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Author Notes:

Correspondence to Steve M. Potter, Laboratory for NeuroEngineering, Coulter Department of Biomedical Engineering, Georgia Institute of Technology, 313 Ferst Dr. NW, Atlanta, GA 30332-0535, USA. e-mail: steve.potter@bme.gatech.edu

Chadwick M. Hales wrote the paper, designed, and conducted all experiments.

Steve M. Potter edited the paper and contributed to experimental design.

Riley Zeller-Townson and Jonathan P. Newman provided technical assistance with the NeuroRighter recording hardware and software.

Jonathan P. Newman edited the paper.

Nathan J. Killian provided support for the power spectral analysis.

James T. Shoemaker performed E18 rat dissections.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


Research Funding:

Research was supported by the Clinical Research Training Fellowship from the American Academy of Neurology Foundation (Chadwick M. Hales) and NSF EFRI (0836017) (Steve M. Potter).


  • Science & Technology
  • Life Sciences & Biomedicine
  • Neurosciences
  • Neurosciences & Neurology
  • multielectrode array
  • microelectrode
  • MEA
  • oscillation
  • gap junction
  • NeuroRighter
  • carbenoxolone
  • microstimulation
  • 100-500 HZ
  • TIME

Stimulus-evoked high frequency oscillations are present in neuronal networks on microelectrode arrays


Journal Title:

Frontiers in Neural Circuits


Volume 6, Number MAY2012


, Pages 1-10

Type of Work:

Article | Final Publisher PDF


Pathological high frequency oscillations (250-600 Hz) are present in the brains of epileptic animals and humans. The etiology of these oscillations and how they contribute to the diseased state remains unclear. This work identifies the presence of microstimulation-evoked high frequency oscillations (250-400 Hz) in dissociated neuronal networks cultured on microelectrode arrays (MEAs). Oscillations are more apparent with higher stimulus voltages. As with in vivo studies, activity is isolated to a single electrode, however, the MEA provides improved spatial resolution with no spread of the oscillation to adjacent electrodes 200 μm away. Oscillations develop across four weeks in vitro. Oscillations still occur in the presence of tetrodotoxin and synaptic blockers, and they cause no apparent disruption in the ability of oscillation-presenting electrodes to elicit directly evoked action potentials (dAPs) or promote the spread of synaptic activity throughout the culture. Chelating calcium with ethylene glycol tetraacetic acid (EGTA) causes a temporal prolongation of the oscillation. Finally, carbenoxolone significantly reduces or eliminates the high frequency oscillations. Gap junctions may play a significant role in maintaining the oscillation given the inhibitory effect of carbenoxolone, the propagating effect of reduced calcium conditions and the isolated nature of the activity as demonstrated in previous studies. This is the first demonstration of stimulus-evoked high frequency oscillations in dissociated cultures. Unlike current models that rely on complex in vivo recording conditions, this work presents a simple controllable model in neuronal cultures on MEAs to further investigate how the oscillations occur at the molecular level and how they may contribute to the pathophysiology of disease. © 2012 Hales, Zeller-Townson, Newman, Shoemaker, Killian and Potter.

Copyright information:

Copyright © 2012 Hales, Zeller-Townson, Newman, Shoemaker, Killian and Potter.

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).
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