Study on the Role of Physical Fields in TMAS to Modulate Synaptic Plasticity in Mice
Xiaoxu Ma, Xin Wang, Kai Zhu, Ren Ma, Fangxuan Chu, Xu Liu, Shunqi Zhang, Tao Yin, Xiaoqing Zhou, Zhipeng Liu
IEEE Transactions on Biomedical Engineering 2024 · 10.1109/tbme.2023.3342012
Abstract
Objective Transcranial magneto-acoustic stimulation (TMAS) is a composite technique combining static magnetic and coupled electric fields with transcranial ultrasound stimulation (TUS) and has shown advantages in neuromodulation. However, the role of these physical fields in neuromodulation is unclear. Synaptic plasticity is the cellular basis for learning and memory. In this paper, we varied the intensity of static magnetic, electric and ultrasonic fields respectively to investigate the modulation of synaptic plasticity by these physical fields. Methods There are control, static magnetic field (0.1 T/0.2 T), TUS (0.15/0.3 MPa), and TMAS (0.15 MPa + 0.2 V/m, 0.3 MPa + 0.2 V/m, 0.3 MPa + 0.4 V/m) groups. Hippocampal areas were stimulated at 5 min daily for 7 days and in vivo electrophysiological experiments were performed. Results TMAS induced greater LTP, LTD, and paired-pulse ratio (PPR) than TUS, reflecting that TMAS has a more significant modulation in both long- and short- term synaptic plasticity. In TMAS, a doubling of the electric field amplitude increases LTP, LTD and PPR to a greater extent than a doubling of the acoustic pressure. Increasing the static magnetic field intensity has no significant effect on the modulation of synaptic plasticity. Conclusion This paper argues that electric fields should be the main reason for the difference in modulation between TMAS and TUS and that changing the amplitude of the electric field affected the modulation of TMAS more than changing the acoustic pressure. Significance This study elucidates the roles of the physical fields in TMAS and provides a parameterisation way to guide TMAS applications based on the dominant roles of the physical fields.
Abstract via europepmc.
Exposures
Exposure 1: Hippocampus, TUS 0.15/0.3 MPa and TMAS (static field 0.1/0.2 T, coupled field 0.2/0.4 V/m); separate magnet-only groups
Target: hippocampus — “hippocampal region (center: Anterior-Posterior (AP) 3 mm, Medial-Lateral (ML) 2.4 mm)”
Device: not reported
| Waveform | pulsed | |
|---|---|---|
| Fundamental frequency (kHz) | 1,000 | ✓✓✓ |
| Pulse duration (ms) | not reportedimplied by duty cycle ÷ PRF: 0.1 ms (not stated by the paper) | ⚑ |
| Pulse repetition frequency (Hz) | 1,000 | ✓✓✓ |
| Duty cycle (%) | 10 | ✓✓✓ |
| Sonication duration (s) | 300 | ✓✓✓ |
| Free-field pressure (kPa) | not reported | |
|---|---|---|
| Free-field Isppa (W/cm²) | not reported | |
| Free-field Ispta (W/cm²) | not reported | |
| In-situ estimate | not 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) | 150, 300swept | ✓?⚑ |
Ultrasonic pulse with a main frequency of 1 MHz, repetition frequency of 1 kHz and duty cycle of 10%, each stimulation lasting 5 minutes, once a day for 7 days.
Flags from extraction
exposures[0].unspecified_domain.pressure_kpa— Psptp 0.15 and 0.3 MPa measured with a needle hydrophone 'placed at the stimulus target' before stimulation; whether in water or through skull is not stated, so recorded as unspecified domain.sham_type— Control group is described only as 'control'; how it was handled (anaesthesia, coupling, no stimulation) is not stated.exposures[0].timing.pulse_duration_ms— Pulse duration not stated; shown only in Fig. 1(d). Not computed from duty cycle and PRF.n_subjects— Text reads '24 2.50 g' (garbled weight); 48 mice in 8 groups of 6 are stated.exposures[0].device— Transducer maker and model not named; only function generator and power amplifier are named.