LTP forms 1, 2 and 3: different mechanisms for the ‘long’ in long-term potentiation

Raymond, Clarke R.

doi:10.1016/j.tins.2007.01.007

Cited by 185 publications

(188 citation statements)

References 87 publications

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“…In fact, VDCCs are assumed to be activated by higher-stimulation frequencies than those activating NMDARs (Morgan & Teyler, 1999). Thus, to induce the NMDAR-dependent LTP, theta-burst stimulation (TBS, containing two trains of five pulses at 100 Hz separated by 200 ms), a type of more physiological relevant stimulus, is introduced (Raymond, 2007;Boric et al, 2008). The LTP of neurotransmission was measured by the changes in field excitatory postsynaptic potentials (fEPSPs) before and after TBS in the CA1 area of the hippocampus.…”

Section: Modulation Of Thiol Redox Status Affects Nmdarmediated Synapmentioning

confidence: 99%

Reversal of aging‐associated hippocampal synaptic plasticity deficits by reductants via regulation of thiol redox and NMDA receptor function

Yang

Long

et al. 2010

Aging Cell

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SummaryDeficits in learning and memory accompanied by agerelated neurodegenerative diseases are closely related to the impairment of synaptic plasticity. In this study, we investigated the role of thiol redox status in the modulation of the N-methyl-D-aspartate receptor (NMDAR)-dependent long-term potentiation (LTP) in CA1 areas of hippocampal slices. Our results demonstrated that the impaired LTP induced by aging could be reversed by acute administration of reductants that can regulate thiol redox status directly, such as dithiothreitol or b-mercaptoethanol, but not by classical anti-oxidants such as vitamin C or trolox. This repair was mediated by the recruitment of aging-related deficits in NMDAR function induced by these reductants and was mimicked by glutathione, which can restore the age-associated alterations in endogenous thiol redox status. Moreover, antioxidant prevented but failed to reverse H 2 O 2 -induced impairment of NMDARmediated synaptic plasticity. These results indicate that the restoring of thiol redox status may be a more effective strategy than the scavenging of oxidants in the treatment of pre-existing oxidative injury in learning and memory.

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Section: Modulation Of Thiol Redox Status Affects Nmdarmediated Synapmentioning

confidence: 99%

Reversal of aging‐associated hippocampal synaptic plasticity deficits by reductants via regulation of thiol redox and NMDA receptor function

Yang

Long

et al. 2010

Aging Cell

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“…It is well known that LTP is not a solitary phenomenon but contains various forms that can be categorized by the general mechanisms in vivo. For example, ionotropic glutamate receptors, metabotropic type glutamate receptors, and dopamine receptors (D1-D5) mediate LTP through different pathways (43). The LTP induced by HFS might be neither protein synthesis-dependent (D1-D5) nor metabotropic type glutamate receptor-dependent based on previous observations (43)(44)(45).…”

Section: Discussionmentioning

confidence: 99%

“…For example, ionotropic glutamate receptors, metabotropic type glutamate receptors, and dopamine receptors (D1-D5) mediate LTP through different pathways (43). The LTP induced by HFS might be neither protein synthesis-dependent (D1-D5) nor metabotropic type glutamate receptor-dependent based on previous observations (43)(44)(45). Therefore, in the present study, we mainly focused on the molecules mediated in the ionotropic glutamate receptor-dependent pathway, including the NMDAR, AMPAR, and CaMKII in postsynaptic regions.…”

Section: Discussionmentioning

confidence: 99%

Loss of α1,6-Fucosyltransferase Decreases Hippocampal Long Term Potentiation

Fukuda

Isaji

et al. 2015

Journal of Biological Chemistry

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Background: High expression levels of core fucosylated N-glycans in brain tissues remain unexplained. Results: Loss of core fucosylation enhanced AMPA receptor heteromerization and decreased long term potentiation. Conclusion: Core fucosylation is required for hippocampal long term potentiation. Significance: Core fucosylation may be very important for the neuronal synaptic plasticity that is required for learning and memory.

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“…Experimentally LTP can be induced by repeated electrical stimulation at high frequency (reviewed in [33]). Induction requires increased cytoplasmic calcium concentration to activate multiple signal transduction pathways, which increase synaptic strength.…”

Section: Introductionmentioning

confidence: 99%

“…Induction requires increased cytoplasmic calcium concentration to activate multiple signal transduction pathways, which increase synaptic strength. This leads to a sustained increase of the fEPSP (at least 30 mins; maintenance), the duration of which depends on the method of induction [33,34]. LTP induction can readily be inhibited, for example by Ca 2+ chelation or NMDA receptor inhibition [31].…”

Section: Introductionmentioning

confidence: 99%

Effects of relative hypoglycemia on LTP and NADH imaging in rat hippocampal slices

2007

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Cognitive and neuronal impairment in diabetes may be associated with iatrogenic hypoglycemia, particularly at low serum glucose levels (< 3 mM). To evaluate cellular impairment, we assessed acute hippocampal slice functioning during decreased ambient glucose, by monitoring evoked field excitatory post-synaptic potentials (fEPSP), and slice nicotinamide adenine dinucleotide (NADH) fluorescence. The effects of lowered glucose levels (60 min) were analyzed by examining the induction and maintenance of long-term potentiation (LTP), and NADH metabolic imaging in the CA1 region. The basal fEPSP response was reduced by lowered ambient glucose, an effect that was reversible in 2.5 mM glucose, partially reversible in 1.25 mM glucose and irreversible in 0 mM glucose, after 25 min recovery. LTP induction and maintenance declined during glucose restriction, demonstrating reversibly failed maintenance in 5 mM and 2.5 mM ambient glucose, and absent induction in 1.25 mM glucose. Peak NADH levels observed during train-induced biphasic transients were significantly reduced during 1.25 mM and 2.5 mM glucose. Significant functional compromise in our slice model occurred at 2.5 mM ambient glucose, equivalent to <1mM tissue glucose in the slice center, due to diffusion limitations and active glucose utilization. This tissue glucose level correlates with human observations of a serum threshold of <3mM for cognitive impairment, since brain tissue glucose is approximately one third of serum levels. The physiological effects of hypoglycemia in our slice model, assessed through fEPSP, LTP, and NADH responses, replicate closely the in vivo situation, confirming the usefulness of this model in assessing consequences of relative hypoglycemia.

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LTP forms 1, 2 and 3: different mechanisms for the ‘long’ in long-term potentiation

Cited by 185 publications

References 87 publications

Reversal of aging‐associated hippocampal synaptic plasticity deficits by reductants via regulation of thiol redox and NMDA receptor function

Reversal of aging‐associated hippocampal synaptic plasticity deficits by reductants via regulation of thiol redox and NMDA receptor function

Loss of α1,6-Fucosyltransferase Decreases Hippocampal Long Term Potentiation

Effects of relative hypoglycemia on LTP and NADH imaging in rat hippocampal slices

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