Journal ArticleDOI
The effects of chronic lead exposure on long-term depression in area CA1 and dentate gyrus of rat hippocampus in vitro
TLDR
It is demonstrated that low-level lead exposure could reduce the range of synaptic plasticity, which might underlie the dysfunction of learning and memory caused by chronic lead exposure.About:
This article is published in Brain Research.The article was published on 1999-02-06. It has received 34 citations till now. The article focuses on the topics: Long-term depression & Long-term potentiation.read more
Citations
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Journal ArticleDOI
Molecular targets of lead in brain neurotoxicity.
TL;DR: This review outlines the most recent hypotheses and evidences that link lead poisoning to impairment of these protein functions, as well as the in vitro experimental approaches that are most likely to provide information on basic mechanicistic processes.
Journal ArticleDOI
Long-Term Potentiation at CA3-CA1 Hippocampal Synapses with Special Emphasis on Aging, Disease, and Stress.
TL;DR: The current review intends to present an overview of the research findings regarding hippocampal LTP with special emphasis on aging, diseases, and psychological insults.
Journal ArticleDOI
Lead stimulates ERK1/2 and p38MAPK phosphorylation in the hippocampus of immature rats.
Fabiano Mendes de Cordova,Ana Lúcia S. Rodrigues,Maria B O Giacomelli,Camila S. Oliveira,Thaís Posser,Peter R. Dunkley,Rodrigo B. Leal +6 more
TL;DR: The results indicate that the phosphorylation of hippocampal ERK1/2 and p38(MAPK) is stimulated by lead in a period of rapid brain development, an effect that may underlie, at least in part, the neurotoxicty elicited by this metal.
Journal ArticleDOI
Effects of Epigallocatechin-3-gallate on lead-induced oxidative damage.
TL;DR: Epigallocatechin-3-gallate (EGCG), a catechin polyphenols component, is found to be an effective antioxidant and could be a potential complementary agent in the treatment of chronic lead intoxication through its antioxidative character.
Journal ArticleDOI
Lead-stimulated p38MAPK-dependent Hsp27 phosphorylation.
TL;DR: This is the first report showing that Pb2+ can modulate the phosphorylation state of Hsp27 via activation of the p38MAPK pathway, a cytotoxic metal ion whose mechanism of action is not established.
References
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Journal ArticleDOI
A synaptic model of memory: long-term potentiation in the hippocampus
TL;DR: The best understood form of long-term potentiation is induced by the activation of the N-methyl-d-aspartate receptor complex, which allows electrical events at the postsynaptic membrane to be transduced into chemical signals which, in turn, are thought to activate both pre- and post Synaptic mechanisms to generate a persistent increase in synaptic strength.
Journal ArticleDOI
Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path.
Timothy V. P. Bliss,T. Lømo +1 more
TL;DR: The after‐effects of repetitive stimulation of the perforant path fibres to the dentate area of the hippocampal formation have been examined with extracellular micro‐electrodes in rabbits anaesthetized with urethane.
Journal ArticleDOI
Homosynaptic long-term depression in area CA1 of hippocampus and effects of N-methyl-D-aspartate receptor blockade.
Serena M. Dudek,Mark F. Bear +1 more
TL;DR: The data suggest that synaptic depression can be triggered by prolonged NMDA receptor activation that is below the threshold for inducing synaptic potentiation, and it is proposed that this mechanism is important for the modifications of hippocampal response properties that underlie some forms of learning and memory.
Journal ArticleDOI
Mechanisms underlying induction of homosynaptic long-term depression in area CA1 of the hippocampus.
TL;DR: Induction of homosynaptic LTD requires an NMDA receptor-dependent change in postsynaptic Ca2+ which may be distinct from that required for long-term potentiation.
Journal ArticleDOI
A mechanism for the Hebb and the anti-Hebb processes underlying learning and memory.
TL;DR: Modeling of the group of Ca2+/calmodulin-dependent protein kinase II molecules contained within a postsynaptic density shows that it can function as an analog computer that can store a synaptic weight and modify it in accord with the Hebb and anti-Hebb learning rules.
Related Papers (5)
Picomolar concentrations of lead stimulate brain protein kinase C
Jasna Markovac,Gary W. Goldstein +1 more