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bp(GO:"long-term synaptic potentiation")

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Entity

Name
long-term synaptic potentiation
Namespace
go
Namespace Version
20180921
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/go-names.belns

Appears in Networks 18

Amyloid β oligomers (AβOs) in Alzheimer’s disease v1.0.0

APP processing in Alzheimer's disease v1.0.1

APP processing in Alzheimer's disease

albuquerque2009 v1.0.0

This file encodes the article Mammalian Nicotinic Acetylcholine Receptors: From Structure to Function by Albuquerque et al, 2009

Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection. v1.0.0

Activation of M1 and M4 muscarinic receptors as potential treatments for Alzheimer's disease and schizophrenia. v1.0.0

This file encodes the article Activation of M1 and M4 muscarinic receptors as potential treatments for Alzheimer’s disease and schizophrenia by Choi et al, 2014

Nicotinic Acetylcholine Receptors and Nicotinic Cholinergic Mechanisms of the Central Nervous System v1.0.0

Neuronal Nicotinic Acetylcholine Receptor Structure and Function and Response to Nicotine v1.0.1

M1 muscarinic acetylcholine receptor in Alzheimer’s disease v1.0.0

This file encodes the article M1 muscarinic acetylcholine receptor in Alzheimer’s disease by Jiang et al, 2014

Role of the nicotinic acetylcholine receptor in Alzheimer's disease pathology and treatment v1.0.1

Neural Systems Governed by Nicotinic Acetylcholine Receptors: Emerging Hypotheses v1.0.0

Naturally-expressed nicotinic acetylcholine receptor subtypes v1.0.0

Adenosine A1 receptor antagonist 64627 alleviates axonopathy caused by human Tau ΔK280 v1.0.0

Activity-dependent tau protein translocation to excitatory synapse is disrupted by exposure to amyloid-beta oligomers v1.0.0

Molecular chaperones and regulation of tau quality control: strategies for drug discovery in tauopathies v1.0.0

The Ubiquitin–Proteasome System and the Autophagic–Lysosomal System in Alzheimer Disease v1.0.0

Extracellular low-n oligomers of tau cause selective synaptotoxicity without affecting cell viability v1.0.0

Nuclear Factor Kappa-light-chain-enhancer of Activated B Cells (NF-κB) - a Friend, a Foe, or a Bystander - in the Neurodegenerative Cascade and Pathogenesis of Alzheimer's Disease v1.0.0

Upstream regulators and downstream effectors of NF-κBinAlzheimer's disease v1.0.0

In-Edges 39

a(HBP:HBP00074) decreases bp(GO:"long-term synaptic potentiation") View Subject | View Object

Moreover, in brain slices, AβOs rapidly inhibited long-term potentiation (LTP) of synapses (Klein et al. 2001). PubMed:29196815

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MeSH
Extracellular Space
Cell Ontology (CL)
neuron
Confidence
High

a(HBP:HBP00074) decreases bp(GO:"long-term synaptic potentiation") View Subject | View Object

In normal rats, impaired memory of a learned behavior was observed after intraventricular application of soluble oligomers of Aβ42 isolated directly from human AD brains (Shankar et al. 2008). Furthermore, AβO injections resulted in reduction of a synapse number and their function in dose-dependent manner. It also led to the inhibition of LTP and enhancement of long-term synaptic depression (LTD) in rodent hippocampus (Shankar et al. 2008). PubMed:29196815

Appears in Networks:
Annotations
MeSH
Extracellular Space
Cell Ontology (CL)
neuron
Confidence
High
MeSH
Hippocampus

a(HBP:HBP00075) decreases bp(GO:"long-term synaptic potentiation") View Subject | View Object

LMW oligomers led to a decrease in the neuronal levels of β2ARs, activated brain microglia, and induced impaired hippocampal LTP in mice in vivo (Yang et al. 2017). PubMed:29196815

Appears in Networks:
Annotations
MeSH
Extracellular Space
Confidence
Medium
MeSH
Hippocampus

a(CHEBI:"amyloid-beta") decreases bp(GO:"long-term synaptic potentiation") View Subject | View Object

Although excessive Abeta causes synaptic dysfunction and synapse loss [142], low levels of Abeta increase hippocampal longterm potentiation and enhances memory, indicating a novel positive, modulatory role on neurotransmission and memory [158,159] PubMed:21214928

