Blockade of long-term depression in neonatal hippocampal slices by a phospholipase A2 inhibitor

Fitzpatrick, John S.; Baudry, Michel

doi:10.1016/0165-3806(94)90012-4

Cited by 35 publications

(17 citation statements)

References 18 publications

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“…Nevertheless, when the effect of PLA2 on 3H-AMPA binding was tested in telencephalic membranes prepared from very young animals, not only did we not detect any stimulation of 3H-AMPA binding, but a marked decrease in binding was obtained [62]. This finding is quite interesting because of previous work suggesting that LTD formation could be related to PLA2 activation [54,63], and it is reasonable to propose that such a reduction in AMPA binding generated by the activation of endogenous PLA2 could represent an important mechanism for LTD expression in the hippocampus. In summary, the above experiments reveal that PLA2-induced modification of AMPA receptors is not present in tissues in which LTP cannot be reproduced, such as following seizure activity or during the neonatal period.…”

Section: Multi-author Review Articlesupporting

confidence: 48%

Modification of glutamate receptors by phospholipase A2: its role in adaptive neural plasticity

Massicotte

2000

CMLS, Cell. Mol. Life Sci.

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Long-term potentiation (LTP) and long-term depression (LTD) are two electrophysiological models that have been studied extensively in recent years as they may represent basic mechanisms in many neuronal networks to store certain types of information. In several brain regions, it has been shown that these two forms of synaptic plasticity require sufficient dendritic depolarization, with the amplitude of the calcium signal being crucial for the generation of either LTP or LTD. The rise in calcium concentration mediated by the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors has been proposed to stimulate various calcium-dependent enzymatic processes that could convert the induction signal into long-lasting changes in synaptic structure; protein kinases and phosphatases have so far been considered predominantly with regard to LTP and LTD formation. According to several lines of experimental evidence, changes in synaptic function observed with LTP and LTD are thought to be the result of modifications of postsynaptic currents mediated by the alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) subtype of glutamate receptors. Moreover, it has become apparent recently that activation of the calcium-dependent enzyme phospholipase A2 (PLA2) could be part of the molecular mechanisms involved in alterations of AMPA receptor properties during long-term changes in synaptic operation. In the present review, we will first describe the results that indicate a critical role of the phospholipases in regulating synaptic function. Next, sections will be devoted to the effects of PLA2 and phospholipids on the binding properties of glutamate receptors, and a revised biochemical model will be presented as an attempt to integrate the PLA2 enzyme into the mechanisms ( in particular kinases and phosphatases) that participate in adaptive neural plasticity. Finally, we will review data relevant to the issue of selective changes in AMPA binding after environmental enrichment and LTP.

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Section: Multi-author Review Articlesupporting

confidence: 48%

Modification of glutamate receptors by phospholipase A2: its role in adaptive neural plasticity

Massicotte

2000

CMLS, Cell. Mol. Life Sci.

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“…Here, we found that FPI increased lipid peroxidation in the SC as evidenced by increased levels of 4-HNE. The phospholipase A 2 (PLA 2 ) family is involved in the metabolism of membrane phospholipids [11], and the calcium-independent PLA 2 (iPLA 2 ) plays an important role in synaptic plasticity [16], [17]. Therefore, our results showing significant changes in iPLA2 levels in the n-3 def animals undergoing FPI provide an indication for the compromise of membrane homeostasis.…”

Section: Discussionmentioning

confidence: 68%

Dietary Omega-3 Deficiency from Gestation Increases Spinal Cord Vulnerability to Traumatic Brain Injury-Induced Damage

et al. 2012

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Although traumatic brain injury (TBI) is often associated with gait deficits, the effects of TBI on spinal cord centers are poorly understood. We seek to determine the influence of TBI on the spinal cord and the potential of dietary omega-3 (n-3) fatty acids to counteract these effects. Male rodents exposed to diets containing adequate or deficient levels of n-3 since gestation received a moderate fluid percussion injury when becoming 14 weeks old. TBI reduced levels of molecular systems important for synaptic plasticity (BDNF, TrkB, and CREB) and plasma membrane homeostasis (4-HNE, iPLA2, syntaxin-3) in the lumbar spinal cord. These effects of TBI were more dramatic in the animals exposed to the n-3 deficient diet. Results emphasize the comprehensive action of TBI across the neuroaxis, and the critical role of dietary n-3 as a means to build resistance against the effects of TBI.

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“…This is supported by experiments in which inhibitors of protein phosphatases 1 and 2A can block or even reverse established LTD (Mulkey et al, 1993). A mix of pre-and postsynaptic changes has been suggested by Fitzpatrick and Baudry (1994) on the basis of changes in both paired-pulse facilitation and response to iontophoresed ClO 4 2 , which is an ion that affects the glutamate affinity of the AMPA receptor. Within the cerebellum, a postsynaptic change underlying associative LTD is implied by the decreased responsiveness of AMPA receptors to iontophoretic application of transmitter or its analogues (Ito et al, 1982).…”

Section: Introductionmentioning

confidence: 87%

Long-lasting decreases of AMPA responses following postsynaptic activity in single hippocampal neurons

Vickery

Bindman

1997

Synapse

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Direct postsynaptic depolarization and firing of single CA1 neurons caused decreased responses to iontophoresed alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA). Since there was no associated change in the excitatory postsynaptic potential (EPSP) evoked by electrical stimulation in the same band of stratum radiatum, we infer that the decreased AMPA response was mediated predominantly by extrasynaptic receptors. The decreased AMPA response developed within 10-30 min after conditioning, a time course similar to the delayed increase in AMPA responses associated with long-term potentiation (LTP) [Davies et al. (1989), Nature, 338:500-503; Sergueeva et al. (1993), Neuropharmacology, 32:933-935]. Our observations suggest the existence of mirror-image processes that may regulate AMPA receptors and possibly synaptic efficacy.

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Blockade of long-term depression in neonatal hippocampal slices by a phospholipase A2 inhibitor

Cited by 35 publications

References 18 publications

Modification of glutamate receptors by phospholipase A2: its role in adaptive neural plasticity

Modification of glutamate receptors by phospholipase A2: its role in adaptive neural plasticity

Dietary Omega-3 Deficiency from Gestation Increases Spinal Cord Vulnerability to Traumatic Brain Injury-Induced Damage

Long-lasting decreases of AMPA responses following postsynaptic activity in single hippocampal neurons

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