Peroxidative oxidation of lipids in slices of olfactory cortex of the rat brain during long-term potentiation

Nilova, N. S.; Polezhaeva, L N

doi:10.1007/bf02391152

Cited by 4 publications

(3 citation statements)

References 9 publications

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“…Cholesterol-content-dependent change of membrane fluidity, reported to affect the ligandreceptor binding (44), could be a candidate mechanism for modulation of synaptic plasticity mediated by cholesterol. It is important to note that membrane fluidity can be also modified by the change of membrane lipid peroxidation, reported to accompany LTP course in slices (45), as well as by the change in the level of cholesterol esterification (46). Another possible mechanism, proposed previously, likely to occur at the postsynaptic locus is the modulation of receptor function by a specific cholesterol-receptor interaction (44) or cholesterol efflux-dependent membrane lipid raft (47) structural and/or functional deterioration.…”

Section: Cholesterol Efflux Synaptic Plasticity and Neurodegenerationmentioning

confidence: 92%

Essential role for cholesterol in synaptic plasticity and neuronal degeneration

2001

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There is no understanding of the role of cholesterol and phospholipids in the mechanisms of synaptic function and neurodegeneration. Here we report that cholesterol disbalance is critical for synaptic transmission and plasticity as investigated by a study of paired pulse facilitation (PPF) and long‐term potentiation (LTP). Extracellular recording of field‐evoked postsynaptic potentials showed enhanced PPF ratio and an impairment of LTP in CA1 subfield of adult rat ex‐vivo hippocampal slices subjected to cyclodextrin‐ or normal human CSF‐HDL3‐mediated cholesterol efflux. Immunofluorescence with antibodies against neurofilament and tau revealed that cholesterol and phospholipids depletion causes alteration of normal hippocampal neurites and the appearance of PHF‐tau in the mossy fibers. We further find that LTP and amyloid β protein increase [14C]acetate label incorporation into newly synthesized hippocampal membrane lipids. Our results indicate the importance of neuronal cholesterol redistribution and synthesis for synaptic plasticity and neurodegeneration.

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Section: Cholesterol Efflux Synaptic Plasticity and Neurodegenerationmentioning

confidence: 92%

Essential role for cholesterol in synaptic plasticity and neuronal degeneration

2001

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“…Studies of brain slice preparations have shown that MLP can modify long-term potentiation of synaptic transmission (6, 7), a form of synaptic plasticity known to be mediated by Ca 2ϩ influx (68). In addition, it has been reported that levels of MLP increase in slices in response to stimulation that induces long-term potentiation (5). Because phosphorylation of VDCCs and other types of ion channels is thought to be a major mechanism for regulating synaptic plasticity, it will be of considerable interest to determine whether 4HN plays a role in modifying synaptic plasticity.…”

Section: Discussionmentioning

confidence: 99%

The Lipid Peroxidation Product 4-Hydroxynonenal Facilitates Opening of Voltage-dependent Ca2+ Channels in Neurons by Increasing Protein Tyrosine Phosphorylation

Lu¹,

Chan²,

Fu³

et al. 2002

Journal of Biological Chemistry

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Calcium influx through voltage-dependent calcium channels (VDCCs) mediates a variety of functions in neurons and other excitable cells, but excessive calcium influx through these channels can contribute to neuronal death in pathological settings. Oxyradical production and membrane lipid peroxidation occur in neurons in response to normal activity in neuronal circuits, whereas excessive lipid peroxidation is implicated in the pathogenesis of of neurodegenerative disorders. We now report on a specific mechanism whereby lipid peroxidation can modulate the activity of VDCCs. The lipid peroxidation product 4-hydroxy-2,3-nonenal (4HN) enhances dihydropyridine-sensitive whole-cell Ca 2؉ currents and increases depolarization-induced increases of intracellular Ca 2؉ levels in hippocampal neurons. Prolonged exposure to 4HN results in neuronal death, which is prevented by treatment with glutathione and attenuated by the L-type Ca 2؉ channel blocker nimodipine. Tyrosine phosphorylation of ␣1 VDCC subunits is increased in neurons exposed to 4HN, and studies using inhibitors of tyrosine kinases and phosphatases indicate a requirement for tyrosine phosphorylation in the enhancement of VDCC activity in response to 4HN. Phosphorylation-mediated modulation of Ca 2؉ channel activity in response to lipid peroxidation may play important roles in the responses of neurons to oxidative stress in both physiological and pathological settings.

