Intracellular amyloid induces impairments on electrophysiological properties of cultured human neurons.
The role of intracellular amyloid beta (iAbeta) in Alzheimer's disease (AD) initiation and progression attracts more and more attention in recent years. To address whether iAbeta induces early alterations of electrophysiological properties in cultured human primary neurons, we delivered iAbeta with adeno-virus and measured the electrophysiological properties of infected neurons with whole-cell recordings. Our results show that iAbeta induces an increase in neuronal resting membrane potentials, a decrease in K(+) currents and a hyperpolarizing shift in voltage-dependent activation of K(+) currents. These results suggest the electrophysiological impairments induced by iAbeta may be responsible for its neuronal toxicity.
Hou
Jun-Feng
JF
Laboratory of Neurobiology and State Key Laboratory of Biomembrane and Membrane Biotechnology, College of Life Sciences, Peking University, Beijing, China.
Cui
Jia
J
Yu
Long-Chuan
LC
Zhang
Yan
Y
D000256:Adenoviridae / Q000235:genetics; D016229:Amyloid beta-Peptides / Q000235:genetics / Q000502:physiology*; D002478:Cells, Cultured; D005822:Genetic Vectors; D006801:Humans; D042541:Intracellular Space / Q000378:metabolism*; D015640:Ion Channel Gating; D008564:Membrane Potentials; D009474:Neurons / Q000502:physiology*; D018408:Patch-Clamp Techniques; D015221:Potassium Channels / Q000502:physiology
D016229:Amyloid beta-Peptides; D015221:Potassium Channels