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Annotations
MeSH
Endosomes
Confidence
High
MeSH
Hippocampus
MeSH
Down Syndrome

act(p(HGNC:CHRNG)) increases bp(GO:"long-term synaptic potentiation") View Subject | View Object

In receptors harboring the gamma subunit, agonist-induced receptor activation results in a long-lasting open channel time. The large agonist-induced current in turn leads to local intermittent depolarization and adjustments to protein-protein interactions that favor receptor clustering. As the depolarization increases, transcription of the epsilon subunit is increased dramatically (183). PubMed:19126755

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Text Location
Review

composite(p(HGNC:MAPK14), p(HGNC:MAPK8)) decreases bp(GO:"long-term synaptic potentiation") View Subject | View Object

Consequently, there is mounting evidence that Abeta affects cholinergic signaling independent of its cytotoxic action. For example, Abeta blocks long-term potentiation, a cellular correlate of learning, through activation of JNK and p38MAPK (Wang et al., 2004). PubMed:19293145

Appears in Networks:

bp(GO:learning) association bp(GO:"long-term synaptic potentiation") View Subject | View Object

M1 mAChRs have been demonstrated to potentiate NMDA-receptor signaling in the hippocampus and cortex,48,49 brain areas intimately associated with learning and memory. In addition, M1 KO mice displayed reduced hippocampal long-term potentiation, a mechanism heavily implicated in learning and memory. Behaviorally, M1 KO animals display deficits in several medial prefrontal cortex-dependent cognitive tasks, including non-matching-to- sample, win-shift radial arm maze, and social discrimination tasks. PubMed:24511233

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

bp(GO:memory) association bp(GO:"long-term synaptic potentiation") View Subject | View Object

M1 mAChRs have been demonstrated to potentiate NMDA-receptor signaling in the hippocampus and cortex,48,49 brain areas intimately associated with learning and memory. In addition, M1 KO mice displayed reduced hippocampal long-term potentiation, a mechanism heavily implicated in learning and memory. Behaviorally, M1 KO animals display deficits in several medial prefrontal cortex-dependent cognitive tasks, including non-matching-to- sample, win-shift radial arm maze, and social discrimination tasks. PubMed:24511233

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

p(HGNC:CHRM1) increases bp(GO:"long-term synaptic potentiation") View Subject | View Object

M1 mAChRs have been demonstrated to potentiate NMDA-receptor signaling in the hippocampus and cortex,48,49 brain areas intimately associated with learning and memory. In addition, M1 KO mice displayed reduced hippocampal long-term potentiation, a mechanism heavily implicated in learning and memory. Behaviorally, M1 KO animals display deficits in several medial prefrontal cortex-dependent cognitive tasks, including non-matching-to- sample, win-shift radial arm maze, and social discrimination tasks. PubMed:24511233

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

sec(a(CHEBI:"glutamate(2-)")) increases bp(GO:"long-term synaptic potentiation") View Subject | View Object

The combination of enhanced glutamatergic release and strong postsynaptic response produces LTP of the glutamatergic afferents. PubMed:17009926

Appears in Networks:
Annotations
Cell Ontology (CL)
glutamatergic neuron

bp(GO:"depolarization of postsynaptic membrane") increases bp(GO:"long-term synaptic potentiation") View Subject | View Object

The combination of enhanced glutamatergic release and strong postsynaptic response produces LTP of the glutamatergic afferents. PubMed:17009926

Appears in Networks:
Annotations
Cell Ontology (CL)
glutamatergic neuron

act(p(MESH:"Receptors, N-Methyl-D-Aspartate")) increases bp(GO:"long-term synaptic potentiation") View Subject | View Object

This depolarization and firing of the DA neurons helps to relieve the divalent cation block of NMDA receptors and, thus, enables the NMDA receptors to participate in long-term synaptic potentiation of glutamatergic afferents onto midbrain dopamine neurons. PubMed:26472524

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Annotations
Cell Ontology (CL)
glutamatergic neuron

p(MGI:Chrm1) increases bp(GO:"long-term synaptic potentiation") View Subject | View Object

