TRPA1 channels promote astrocytic Ca²⁺ hyperactivity and synaptic dysfunction mediated by oligomeric forms of amyloid-β peptide.

ABSTRACT:

Background

Excessive synaptic loss is thought to be one of the earliest events in Alzheimer's disease (AD). However, the key mechanisms that maintain plasticity of synapses during adulthood or initiate synapse dysfunction in AD remain unknown. Recent studies suggest that astrocytes contribute to functional changes observed during synaptic plasticity and play a major role in synaptic dysfunction but astrocytes behavior and involvement in early phases of AD remained largely undefined.

Methods

We measure astrocytic calcium activity in mouse CA1 hippocampus stratum radiatum in both the global astrocytic population and at a single cell level, focusing in the highly compartmentalized astrocytic arbor. Concurrently, we measure excitatory post-synaptic currents in nearby pyramidal n

SUBMITTER: Bosson A 

PROVIDER: S-EPMC5501536 | biostudies-literature | 2017 Jul

REPOSITORIES: biostudies-literature