Topic: Pyk2

BDNF mediates long-term potentiation (LTP) of hippocampal CA1 synapses by a translation-dependent mechanism. A master regulator of local protein synthesis at the synapse is fragile-X-messenger ribonucleoprotein (FMRP), however it is unclear to what extent FMRP mediates the effects of BDNF on the synaptic proteome. In this work we investigated whether FMRP regulates the synaptic content of GluN2B-containing NMDA receptors (NMDAR) with implication in synaptic plasticity. Acute hippocampal slices were prepared from WT and Fmr1y/- mice, and LTP was triggered with five theta-bursts, which induces B

Alzheimer's disease (AD) is characterized by an early hippocampus hyperactivity triggered by Aβ oligomers (Aβo) in humans and AD mouse models, followed by hypoactivity and synaptic loss occurring before cognitive decline. GWAS identified PTK2B gene encoding for Pyk2, a tyrosine kinase involved in synaptic plasticity, as a new AD risk factor. Several studies have validated Pyk2 involvement in AD pathophysiology, but its exact role is still debated due to conflicting results. The objective of this project is to decipher the role of Pyk2 in synaptic dysfunctions observed in this disease. We first

Temporal lobe epilepsy (TLE) is one of the most common forms of drug-resistant epilepsy and its precise etiology is still unknown making it imperative to understand the molecular pathways contributing to the disease. It is, therefore, crucial to study the therapeutic targets and signalling pathways involved in the treatment of this disease. Pyk2 has previously been shown to be activated in stress-mediated pathways in the brain. Consequently, we hypothesized that Pyk2 activation might contribute to the pathogenesis of the disease. A pilocarpine model of TLE was used to examine p-Pyk2Tyr402 prot