Among the mAChR family members, the M1 subtype makes up 50–60% of the total and is predominantly expressed in all major areas of the forebrain, including the hippocampus, cerebral cortex, corpus striatum, and thalamus[36-38]. M1 mAChR-knockout mice show a series of cognitive defi cits and impairments in long-term potentiation, indicating that the M1 subtype is physiologically linked to multiple functions such as synaptic plasticity, neuronal excitability, neuronal differentiation during early development, and learning and memory PubMed:24590577

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a(CHEBI:"amyloid-beta polypeptide 42") increases bp(GO:"long-term synaptic potentiation") View Subject | View Object

Subsequent to incubation with pM concentrations of Abeta1-42 monomers and oligomers, an increase of hippocampal LTP was observed PubMed:25514383

Appears in Networks:

a(CHEBI:nicotine) increases bp(GO:"long-term synaptic potentiation") View Subject | View Object

Wild-type mice treated with nicotine or with SSR180711, another partial agonist of alpha7 (Biton et al., 2006), showed increased LTP, while the transgenic AD model APPSwe/PS1DE9 showed no effect on LTP following SSR180711 treatment PubMed:25514383

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(HBP:"amyloid-beta 42 oligomers") increases bp(GO:"long-term synaptic potentiation") View Subject | View Object

Subsequent to incubation with pM concentrations of Abeta1-42 monomers and oligomers, an increase of hippocampal LTP was observed PubMed:25514383

Appears in Networks:

a(PUBCHEM:9928899) increases bp(GO:"long-term synaptic potentiation") View Subject | View Object

Wild-type mice treated with nicotine or with SSR180711, another partial agonist of alpha7 (Biton et al., 2006), showed increased LTP, while the transgenic AD model APPSwe/PS1DE9 showed no effect on LTP following SSR180711 treatment PubMed:25514383

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:nicotine) increases bp(GO:"long-term synaptic potentiation") View Subject | View Object

Chronic or acute nicotine enhances LTP in several regions of hippocampus, especially dentate gyrus (Nashmi et al., 2007; TangandDani, 2009;Pentonet al., 2011) PubMed:21482353

Appears in Networks:
Annotations
MeSH
Dentate Gyrus
MeSH
Hippocampus

a(HBP:"alpha-7-containing nAChR") association bp(GO:"long-term synaptic potentiation") View Subject | View Object

For example, Bgt-sensitive a7-nAChRs have been implicated in processes such as vicinal control of neurotransmitter release [7,14], development and maintenance of neurites and synapses [18–20], long-term potentiation [95,96], seizures [97], and neuronal viability/death [21–24]. These intriguing findings underscore the need for further characterization of functional a7-nAChRs. PubMed:21787755

Appears in Networks:

a(CHEBI:adenosine) decreases bp(GO:"long-term synaptic potentiation") View Subject | View Object

Adenosine downmodulates neuronal activity (cFos levels), impairs the presynapse, and attenuates long-term potentiation (LTP) via the A1 receptor (21) PubMed:27671637

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act(p(MGI:Adora1)) decreases bp(GO:"long-term synaptic potentiation") View Subject | View Object

Adenosine downmodulates neuronal activity (cFos levels), impairs the presynapse, and attenuates long-term potentiation (LTP) via the A1 receptor (21) PubMed:27671637

Appears in Networks:

p(HGNC:MAPT, loc(GO:synapse)) positiveCorrelation bp(GO:"long-term synaptic potentiation") View Subject | View Object

Therefore, during a long-lasting synaptic activation, we observed an increase in tau, fyn, actin, GluA1, and PSD-95 content in the PSD-positive fraction, which is consistent with the characteristic features of synaptic plasticity (Ehlers, 2003). PubMed:24760868

Appears in Networks:
Annotations
Text Location
Results

tloc(p(HGNC:MAPT), fromLoc(GO:"dendritic shaft"), toLoc(GO:synapse)) positiveCorrelation bp(GO:"long-term synaptic potentiation") View Subject | View Object

These results suggest that tau translocates from the dendritic shaft to the synapse during activation and probably takes part in the activity-driven synaptic reorganization that underlies synaptic plasticity PubMed:24760868

Appears in Networks:
Annotations
Text Location
Results

p(HGNC:MAPT) positiveCorrelation bp(GO:"long-term synaptic potentiation") View Subject | View Object

