The ability of aged rats to sustain long-term potentiation is restored when the age-related decrease in membrane arachidonic acid concentration is reversed

McGahon, B.; Clements, Melanie; Lynch, Marina A.

doi:10.1016/s0306-4522(97)00116-4

Cited by 121 publications

(81 citation statements)

References 39 publications

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“…[79]) This effect of the oxidative stress is Ca 2+ dependent [87,88,91,92,133,134]; a finding consistent with the fact that calcium inhibits synaptic plasticity. It is noteworthy that treatment with n-3 fatty acids can restore the LTP in aged rats [70,71,[77][78][79]. Although a detailed account of the role of sodium, potassium, and calcium in the brain is beyond the scope of this review [2,49], it is worth noting that PUFA has also been shown to modulate sodium and calcium currents in the CA1 hippocampus neurons.…”

Section: Oxidative Stress and Ltpmentioning

confidence: 98%

The role of polyunsaturated fatty acids in restoring the aging neuronal membrane

Yehuda¹,

Rabinovitz²,

Carasso³

et al. 2002

Neurobiology of Aging

353

200

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In addition to a gradual loss of neurons in various brain regions, major biochemical changes in the brain affect the neuronal membrane that is the "site of action" for many essential functions including long-term potentiation (LTP), learning and memory, sleep, pain threshold, and thermoregulation. Normal physiological functioning includes the transmission of axonal information, regulation of membrane-bound enzymes, control of ionic channels and various receptors. All are highly dependent on membrane fluidity, where rigidity is increased during aging. The significantly higher level of cholesterol in aging neuronal membrane, the slow rate of cholesterol turnover, and the decreased level of total polyunsaturated fatty acids (PUFA) may result from poor passage rate via the blood-brain barrier, or from a decreased rate of incorporation into the membrane, or a decrease in the activities of delta-6 and delta-9 desaturase enzymes. The added oxidative stress, which leads to an increase of free radicals leading to a decrease in membrane fluidity, may respond to a restricted diet, and thereby overcome the damaging effects of the free radicals. A central focus of this review is that a specific ratio of n-3/n-6 PUFA can restore many of these age-related effects.

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Section: Oxidative Stress and Ltpmentioning

confidence: 98%

The role of polyunsaturated fatty acids in restoring the aging neuronal membrane

Yehuda¹,

Rabinovitz²,

Carasso³

et al. 2002

Neurobiology of Aging

353

200

View full text Add to dashboard Cite

show abstract

“…There are just as many experiments, however, reporting age-related LTP induction deficits (Lynch and Voss, 1994;McGahon et al, 1997;Murray and Lynch, 1998a,b;Tielen et al, 1983). Given that most of the experiments reporting deficits come from a single laboratory, they have been largely discounted and their findings attributed to crucial methodological differences and possibly the strain of rat used (see a review by Geinisman et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

The aging hippocampus: A multi-level analysis in the rat

et al. 2006

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The purpose of the current thesis was twofold: (1) to examine various factors that might be contributing to age-related learning and memory deficits specifically related to the hippocampus, and (2) to validate our rat model of aging, employing a multilevel analysis. We found age-related deficits on both spatial and non-spatial hippocampus-dependent tasks that were accompanied by structural alterations observed both in vivo (volume, but not neuronal metabolic function) and post mortem (neuronal density and neurogenesis, but not synaptic or mitochondrial density). Furthermore, our results suggest that the observed hippocampal structural changes, namely decreased volume and neurogenesis, predict learning and memory deficits, and both can be accounted for by neurogenic reduction. In addition, the above-mentioned pattern of age-related deficits closely resembles that seen in humans, suggesting the present rat version of aging to be a very useful model for investigating hippocampal aging in humans.

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“…Alterations in AA-containing phospholipids and/or PLA 2 activity have been reported in normal aging and neuropsychiatric disorders (Farooqui et al, 1988;Nitsch et al, 1992;McGahon et al, 1997;Smalheiser and Swanson, 1998;Hudson et al, 1999;Patrick et al, 2000). Studies in rats with a unilateral lesion of the nucleus basalis magnocellularis or of the substantia nigra, animal models of Alzheimer and Parkinson disease, respectively, have also demonstrated alterations in PLA 2 -mediated cholinergic and dopaminergic signaling Hayakawa et al, 1998).…”

mentioning

confidence: 99%

Brain Incorporation of [¹¹C]Arachidonic Acid in Young Healthy Humans Measured with Positron Emission Tomography

Giovacchini

Chang

Channing³

et al. 2002

J Cereb Blood Flow Metab

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Summary: Arachidonic acid (AA) is an important second messenger involved in signal transduction mediated by phospholipase A 2 . The goal of this study was to establish an in vivo quantitative method to examine the role of AA in this signaling process in the human brain. A simple irreversible uptake model was derived from rat studies and modified for positron emission tomography (PET) to quantify the incorporation rate K* of [ 11 C]AA into brain. Dynamic 60-minute three-dimensional scans and arterial input functions were acquired in 8 young healthy adults studied at rest. Brain radioactivity was corrected for uptake of the metabolite [ 11 C]CO 2 . K* and cerebral blood volume (V b ) were estimated pixel-by-pixel and were calculated in regions of interest. K* equaled 5.6 ± 1.2 and 2.6 ± 0.5 L · min −1 · mL −1 in gray and white matter, respectively. K* and V b values were found to be unchanged with data analysis periods from 20 to 60 minutes. Thus, PET can be used to obtain quantitative images of the incorporation rate K* of [ 11 C]AA in the human brain. As brain incorporation of labeled AA has been shown in awake rats to be increased by pharmacological activation associated with phospholipase A 2 -signaling, PET and [ 11 C]AA may be useful to measure signal transduction in the human brain.

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The ability of aged rats to sustain long-term potentiation is restored when the age-related decrease in membrane arachidonic acid concentration is reversed

Cited by 121 publications

References 39 publications

The role of polyunsaturated fatty acids in restoring the aging neuronal membrane

The role of polyunsaturated fatty acids in restoring the aging neuronal membrane

The aging hippocampus: A multi-level analysis in the rat

Brain Incorporation of [¹¹C]Arachidonic Acid in Young Healthy Humans Measured with Positron Emission Tomography

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The ability of aged rats to sustain long-term potentiation is restored when the age-related decrease in membrane arachidonic acid concentration is reversed

Cited by 121 publications

References 39 publications

The role of polyunsaturated fatty acids in restoring the aging neuronal membrane

The role of polyunsaturated fatty acids in restoring the aging neuronal membrane

The aging hippocampus: A multi-level analysis in the rat

Brain Incorporation of [11C]Arachidonic Acid in Young Healthy Humans Measured with Positron Emission Tomography

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Brain Incorporation of [¹¹C]Arachidonic Acid in Young Healthy Humans Measured with Positron Emission Tomography