Measurements and models of electric fields in the in vivo human brain during transcranial electric stimulation
- City College of the City University of New York, United States
- New York University School of Medicine, United States
- Mayo Clinic, United States
Abstract
Transcranial electric stimulation aims to stimulate the brain by applying weak electrical currents at the scalp. However, the magnitude and spatial distribution of electric fields in the human brain are unknown. We measured electric potentials intracranially in ten epilepsy patients and estimate electric fields across the entire brain by leveraging calibrated current-flow models. When stimulating at 2 mA, cortical electric fields reach 0.4 V/m, the lower limit of effectiveness in animal studies. When individual whole-head anatomy is considered, the predicted electric field magnitudes correlate with the recorded values in cortical (r=0.89) and depth (r=0.84) electrodes. Accurate models require adjustment of tissue conductivity values reported in the literature, but accuracy is not improved when incorporating white matter anisotropy or different skull compartments. This is the first study to validate and calibrate current-flow models with in vivo intracranial recordings in humans, providing a solid foundation to target stimulation and interpret clinical trials.
Article and author information
Author details
Funding
National Institute of Neurological Disorders and Stroke
- Yu Huang
- Anli A Liu
- Belen Lafon
- Daniel Friedman
- Michael Dayan
- Xiuyuan Wang
- Marom Bikson
- Werner K Doyle
- Orrin Devinsky
- Lucas C Parra
National Institute of Mental Health
- Yu Huang
- Anli A Liu
- Belen Lafon
- Daniel Friedman
- Michael Dayan
- Xiuyuan Wang
- Marom Bikson
- Werner K Doyle
- Orrin Devinsky
- Lucas C Parra
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Ethics
Human subjects: This study was performed at the New York University Medical Center (NYUMC). The protocol was approved by the NYUMC Institutional Review Board(IRB) and all patients provided written informed consent prior to their participation in the study. A physician was present at the bedside during the entire procedure to monitor for clinical safety.
Copyright
© 2017, Huang et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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Measurements and models of electric fields in the in vivo human brain during transcranial electric stimulation
eLife 6:e18834.
https://doi.org/10.7554/eLife.18834
Further reading
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- Neuroscience
The reward and novelty-related neuromodulator dopamine plays an important role in hippocampal long-term memory, which is thought to involve protein-synthesis-dependent synaptic plasticity. However, the direct effects of dopamine on protein synthesis, and the functional implications of newly synthesised proteins for synaptic plasticity, have not yet been investigated. We have previously reported that timing-dependent synaptic depression (t-LTD) can be converted into potentiation by dopamine application during synaptic stimulation (Brzosko et al., 2015) or postsynaptic burst activation (Fuchsberger et al., 2022). Here, we show that dopamine increases protein synthesis in mouse hippocampal CA1 neurons, enabling dopamine-dependent long-term potentiation (DA-LTP), which is mediated via the Ca2+-sensitive adenylate cyclase (AC) subtypes 1/8, cAMP, and cAMP-dependent protein kinase (PKA). We found that neuronal activity is required for the dopamine-induced increase in protein synthesis. Furthermore, dopamine induced a protein-synthesis-dependent increase in the AMPA receptor subunit GluA1, but not GluA2. We found that DA-LTP is absent in GluA1 knock-out mice and that it requires calcium-permeable AMPA receptors. Taken together, our results suggest that dopamine together with neuronal activity controls synthesis of plasticity-related proteins, including GluA1, which enable DA-LTP via a signalling pathway distinct from that of conventional LTP.