We observed a similar LTPinduced increase in tau content within the PSD-enriched fraction from CA1 synaptosomes (29.86 +-4.86 to 70.15 +- 4.86, **p = 0.0011; Fig. 3B). As expected, actin and GluA1 were also increased, strengthening the idea that tau is involved in synaptic reorganization processes necessary for synaptic plasticity PubMed:24760868

Appears in Networks:
Annotations
MeSH
Post-Synaptic Density
Text Location
Results

complex(complex(GO:"filamentous actin"), p(HGNC:MAPT)) association bp(GO:"long-term synaptic potentiation") View Subject | View Object

Finally, we performed a phalloidin precipitation assay after a 15 min Abetao treatment on our neuron culture (Fig. 8A) and observed that tau/F-actin content was increased (**,*p 0.05 relative to control, #p  0.05 relative to Abetao, 1-way ANOVA; control 15.45  1.529, Abetao 32.90  3.181, Abetao Bic/ 4-AP 20.182671 for actin; control 16.342.618, Abetao 31.77 1.952, Abetao Bic/4-AP 17.704.080 for tau,N5 independent cultures Fig. 8B). A subsequent synaptic activation did alter tau interaction with F-actin. PubMed:24760868

Appears in Networks:
Annotations
MeSH
Neurons
Text Location
Results

p(HGNC:DLG4, loc(GO:synapse)) positiveCorrelation bp(GO:"long-term synaptic potentiation") View Subject | View Object

Therefore, during a long-lasting synaptic activation, we observed an increase in tau, fyn, actin, GluA1, and PSD-95 content in the PSD-positive fraction, which is consistent with the characteristic features of synaptic plasticity (Ehlers, 2003). PubMed:24760868

Appears in Networks:
Annotations
Text Location
Results

p(HGNC:FYN, loc(GO:synapse)) positiveCorrelation bp(GO:"long-term synaptic potentiation") View Subject | View Object

Therefore, during a long-lasting synaptic activation, we observed an increase in tau, fyn, actin, GluA1, and PSD-95 content in the PSD-positive fraction, which is consistent with the characteristic features of synaptic plasticity (Ehlers, 2003). PubMed:24760868

Appears in Networks:
Annotations
Text Location
Results

p(HGNC:GRIA1, loc(GO:synapse)) positiveCorrelation bp(GO:"long-term synaptic potentiation") View Subject | View Object

Therefore, during a long-lasting synaptic activation, we observed an increase in tau, fyn, actin, GluA1, and PSD-95 content in the PSD-positive fraction, which is consistent with the characteristic features of synaptic plasticity (Ehlers, 2003). PubMed:24760868

Appears in Networks:
Annotations
Text Location
Results

p(HGNC:GRIA1) positiveCorrelation bp(GO:"long-term synaptic potentiation") View Subject | View Object

We observed a similar LTPinduced increase in tau content within the PSD-enriched fraction from CA1 synaptosomes (29.86 +-4.86 to 70.15 +- 4.86, **p = 0.0011; Fig. 3B). As expected, actin and GluA1 were also increased, strengthening the idea that tau is involved in synaptic reorganization processes necessary for synaptic plasticity PubMed:24760868

Appears in Networks:
Annotations
MeSH
Post-Synaptic Density
Text Location
Results

p(MESH:Actins, loc(GO:synapse)) positiveCorrelation bp(GO:"long-term synaptic potentiation") View Subject | View Object

Therefore, during a long-lasting synaptic activation, we observed an increase in tau, fyn, actin, GluA1, and PSD-95 content in the PSD-positive fraction, which is consistent with the characteristic features of synaptic plasticity (Ehlers, 2003). PubMed:24760868

Appears in Networks:
Annotations
Text Location
Results

p(MESH:Actins) positiveCorrelation bp(GO:"long-term synaptic potentiation") View Subject | View Object

We observed a similar LTPinduced increase in tau content within the PSD-enriched fraction from CA1 synaptosomes (29.86 +-4.86 to 70.15 +- 4.86, **p = 0.0011; Fig. 3B). As expected, actin and GluA1 were also increased, strengthening the idea that tau is involved in synaptic reorganization processes necessary for synaptic plasticity PubMed:24760868

