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Transcranial Ultrasound Stimulation Directly Influences the Cortical Excitability of the Motor Cortex in Parkinsonian Mice

Zhijie Wang, Jiaqing Yan, Xingrang Wang, Yi Yuan, Xiaoli Li

Movement Disorders 2020, 35, 693-698 · 10.1002/mds.27952

rodentparkinsons diseaseinvasive electrophysiology

Abstract

Background Low-intensity transcranial ultrasound stimulation is a new noninvasive brain modulation method with high spatial resolution and high penetration depth. However, until now, it was unclear whether transcranial ultrasound stimulation has a significant effect on PD. Objectives In order to evaluate the effect of transcranial ultrasound stimulation on PD. Methods We used transcranial ultrasound stimulation to modulate parkinsonian-related activity in mice administered MPTP and recorded local field potentials in the motor cortex before and after ultrasound stimulation. We analyzed neuronal oscillatory activity known to be relevant to the pathophysiology of PD. Results After ultrasound stimulation, mean power intensity in the beta band (13-30 Hz) significantly decreased, and the phase-amplitude coupling strength between the beta and high gamma (55-100 Hz) bands and between the beta and ripple (100-200 Hz) bands also became significantly weaker. Conclusions This study demonstrates that ultrasonic neuromodulation can significantly decrease parkinsonian-related activity in mice administered MPTP. © 2019 International Parkinson and Movement Disorder Society.

Abstract via europepmc.

Speciesmouse (C57BL/6)
Subjects11 animals
Sessions per subject1
Randomisedyes
Blindingnot reported
Sham / controlinactive transducer
Auditory controldeafened subjects
Readout timingoffline
Anaesthesiaanaesthetised
Readoutsinvasive electrophysiology
Direction of effectinhibitoryTUS to the STN significantly decreased beta-band LFP power in motor cortex and significantly weakened beta/high-gamma and beta/ripple phase-amplitude coupling, compared to before TUS and to the PD+Sham group.
Adverse eventsnot reported

Exposures

Exposure 1: TUS targeting STN in MPTP-treated (parkinsonian) mice

Target: subthalamic nucleus — “STN
Device: Olympus / Panametrics · Olympus America, Inc. · V301-SU

Pulse timing
Waveformpulsed
Fundamental frequency (kHz)500✓✓
Pulse duration (ms)not reportedimplied by duty cycle ÷ PRF: 0.05 ms (not stated by the paper)
Pulse repetition frequency (Hz)1,000✓✓
Duty cycle (%)5✓✓
Sonication duration (s)0.05✓✓
Pressure and intensity, by domain
Free-field pressure (kPa)not reported
Free-field Isppa (W/cm²)not reported
Free-field Ispta (W/cm²)not reported
In-situ estimatenot reported
In-situ pressure (kPa)not reported
In-situ Isppa (W/cm²)not reported
In-situ Ispta (W/cm²)not reported
Pressure, domain unspecified (kPa)390✓✓
Isppa, domain unspecified (W/cm²)5.1✓✓
Protocol, in the paper’s words

The ultrasound parameters fundamental frequency (FF), pulsed repetition frequency (PRF), duty cycle (DC), and stimulation duration (SD) were 500 kHz, 1 kHz, 5%, and 50 ms, respectively. The interstimulus interval was 1 second, and the total stimulation time was 5 minutes. In the PD + TUS group, we continuously recorded LFPs for 5 minutes and then stimulated the STN by TUS for 5 minutes (LFPs were not recorded during stimulation); finally, we recorded LFPs for another 5 minutes.

Flags from extraction

  • exposures[0].unspecified_domain.pressure_kpaPaper does not state whether the 0.39 MPa / 5.1 W/cm2 field measurement (by needle hydrophone) was made in free field/water or in situ; domain left unspecified.
  • n_subjectsN=11 is the PD+TUS group size (the only group receiving active TUS); healthy, PD, and PD+Sham groups (N=6 each, total 77 mice used study-wide across this and related work) were not counted.