H magnetic resonance spectroscopy

Dietary Supplementation with Vitamin E Reverses the Age-related Deficit in Long Term Potentiation in Dentate Gyrus

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