Appears in Networks:
Annotations
MeSH
Post-Synaptic Density
Text Location
Results

p(HGNC:HSPB1) positiveCorrelation bp(GO:"long-term synaptic potentiation") View Subject | View Object

Recently, our group demonstrated that viral delivery of wild-type Hsp27 into the brains of tau-transgenic mice reduced tau levels and rescued long-term potentiation deficits. PubMed:21882945

Appears in Networks:

a(HBP:AβOs) decreases bp(GO:"long-term synaptic potentiation") View Subject | View Object

Soluble Ab oligomers inhibit hippocampal long-term potentiation and alter memory and learning performance PubMed:22908190

Appears in Networks:

act(p(HGNC:RAB5A)) negativeCorrelation bp(GO:"long-term synaptic potentiation") View Subject | View Object

Pathological Rab5 activation driving endocytic dysfunction in AD may negatively impact longterm potentiation (LTP) and long-term depression (LTD) aspects of synaptic plasticity closely associated with learning and memory (Kessels et al. 2009) PubMed:22908190

Appears in Networks:

p(HGNC:RIN1) decreases bp(GO:"long-term synaptic potentiation") View Subject | View Object

Conversely, deletion of the neuronal rab5 GEF, rin1, reduces rab5 activation, increases LTP induction in the amygdala, and enhances fear learning and memory, most likely by increasing surface levels of AMPA receptors (Dhaka et al. 2003). PubMed:22908190

Appears in Networks:
Annotations
MeSH
Amygdala

a(HBP:"Tau oligomers") decreases bp(GO:"long-term synaptic potentiation") View Subject | View Object

Recently, extracellular tau oligomers were shown to impair long term potentiation (LTP) and memory [40]. PubMed:28528849

Appears in Networks:
Annotations
MeSH
Extracellular Space

p(HGNC:NFKB1) increases bp(GO:"long-term synaptic potentiation") View Subject | View Object

p50 knock-out mice exhibit deficits in late LTP resulting in compromised spatial memory PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:RELA) increases bp(GO:"long-term synaptic potentiation") View Subject | View Object

The indispensable role of NF-κB in synaptic transmission is corroborated by the fact that the mice that are deficient in neuronal p65, exhibit severe deficits in hippocampal basal synaptic transmission and long term potentiation (LTP) PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:"advanced glycation end-product") decreases bp(GO:"long-term synaptic potentiation") View Subject | View Object

AGEs induce tau hyperphosphorylation, memory deterioration, decline of synaptic proteins, and impairment of long-term potentiation in rats [10]. PubMed:27288790

Appears in Networks:

Out-Edges 20

bp(GO:"long-term synaptic potentiation") increases bp(GO:"depolarization of postsynaptic membrane") View Subject | View Object

In receptors harboring the gamma subunit, agonist-induced receptor activation results in a long-lasting open channel time. The large agonist-induced current in turn leads to local intermittent depolarization and adjustments to protein-protein interactions that favor receptor clustering. As the depolarization increases, transcription of the epsilon subunit is increased dramatically (183). PubMed:19126755

Appears in Networks:
Annotations
Text Location
Review

bp(GO:"long-term synaptic potentiation") association bp(GO:learning) View Subject | View Object

M1 mAChRs have been demonstrated to potentiate NMDA-receptor signaling in the hippocampus and cortex,48,49 brain areas intimately associated with learning and memory. In addition, M1 KO mice displayed reduced hippocampal long-term potentiation, a mechanism heavily implicated in learning and memory. Behaviorally, M1 KO animals display deficits in several medial prefrontal cortex-dependent cognitive tasks, including non-matching-to- sample, win-shift radial arm maze, and social discrimination tasks. PubMed:24511233

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

bp(GO:"long-term synaptic potentiation") association bp(GO:memory) View Subject | View Object

M1 mAChRs have been demonstrated to potentiate NMDA-receptor signaling in the hippocampus and cortex,48,49 brain areas intimately associated with learning and memory. In addition, M1 KO mice displayed reduced hippocampal long-term potentiation, a mechanism heavily implicated in learning and memory. Behaviorally, M1 KO animals display deficits in several medial prefrontal cortex-dependent cognitive tasks, including non-matching-to- sample, win-shift radial arm maze, and social discrimination tasks. PubMed:24511233