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“…1998). Given that lipid peroxidation can occur in neurons in association with conditions of plasticity including long‐term potentiation (Nilova and Polezhaeva 1996) and epileptic seizures (Ueda et al . 1997), it is reasonable to consider that 4HN modulates these processes.…”

Section: Discussionmentioning

confidence: 99%

Selective and biphasic effect of the membrane lipid peroxidation product 4‐hydroxy‐2,3‐nonenal on N‐methyl‐d‐aspartate channels

Chan

Haughey

et al. 2001

Journal of Neurochemistry

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Increased oxyradical production and membrane lipid peroxidation occur in neurons under physiological conditions and in neurodegenerative disorders. Lipid peroxidation can alter synaptic plasticity and may increase the vulnerability of neurons to excitotoxicity, but the underlying mechanisms are unknown. We report that 4-hydroxy-2,3-nonenal (4HN), an aldehyde product of lipid peroxidation, exerts a biphasic effect on NMDA-induced current in cultured rat hippocampal neurons with current being increased during the ®rst 2 h and decreased after 6 h. Similarly, 4HN causes an early increase and a delayed decrease in NMDA-induced elevation of intracellular Ca 21 levels. In contrast, 4HN affects neither the ion current nor the Ca 21 response to a-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA). The initial enhancement of NMDA-induced current is associated with increased phosphorylation of the NR1 receptor subunit, whereas the delayed suppression of current is associated with cellular ATP depletion and mitochondrial membrane depolarization. Cell death induced by 4HN is attenuated by an NMDA receptor antagonist, but not by an AMPA receptor antagonist. A secreted form of amyloid precursor protein, previously shown to protect neurons against oxidative and excitotoxic insults, prevented each of the effects of 4HN including the early and late changes in NMDA current, delayed ATP depletion, and cell death. These ®ndings show that the membrane lipid peroxidation product 4HN can modulate NMDA channel activity, suggesting a role for this aldehyde in physiological and pathophysiological responses of neurons to oxidative stress. Keywords: Alzheimer's disease, amyloid precursor protein, calcium, excitotoxicity, mitochondrial depolarization, synaptic plasticity. Neurons are subjected to considerable oxidative stress under physiological conditions as the result of oxyradical production that occurs during mitochondrial respiration and activities of enzymes such as nitric oxide synthase and cyclooxygenases (Dagani et al. 1988;Lipton et al. 1994;Kaufmann et al. 1997). However, excessive oxyradical production may contribute to the dysfunction and death of neurons that occurs in several neurodegenerative disorders (Chan 1996;Lovell et al. 1997;Mattson and Pedersen 1998;Olanow and Tatton 1999;Mattson et al. 2000a). Free radical attack on unsaturated bonds of membrane fatty acids results in an autocatalytic process called membrane lipid peroxidation, which can be triggered by production of hydroxyl, superoxide and nitric oxide radicals (Gutteridge 1995;Traylor and Mayeux 1997;Guo et al. 1999). Lipid peroxidation can impair the function of several membrane transport proteins including the Na 1 /K 1 ATPase (Mark et al. 1995(Mark et al. , 1997a) the Ca 21 -ATPase (Mark et al. 1995) and glucose and glutamate transporters (Mark et al. 1997b;Blanc et al. 1998). The mechanism whereby lipid peroxidation causes dysfunction and death of cells may involve an aldehyde called 4-hydroxy-2,3-nonenal (4HN), which is liberated from peroxidized f...

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Peroxidative oxidation of lipids in slices of olfactory cortex of the rat brain during long-term potentiation

Cited by 4 publications

References 9 publications

Essential role for cholesterol in synaptic plasticity and neuronal degeneration

Essential role for cholesterol in synaptic plasticity and neuronal degeneration

The Lipid Peroxidation Product 4-Hydroxynonenal Facilitates Opening of Voltage-dependent Ca2+ Channels in Neurons by Increasing Protein Tyrosine Phosphorylation

Selective and biphasic effect of the membrane lipid peroxidation product 4‐hydroxy‐2,3‐nonenal on N‐methyl‐d‐aspartate channels

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