MAPK cascade signalling and synaptic plasticity
By Gareth M. Thomas, Richard L. Huganir. 2004
1,522 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Neurology
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In Cellular and Molecular Neuroscience
In Molecular Biology
In Neurology
- L. Minichiello
- A. Citri
- S. Waddell
- Pedro F. Jacob
- Michael D. Ehlers
- Richard L. Huganir
- Yi Zhong
- Qian Li
Citations in the corpus
- Genetic dissection of mutual interference between two consecutive learning tasks in Drosophila (2022, background): “Feeding U0126, a widely used inhibitor of the MAPK pathway (Thomas & Huganir, 2004), did not affect single-task learning, but significantly exacerbated Pro-I when learning two consecutive tasks (Figure 4A).”
- Distinct Roles of NR2A and NR2B Cytoplasmic Tails in Long-Term (2010, neutral): “, 2005)] or by stimulating the LTD signaling pathways [such as Rap and p38 mitogen-activated protein kinase) (Thomas and Huganir, 2004; Zhu et al., 2005; Li et al., 2006)].”
- TrkB signalling pathways in LTP and learning (2009, background): “PKA, CaMKIV and extracellular signal-regulated kinase ( ERK ) signalling to the nucleus activates key transcription factors, including cyclic AMP-responsive element-binding protein ( CREB ), that trigger the synthesis of proteins that underlie L-LTP maintenanc”
- Activity level controls postsynaptic composition and signaling via the ubiquitin-proteasome system (2003, background): “Similarly, the overexpression of high-affinity mRFP-RBD-mRFP slowed the decay of Ras activation by reducing free [RasGTP] (equation (2)).”
- Synaptic activity-responsive element in the Arc/Arg3.1 promoter essential for synapse-to-nucleus signaling in activated neurons (2009, background): “1 gene that lied downstream of activity-regulated signaling mechanisms, such as CaMK and MAPK cascades, both of which were previously shown to underlie many aspects of neuronal adaptive responses (8, 26).”
- Stress-Induced p38 Mitogen-Activated Protein Kinase Activation Mediates κ-Opioid-Dependent Dysphoria (2007, background): “…that the KOR-dependent p38 MAPK activity after chronic stress and repeated sustained agonist exposure may act to “store” the aversion experience by effects on plasticity as suggested for MAPKs in other models (Thomas and Huganir, 2004); however, this hypothesis requires additional validation.”
- Neurobiology of the incubation of drug craving (2011, positive): “ERK is a component of the mitogen-activated protein kinase (MAPK) intracellular signaling pathway and its activation plays an important role in synaptic plasticity mechanisms underlying learning and memory [59, 60].”
- Synaptic Plasticity: Multiple Forms, Functions, and Mechanisms (2008, background): “The signaling to the nucleus required for long-lasting LTP has been suggested to depend on a number of protein kinases including PKA, CaMKIV, and Erk-MAPK, which activate key transcription factors that may include cAMP response element-binding protein and immediate-early genes such as c-Fos and Zif2”
- Spaced Training Forms Complementary Long-Term Memories of Opposite Valence in Drosophila (2019, positive): “In parallel with mechanisms of plasticity in other species, activated ERK phosphorylates and activates gene expression driven by the cAMP-response element binding (CREB) transcription factor (Bartsch et al., 1998; Impey et al., 1998; Thomas and Huganir, 2004; Miyashita et al., 2018).”
- Whole-brain activity mapping onto a zebrafish brain atlas (2015, background): “…kinase (ERK, also known as Mitogen activated protein kinase) 15–17 In response to depolarization, calcium influx through L-type voltage gated calcium channels activates the Ras-Erk pathway 18 leading to the phosphorylation of transcription factors such as CREB and Elk, and IEG expression 19 .”
- Regulation of Dendritic Morphogenesis by Ras–PI3K–Akt–mTOR and Ras–MAPK Signaling Pathways (2005, background): “In addition, Ras is well known to activate the Raf–MEK– MAPK pathway to regulate long-term synaptic plasticity and memory formation (Weeber and Sweatt, 2002; Thomas and Huganir, 2004).”
- The cell biology of synaptic plasticity: AMPA receptor trafficking. (2007, background): “If left unchecked, LTP and LTD can saturate synaptic strength.”