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

bp(GO:"long-term synaptic potentiation") association a(HBP:"alpha-7-containing nAChR") View Subject | View Object

For example, Bgt-sensitive a7-nAChRs have been implicated in processes such as vicinal control of neurotransmitter release [7,14], development and maintenance of neurites and synapses [18–20], long-term potentiation [95,96], seizures [97], and neuronal viability/death [21–24]. These intriguing findings underscore the need for further characterization of functional a7-nAChRs. PubMed:21787755

Appears in Networks:

bp(GO:"long-term synaptic potentiation") positiveCorrelation p(HGNC:MAPT, loc(GO:synapse)) View Subject | View Object

Therefore, during a long-lasting synaptic activation, we observed an increase in tau, fyn, actin, GluA1, and PSD-95 content in the PSD-positive fraction, which is consistent with the characteristic features of synaptic plasticity (Ehlers, 2003). PubMed:24760868

Appears in Networks:
Annotations
Text Location
Results

bp(GO:"long-term synaptic potentiation") positiveCorrelation tloc(p(HGNC:MAPT), fromLoc(GO:"dendritic shaft"), toLoc(GO:synapse)) View Subject | View Object

These results suggest that tau translocates from the dendritic shaft to the synapse during activation and probably takes part in the activity-driven synaptic reorganization that underlies synaptic plasticity PubMed:24760868

Appears in Networks:
Annotations
Text Location
Results

bp(GO:"long-term synaptic potentiation") positiveCorrelation p(HGNC:MAPT) View Subject | View Object

We observed a similar LTPinduced increase in tau content within the PSD-enriched fraction from CA1 synaptosomes (29.86 +-4.86 to 70.15 +- 4.86, **p = 0.0011; Fig. 3B). As expected, actin and GluA1 were also increased, strengthening the idea that tau is involved in synaptic reorganization processes necessary for synaptic plasticity PubMed:24760868

Appears in Networks:
Annotations
MeSH
Post-Synaptic Density
Text Location
Results

bp(GO:"long-term synaptic potentiation") positiveCorrelation p(MESH:Actins, loc(GO:synapse)) View Subject | View Object

Therefore, during a long-lasting synaptic activation, we observed an increase in tau, fyn, actin, GluA1, and PSD-95 content in the PSD-positive fraction, which is consistent with the characteristic features of synaptic plasticity (Ehlers, 2003). PubMed:24760868

Appears in Networks:
Annotations
Text Location
Results

bp(GO:"long-term synaptic potentiation") positiveCorrelation p(MESH:Actins) View Subject | View Object

We observed a similar LTPinduced increase in tau content within the PSD-enriched fraction from CA1 synaptosomes (29.86 +-4.86 to 70.15 +- 4.86, **p = 0.0011; Fig. 3B). As expected, actin and GluA1 were also increased, strengthening the idea that tau is involved in synaptic reorganization processes necessary for synaptic plasticity PubMed:24760868

Appears in Networks:
Annotations
MeSH
Post-Synaptic Density
Text Location
Results

bp(GO:"long-term synaptic potentiation") positiveCorrelation p(HGNC:FYN, loc(GO:synapse)) View Subject | View Object

Therefore, during a long-lasting synaptic activation, we observed an increase in tau, fyn, actin, GluA1, and PSD-95 content in the PSD-positive fraction, which is consistent with the characteristic features of synaptic plasticity (Ehlers, 2003). PubMed:24760868

Appears in Networks:
Annotations
Text Location
Results

bp(GO:"long-term synaptic potentiation") positiveCorrelation p(HGNC:GRIA1, loc(GO:synapse)) View Subject | View Object

Therefore, during a long-lasting synaptic activation, we observed an increase in tau, fyn, actin, GluA1, and PSD-95 content in the PSD-positive fraction, which is consistent with the characteristic features of synaptic plasticity (Ehlers, 2003). PubMed:24760868

Appears in Networks:
Annotations
Text Location
Results

bp(GO:"long-term synaptic potentiation") positiveCorrelation p(HGNC:GRIA1) View Subject | View Object

