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Simultaneous Transcranial Alternating Current Stimulation and Functional Magnetic Resonance Imaging
Published on: June 5, 2017
High frequency stimulation abolishes thalamic network oscillations: an electrophysiological and computational
Kendall H Lee1, Frederick L Hitti, Su-Youne Chang
1Department of Neurologic Surgery, Mayo Clinic, 200 First Street SW, Rochester, MN 55902, USA.
Journal of Neural Engineering
|May 31, 2011
Summary
High-frequency stimulation (HFS) of the thalamus for epilepsy disrupts brain oscillations by increasing glutamate release. This mechanism, involving glutamate and ion channel modulation, offers insights into deep brain stimulation (DBS) efficacy.
Area of Science:
- Neuroscience
- Epilepsy Research
- Computational Modeling
Background:
- Thalamic deep brain stimulation (DBS) is an effective epilepsy treatment.
- The precise mechanism of thalamic DBS action remains incompletely understood.
Purpose of the Study:
- To investigate the mechanism of action of thalamic DBS.
- To examine the effects of high-frequency stimulation (HFS) on thalamic network oscillations.
Main Methods:
- Electrophysiological recordings (intracellular and extracellular) in ferret thalamic slices (nucleus reticularis thalami and lateral geniculate nucleus).
- High-frequency stimulation (100 Hz) applied to thalamocortical relay (TC) and nucleus reticularis (nRt) neurons.
- Measurement of extracellular glutamate levels.
- Computational modeling of the thalamic network.
Main Results:
- HFS of TC neurons increased neuronal activity, reduced input resistance, elevated extracellular glutamate, and abolished spindle oscillations.
- HFS of nRt also suppressed spindle oscillations.
- Prolonged suppression of spindle oscillations was observed, linked to glutamate release and modulation of hyperpolarization-activated current (I(h)) in computational models.
Conclusions:
- Thalamic DBS may exert its anti-epileptic effects through prolonged glutamate release.
- Glutamate release modulates ion channels (e.g., I(h)), decreases neuronal input resistance, and disrupts pathological thalamic network oscillations.
