Author: Plaksin M1, Kimmel E1, Shoham S1
Affiliation: <sup>1</sup>Faculty of Biomedical Engineering and Russell Berrie Nanotechnology Institute, Technion-Israel Institute of Technology , Haifa 32000, Israel.
Conference/Journal: eNeuro.
Date published: 2016 Jun 22
Other:
Volume ID: 3 , Issue ID: 3 , Special Notes: doi: 10.1523/ENEURO.0136-15.2016. eCollection 2016 May-Jun. , Word Count: 191
Diverse translational and research applications could benefit from the noninvasive ability to reversibly modulate (excite or suppress) CNS activity using ultrasound pulses, however, without clarifying the underlying mechanism, advanced design-based ultrasonic neuromodulation remains elusive. Recently, intramembrane cavitation within the bilayer membrane was proposed to underlie both the biomechanics and the biophysics of acoustic bio-effects, potentially explaining cortical stimulation results through a neuronal intramembrane cavitation excitation (NICE) model. Here, NICE theory is shown to provide a detailed predictive explanation for the ability of ultrasonic (US) pulses to also suppress neural circuits through cell-type-selective mechanisms: according to the predicted mechanism T-type calcium channels boost charge accumulation between short US pulses selectively in low threshold spiking interneurons, promoting net cortical network inhibition. The theoretical results fit and clarify a wide array of earlier empirical observations in both the cortex and thalamus regarding the dependence of ultrasonic neuromodulation outcomes (excitation-suppression) on stimulation and network parameters. These results further support a unifying hypothesis for ultrasonic neuromodulation, highlighting the potential of advanced waveform design for obtaining cell-type-selective network control.
KEYWORDS: Hodgkin and Huxley; T-type calcium channels; action potential; model; neurons; ultrasound
PMID: 27390775 PMCID: PMC4917736 DOI: 10.1523/ENEURO.0136-15.2016