Astrocytes with previous chronic exposure to amyloid β-peptide fragment 1-40 suppress excitatory synaptic transmission

Journal of Neurochemistry
Hiroyuki KawanoKatsunori Iwasaki

Abstract

Synaptic dysfunction and neuronal death are responsible for cognitive and behavioral deficits in Alzheimer's disease (AD). It is well known that such neurological abnormalities are preceded by long-term exposure of amyloid β-peptide (Aβ) and/or hyperphosphorylated tau prior. In addition to the neurological deficit, astrocytes as a major glial cell type in the brain, significantly participate in the neuropathogenic mechanisms underlying synaptic modulation. Although astrocytes play a significant key role in modulating synaptic transmission, little is known on whether astrocyte dysfunction caused by such long-term Aβ exposure affects synapse formation and function. Here, we show that synapse formation and synaptic transmission are attenuated in hippocampal-naïve neurons co-cultured with astrocytes that have previously experienced chronic Aβ1-40 exposure. In this abnormal astrocytic condition, hippocampal neurons exhibit decrements of evoked excitatory post-synaptic currents (EPSCs) and miniature EPSC frequency. Furthermore, size of readily releasable synaptic pools and number of excitatory synapses were also significantly decreased. Contrary to these negative effects, release probability at individual synapses was significantly i...Continue Reading

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Citations

Jan 31, 2019·Journal of Neurophysiology·Courtney Clyburn, Kirsteen N Browning
Oct 12, 2018·Journal of Neurogenetics·Alicia MansillaAlberto Ferrús
Aug 14, 2020·Neural Regeneration Research·Mariana ToricelliTania Araujo Viel
Aug 2, 2020·Journal of Pharmacological Sciences·Kohei OyabuKatsunori Iwasaki

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