Acute Pannexin 1 Blockade Mitigates Early Synaptic Plasticity Defects in a Mouse Model of Alzheimer’s Disease

Área de publicación Neurociencia Cognitiva
Tipo de publicación Articles
Lugar de publicación Front. Cell. Neurosci
Fecha de publicación 2020
Autores Claudia Duran-Aniotz - Flores-Muñoz, C., Gómez, B., Mery, E., Mujica, P., Gajardo, I., Córdova, C., Lopez-Espíndola, D., Hetz, C., Muñoz, P., Gonzalez-Jamett, A.M., Ardiles, Á.O.

The acute inhibition of Panx1 activity with the drug probenecid (PBN) did not change neurodegenerative parameters such as amyloid deposition or astrogliosis, but it significantly reduced excitatory synaptic defects in the AD model by normalizing long-term potentiation (LTP) and depression and improving dendritic arborization and spine density in hippocampal neurons of the Tg mice. These results suggest a major contribution of Panx1 in the early mechanisms leading to the synaptopathy in AD.

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