LTP inhibits LTD in the hippocampus via regulation of GSK3beta.

By S. Peineau, C. Taghibiglou, Clarrisa Bradley, T. Wong, Lidong Liu, Jie Lu, Edmond Lo, Dongchuan Wu, Emilia Saule, T. Bouschet and 5 more. Neuron, 2007

736 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/96dbfdf5376cca36710802909009fa57a29745dd

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. D. Selkoe
2. L. Mucke
3. A. Citri
4. G. Shankar
5. Nina E. Shepardson
6. Shaomin Li
7. D. Walsh
8. R. Malenka

In Genetics

1. R. Malenka
2. A. Citri
3. L. Mucke

In Molecular Biology

1. D. Selkoe
2. L. Mucke
3. Eléonore Beurel
4. A. Citri
5. S. Grieco
6. G. Shankar
7. D. Walsh
8. R. Malenka

Citations in the corpus

• The GSK3 hypothesis of Alzheimer's disease (2008, background): “Thus, it would appear that GSK3b is critical for the induction of memory formation, switching off LTD and allowing LTP to occur.”
• Glycogen synthase kinase-3 (GSK3): regulation, actions, and diseases (2014, background): “Thus, while it is clear that GSK3 impairs LTP and promotes LTD, which has been linked to impaired cognition in several disorders (King et al., 2014), further approaches are needed to clarify the roles of each GSK3 isoform in these processes.”
• The Many Faces of Tau (2011, background): “In addition, reduction of GSK-3b impairs NMDAR-mediated long-term depression (Peineau et al., 2007) and memory consolidation (Kimura et al., 2008), raising concerns about potential side effects of GSK-3b inhibitors.”
• Soluble oligomers of amyloid β-protein facilitate hippocampal long-term depression by disrupting neuronal glutamate uptake (2009, positive): “signaling cascades involved in LTD induction, including PP2B, p38 MAPK, and GSK3 (Mulkey et al., 1994; Bolshakov et al., 2000; Li et al., 2006; Peineau et al., 2007).”
• Synaptic Plasticity: Multiple Forms, Functions, and Mechanisms (2008, background): “…proteins other than phosphatases have been suggested to play key roles in LTD (Bolshakov et al, 2000; Dan and Poo, 2006; Palmer et al, 2005; Peineau et al, 2007), the hypothesis that LTP involves preferential activation of protein kinases while LTD involves activation of phosphatases…”