experiments overviewOverview of experiments used for figures 3,4,5exp2015-10-15confocal images used for counting inclusion bodiesexp2013-05-06exp2013-05-29exp2013-07-25See experiments overview for detailsexp2013-12-12See experiments overview for detailsexp2014-05-28See experiements overview for detailsexp2014-05-28bSee experiements overview for detailsexp2014-07-07exp2014-07-30exp2014-08-04See experiements overview for detailsexp2015-08-31 BSA TrisSee experiements overview for detailsexp2015-11-16aSee experiements overview for detailsexp2015-11-16bSee experiments overview for detailsexp2016-01-11aSee experiments overview for detailsexp2016-01-11bSee experiments overview for detailsexp2016-01-18aexp2016-01-18bSee experiments overview for detailsexp2016-01-27See experiments overview for detailsexp2016-03-14 BSA Tris aSee experiments overview for detailsexp2016-05-26 BSA TrisSee experiments overview for detailsexp2016-06-27 BSA TrisSee experiments overview for detailsexp2016-03-14 BSA Tris bSee experiments overview for detailsexp2016-03-14 BSA Tris cSee experiments overview for detailsReadXDatMatlab script to read the data. the Script will produce a timestamp (Ts) per fired action potential, a waveshape (Us; 96 data points), and a electrode number from which the event is recorded.

Amyloid aggregates of the protein α-synuclein (αS) called Lewy Bodies (LB) and Lewy Neurites (LN) are the pathological hallmark of Parkinson's disease (PD) and other synucleinopathies. We have previously shown that high extracellular αS concentrations can be toxic to cells and that neurons take up αS. Here we aimed to get more insight into the toxicity mechanism associated with high extracellular αS concentrations (50-100 μM). High extracellular αS concentrations resulted in a reduction of the firing rate of the neuronal network by disrupting synaptic transmission, while the neuronal ability to fire action potentials was still intact. Furthermore, many cells developed αS deposits larger than 500 nm within five days, but otherwise appeared healthy. Synaptic dysfunction clearly occurred before the establishment of large intracellular deposits and neuronal death, suggesting that an excessive extracellular αS concentration caused synaptic failure and which later possibly contributed to neuronal death.