bp(GO:"regulation of synaptic plasticity")

Entity

Name

regulation of synaptic plasticity

Namespace

go

Namespace Version

20180921

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/go-names.belns

PrPC was identified as AβO co-receptor, which mediates an impairment of synaptic plasticity by AβOs, although the infectious form PrPSc conformation is not necessary (Lauren et al. 2009). PubMed:29196815

By modulating activity-dependent events, nAChRs participate in fundamental aspects of synaptic plasticity that are involved in attention, learning, memory, and development (3, 12–16). PubMed:17009926

Nicotinic stimulation enhances glutamate release on multiple timescales, extending from seconds to a few minutes (81), and contributes to the induction of synaptic plasticity (4, 13, 14, 16, 88). PubMed:17009926

Nicotinic receptors also modulate glutamatergic synaptic plasticity. PubMed:17009926

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

It has acute effects on the synapse, serving as an activity-dependent regulator of synaptic plas- ticity and participating in rapid synaptic transmission [150,151,156–159], in the maturation of GABAergic signaling and in the stabilization of newly formed synapses [151,160–163]. PubMed:22040696

Interestingly, the UPS is important for elimination of tau and other neurotoxic proteins in post synaptic dendritic compartments (a key site of spreading), where it plays a more general role favouring synaptic plasticity, den- dritogenesis and memory formation 49,52 . PubMed:30116051

This results in the activation of mitogen-activated protein kinase kinase kinase 1 (MAP3K1), 114 which then activates a cascade of kinases that eventually leads to the translocation of JNK to the nucleus or other target sites to phosphorylate downstream effectors, thereby affecting significant aspects of neuronal function such as neurite outgrowth, mitochondrial function, synaptic plasticity and apoptosis. 1 PubMed:30444369

The earliest symptoms of AD are believed to be due to synaptic dysfunction, and in this context, numerous studies have established a significant role of the UPS in the regulation of synaptic plasticity. PubMed:22908190

Autophagy may also modulate synaptic plasticity, which involves structural remodeling of nerve terminals (Boland et al. 2006) and the trafficking and degradation of receptors and other synaptic proteins (Leil et al. 2004; Rowland et al. 2006). PubMed:22908190

Although key to the survival of all cells, endocytosis supports unique neuronal functions, including aspects of synaptic transmission and plasticity underlying memory and learning. PubMed:22908190

To date, the physiological function of dendritic tau has not been well characterized. It may be involved in the regulation of synaptic plasticity, as pharmacological synaptic activation induces translocation of endogenous tau from the dendritic shaft to excitatory postsynaptic compartments in cultured mouse neurons and in acute hippocampal slices PubMed:26631930

In the nervous system, NF-κB has been proposed to serve important function by acting as a transcription regulator: it has roles in inflammation, neuronal survival, differentiation, apoptosis, neurite outgrowth, and synaptic plasticity [5], which are impaired in the progression of various neurodegenerative diseases especially in AD. PubMed:27288790

In the nervous system, NF-κB has been proposed to serve important function by acting as a transcription regulator: it has roles in inflammation, neuronal survival, differentiation, apoptosis, neurite outgrowth, and synaptic plasticity [5], which are impaired in the progression of various neurodegenerative diseases especially in AD. PubMed:27288790

Figure 3, Supplemental Figure 5 (younger age group), Supplemental Figure 6 (older age group), and Supplemental Tables 5 and 8 reveal an overall similar pattern of Adnp genotype–and NAP treatment–regulated human and mouse protein product interactions across ages with Akt1 (the mosaic mutations of which lead to the Proteus syndrome, characterized by the overgrowth of skin, connective tissue, brain, and other tissues; ref. 37) and discs large MAGUK scaffold protein 4 (Dlg4, also known as Psd95), a key regulator of synaptic plasticity (see above) that plays central roles associated with ADNP and NAP function. PubMed:30106381

By modulating activity-dependent events, nAChRs participate in fundamental aspects of synaptic plasticity that are involved in attention, learning, memory, and development (3, 12–16). PubMed:17009926

Nicotinic receptors also modulate glutamatergic synaptic plasticity. PubMed:17009926

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

This results in the activation of mitogen-activated protein kinase kinase kinase 1 (MAP3K1), 114 which then activates a cascade of kinases that eventually leads to the translocation of JNK to the nucleus or other target sites to phosphorylate downstream effectors, thereby affecting significant aspects of neuronal function such as neurite outgrowth, mitochondrial function, synaptic plasticity and apoptosis. 1 PubMed:30444369

The earliest symptoms of AD are believed to be due to synaptic dysfunction, and in this context, numerous studies have established a significant role of the UPS in the regulation of synaptic plasticity. PubMed:22908190

Although key to the survival of all cells, endocytosis supports unique neuronal functions, including aspects of synaptic transmission and plasticity underlying memory and learning. PubMed:22908190

Autophagy may also modulate synaptic plasticity, which involves structural remodeling of nerve terminals (Boland et al. 2006) and the trafficking and degradation of receptors and other synaptic proteins (Leil et al. 2004; Rowland et al. 2006). PubMed:22908190

To date, the physiological function of dendritic tau has not been well characterized. It may be involved in the regulation of synaptic plasticity, as pharmacological synaptic activation induces translocation of endogenous tau from the dendritic shaft to excitatory postsynaptic compartments in cultured mouse neurons and in acute hippocampal slices PubMed:26631930

In the nervous system, NF-κB has been proposed to serve important function by acting as a transcription regulator: it has roles in inflammation, neuronal survival, differentiation, apoptosis, neurite outgrowth, and synaptic plasticity [5], which are impaired in the progression of various neurodegenerative diseases especially in AD. PubMed:27288790

In the nervous system, NF-κB has been proposed to serve important function by acting as a transcription regulator: it has roles in inflammation, neuronal survival, differentiation, apoptosis, neurite outgrowth, and synaptic plasticity [5], which are impaired in the progression of various neurodegenerative diseases especially in AD. PubMed:27288790

Figure 3, Supplemental Figure 5 (younger age group), Supplemental Figure 6 (older age group), and Supplemental Tables 5 and 8 reveal an overall similar pattern of Adnp genotype–and NAP treatment–regulated human and mouse protein product interactions across ages with Akt1 (the mosaic mutations of which lead to the Proteus syndrome, characterized by the overgrowth of skin, connective tissue, brain, and other tissues; ref. 37) and discs large MAGUK scaffold protein 4 (Dlg4, also known as Psd95), a key regulator of synaptic plasticity (see above) that plays central roles associated with ADNP and NAP function. PubMed:30106381