Biology subjects

Bikson, M.

Publications and source records attributed to Bikson, M..

4 recordsLinked to original sources

bioRxiv2018

transcranial Direct Current Stimulation Studies Open Database (tDCS-OD)

Transcranial direct current stimulation (tDCS) is increasingly evaluated for a myriad of clinical indications and performance enhancement mainly related to cognitive and motor applications. As a result tDCS has been tested with diverse inclusion criteria and subject populations. tDCS is customized for applications by many factors, including stimulation dose (montage, current, time), associated training and subject inclusion/exclusion criteria. The rapid proliferation of applications, technological advancements and emerging scientific discoveries presents challenges to the organization and consolidation of tDCS data - which can lead to scientific, clinical and public confusions. In this paper, we develop a system to summarize and consolidate methodological aspects of tDCS, concentrating on study design and the physical parameters of the stimulation. We introduce a community-driven, open access database, where these parameters, including stimulation intensities, duration, electrode sizes, montages, and subject information, are noted for relevant tDCS publications. The transcranial Direct Current Stimulation Studies Open Database (tDCS-OD) (http://tdcsdatabase.com) will support constructive dialogue on research and clinical tDCS applications, critical evaluation of past work, and identification of promising protocols, while reducing ambiguity about stimulation methodology. The database design allows ongoing updates and editing, with transparent version control. At the moment, the database includes information about 56,613 tDCS sessions.

neuroscience↗

bioRxiv2018

Synaptic transmission modulates while non-synaptic processes govern the transition from pre-ictal to seizure activity in vitro

It is well established that non-synaptic mechanisms can generate electrographic seizures after blockade of synaptic function. We investigated the interaction of intact synaptic activity with non-synaptic mechanisms in the isolated CA1 region of rat hippocampal slices using the \"elevated-K+\" model of epilepsy. Elevated K+ ictal bursts share waveform features with other models of electrographic seizures, including non-synaptic models where chemical synaptic transmission is suppressed, such as the low-Ca2+model. These features include a prolonged (several seconds) negative field shift associated with neuronal depolarization and superimposed population spikes. When population spikes are disrupted for up to several seconds, intracellular recording demonstrated that the prolonged suppression of population spikes during ictal activity was due to depolarization block of neurons. Elevated-K+ ictal bursts were often preceded by a build-up of \"pre-ictal\" epileptiform discharges that were characterized as either \"slow-transition\" (localized and with a gradual increase in population spike amplitude, reminiscent non-synaptic neuronal aggregate formation, presumed mediated by extracellular K+ concentrations ([K+])o accumulation), or \"fast-transition\" (with a sudden increase in population spike amplitude, presumed mediated by field effects). When ictal activity had a fast-transition it was preceded by fast-transition pre-ictal activity; otherwise population spikes developed gradually at ictal event onset. Addition of bicuculline, a GABAA receptor antagonist, suppressed population spike generation during ictal activity, reduced pre-ictal activity, and increased the frequency of ictal discharges. Nipecotic acid and NNC-711, both of which block GABA re-uptake, increased population spike amplitude during ictal bursts and promoted the generation of preictal activity. By contrast, addition of ionotropic glutamate-receptor antagonists (NBQX, D-APV) had no consistent effect on ictal burst waveform or frequency and did not fully suppress pre-ictal activity. Similarly, CGP 55848, a GABAB receptor antagonist, has no significant effect on pre-ictal activity or burst frequency (although it did increase burst duration slightly). Our results are consistent with the hypothesis that non-synaptic mechanisms underpin the generation of ictal bursts in CA1 and that GABAA synaptic mechanisms can shape event development by delaying event initiation and counteracting depolarization block.

neuroscience↗

bioRxiv2017

Realistic vOlumetric-Approach to Simulate Transcranial Electric Stimulation -- ROAST -- a fully automated open-source pipeline

Research in the area of transcranial electrical stimulation (TES) often relies on computational models of current flow in the brain. Models are built based on the magnetic resonance images (MRI) of the human head to capture detailed individual anatomy. To simulate current flow on an individual, the subjects MRI is segmented, virtual electrodes are placed on this anatomical model, the volume is tessellated into a mesh, and a finite element model (FEM) is solved numerically to estimate the current flow. Various software tools are available for each step, as well as processing pipelines that connect these tools for automated or semi-automated processing. The goal of the present tool - ROAST - is to provide an end-to-end pipeline that can automatically process individual heads with realistic volumetric anatomy leveraging open-source software and custom scripts to improve segmentation and execute electrode placement. The electric field estimated with the open-source tools used by ROAST differ little from the results obtained with commercial meshing and FEM solving software. We also do not find large differences between the various automated segmentation methods used by ROAST and SimNIBS, a well-established open-source modeling pipeline. However, we do find large differences when volumetric segmentation are converted into surfaces that are used in SimNIBS to generate volumetric meshes. Evaluation on intracranial recordings from human subjects suggests that ROAST outperforms newer versions of SimNIBS in predicting field distribution and magnitudes, but that an older version of SimNIBS performs similarly. We hope that the detailed comparisons presented here of various choices in this modeling pipeline can provide guidance for future tool development. We release ROAST as an open-source, easy-to-install and fully-automated pipeline for individualized TES modeling at https://www.parralab.org/roast/.

biophysics↗

bioRxiv2017

tDCS changes in motor excitability are specific to orientation of current flow

Measurements and models of current flow in the brain during transcranial Direct Current Stimulation (tDCS) indicate stimulation of regions in-between electrodes. Moreover, the cephalic cortex result in local fluctuations in current flow intensity and direction, and animal studies suggest current flow direction relative to cortical columns determines response to tDCS. Here we test this idea by measuring changes in cortico-spinal excitability by Transcranial Magnetic Stimulation Motor Evoked Potentials (TMS-MEP), following tDCS applied with electrodes aligned orthogonal (across) or parallel to M1 in the central sulcus. Current flow models predicted that the orthogonal electrode montage produces consistently oriented current across the hand region of M1 that flows along cortical columns, while the parallel electrode montage produces none-uniform current directions across the M1 cortical surface. We find that orthogonal, but not parallel, orientated tDCS modulates TMS-MEPs. We also show modulation is sensitive to the orientation of the TMS coil (PA or AP), which is through to select different afferent pathways to M1. Our results are consistent with tDCS producing directionally specific neuromodulation in brain regions in-between electrodes, but shows nuanced changes in excitability that are presumably current direction relative to column and axon pathway specific. We suggest that the direction of current flow through cortical target regions should be considered for targeting and dose-control of tDCS.\n\nHighlights O_LIDirection of current flow is important for tDCS after-effects.\nC_LIO_LItDCS modulates excitability between two electrodes.\nC_LIO_LItDCS differentially modulates PA and AP inputs into M1.\nC_LI\n\nAbbreviations\n\nFundingThis research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

neuroscience↗