Topic: hippocampal hyperactivity

Alzheimer’s disease (AD) is characterized by a long asymptomatic phase associated with the toxic accumulation of oligomeric form of amyloid-beta peptide (Aβo). One of the first event reported in this phase seems to be a specific hippocampal hyperactivity in both humans and AD mouse model. We highlighted that this early hyperactivity starts with an abnormal increase of calcium activity in astrocytes which affects neighbouring neurons in the hippocampus. We identified an astrocytic calcium channel, transient receptor potential ankyrin-1 (TRPA1), implicated in the Aβo-induced hippocampal hyperact

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

The subiculum, a hippocampal subfield that functions as the final gate for most hippocampal outputs, is implicated in various psychiatric disorders. Accumulating evidence suggests that dysfunction in multiple GABAergic interneuron types is a key factor in the pathologic presentation of hippocampal hyperactivity associated with these disorders. We posit that dysfunction in the inhibitory control of interneurons in the subiculum may be a key network mechanism for the emergence of hippocampal hyperactivity. In several brain regions, a special class of interneurons known as vasoactive intestinal p