We observed a similar LTPinduced increase in tau content within the PSD-enriched fraction from CA1 synaptosomes (29.86 +-4.86 to 70.15 +- 4.86, **p = 0.0011; Fig. 3B). As expected, actin and GluA1 were also increased, strengthening the idea that tau is involved in synaptic reorganization processes necessary for synaptic plasticity PubMed:24760868

Appears in Networks:
Annotations
MeSH
Post-Synaptic Density
Text Location
Results

bp(GO:"long-term synaptic potentiation") positiveCorrelation p(HGNC:DLG4, loc(GO:synapse)) View Subject | View Object

Therefore, during a long-lasting synaptic activation, we observed an increase in tau, fyn, actin, GluA1, and PSD-95 content in the PSD-positive fraction, which is consistent with the characteristic features of synaptic plasticity (Ehlers, 2003). PubMed:24760868

Appears in Networks:
Annotations
Text Location
Results

bp(GO:"long-term synaptic potentiation") association complex(complex(GO:"filamentous actin"), p(HGNC:MAPT)) View Subject | View Object

Finally, we performed a phalloidin precipitation assay after a 15 min Abetao treatment on our neuron culture (Fig. 8A) and observed that tau/F-actin content was increased (**,*p 0.05 relative to control, #p  0.05 relative to Abetao, 1-way ANOVA; control 15.45  1.529, Abetao 32.90  3.181, Abetao Bic/ 4-AP 20.182671 for actin; control 16.342.618, Abetao 31.77 1.952, Abetao Bic/4-AP 17.704.080 for tau,N5 independent cultures Fig. 8B). A subsequent synaptic activation did alter tau interaction with F-actin. PubMed:24760868

Appears in Networks:
Annotations
MeSH
Neurons
Text Location
Results

bp(GO:"long-term synaptic potentiation") increases p(HGNC:MAPT, pmod(Ph, Thr, 205)) View Subject | View Object

Thr-205 phosphorylated tau was only increased under synaptic activation in the PSD fraction (control 24.57  0.9754 vs Bic/4-AP 38.90  1.936; Fig. 9E), whereas it was decreased after Abetao treatment (control 24.57  0.9754 vs Abeta 13.64  2.416). Synaptic activation after Abetao exposure did not produce any significant Thr-205 phosphorylation of tau (Abeta Bic/4-AP 22.892.796 vs Bic/ 4-AP 38.90  1.93 vs Abeta 13.642.50). PubMed:24760868

Appears in Networks:
Annotations
MeSH
Post-Synaptic Density
Text Location
Results

bp(GO:"long-term synaptic potentiation") increases p(HGNC:MAPT, var("p.T205A"), loc(MESH:"Dendritic Spines")) View Subject | View Object

We observed that synaptic activation promoted EGFP-Tau T205A translocation to the spine but FRAP experiments revealed a shorter tau turnover time in the spine (Fig. 9B), whereas Abetao driven translocation to the spine was no longer observable in EGFP-Tau S404A-transfected neurons (Fig. 9F,G). These experiments highlight the pivotal role of these phosphorylations in tau translocation features to the spine. PubMed:24760868

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Text Location
Results

bp(GO:"long-term synaptic potentiation") positiveCorrelation p(HGNC:HSPB1) View Subject | View Object

Recently, our group demonstrated that viral delivery of wild-type Hsp27 into the brains of tau-transgenic mice reduced tau levels and rescued long-term potentiation deficits. PubMed:21882945

Appears in Networks:

bp(GO:"long-term synaptic potentiation") negativeCorrelation act(p(HGNC:RAB5A)) View Subject | View Object

Pathological Rab5 activation driving endocytic dysfunction in AD may negatively impact longterm potentiation (LTP) and long-term depression (LTD) aspects of synaptic plasticity closely associated with learning and memory (Kessels et al. 2009) PubMed:22908190

Appears in Networks:

bp(GO:"long-term synaptic potentiation") decreases p(HGNC:NFKB1) View Subject | View Object

The expression of p65 and p50 is induced in response to long-term changes in synaptic strength and transmission such as LTP [39] and LTD PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

bp(GO:"long-term synaptic potentiation") decreases p(HGNC:RELA) View Subject | View Object

The expression of p65 and p50 is induced in response to long-term changes in synaptic strength and transmission such as LTP [39] and LTD PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.