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Low intensity transcranial ultrasound stimulation induces hemodynamic responses through neurovascular coupling

Hang Song, Ruoyu Chen, Liyuan Ren, Yinuo Zeng, Junfeng Sun, Shanbao Tong

iScience 2024 · 10.1016/j.isci.2024.110269

rodenthealthyinvasive electrophysiologycerebral haemodynamics

Abstract

Collective studies have demonstrated that transcranial ultrasound stimulation (TUS) can elicit activation in hemodynamics, implying its potential in treating cerebral or peripheral vessel-related malfunction. The theory for hemodynamic response to TUS is neurovascular coupling (NVC) following the ultrasound-induced cellular (de)polarization. However, it was not conclusive due to the co-existence of the pathway of direct ultrasound-vessel interactions. This study thus aims to investigate and provide direct evidence for NVC pathway in a rodent model of TUS by inhibiting neural activity with sodium valproate (VPA), a GABAergic agent. Twenty Sprague-Dawley rats were randomly assigned to VPA and Saline groups. Microelectrode and optical imaging were utilized to record local field potential and relative cerebral blood flow (rCBF) during baseline, before, and after TUS periods. We found the attenuated neural activity was associated with reduced rCBF responses. These results provided direct evidence for the presence of NVC pathway in hemodynamic modulation by TUS.

Abstract via europepmc.

Speciesrat (Sprague-Dawley)
Subjects20 animals
Sessions per subjectnot reported
Randomisedyes
Blindingnot reported
Sham / controlnone
Auditory controlnot reported
Readout timingoffline
Anaesthesiaanaesthetised
Readoutsinvasive electrophysiology, cerebral haemodynamics — LFP power (tungsten microelectrode); laser speckle contrast imaging of rCBF
Direction of effectexcitatoryTUS increased LFP power and rCBF in the Saline group; after VPA (neural inhibition) the TUS-induced rCBF increase was not significant and the Group x Stage interaction was significant.
Adverse eventsnot reportedThe text states the TUS parameters generated negligible temperature change (less than 0.02 C), citing the authors' prior study.

Exposures

Exposure 1: TUS to S1 after VPA or saline i.p.

Target: primary somatosensory cortex — “The primary sensory cortex (S1, ML: 3 mm, AP: 0.84 mm)”
Device: Olympus / Panametrics · Olympus NDT · V301-SU ✓

Pulse timing
Waveformpulsed
Fundamental frequency (kHz)500✓✓✓
Pulse duration (ms)0.4✓✓✓
Pulse repetition frequency (Hz)1,500✓✓✓
Duty cycle (%)not reportedpulse duration × PRF gives 60%⚑
Sonication duration (s)1✓✓✓
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
Isppa, domain unspecified (W/cm²)8.92✓✓✓⚑
Protocol, in the paper’s words

5-min sonication with ISI = 4 s, sonication duration = 1 s, PRF = 1.5 kHz and tone burst duration = 0.4 ms; 20-s LFP-LSCI blocks recorded at baseline, 10 min after VPA/saline i.p., and immediately after TUS.

Flags from extraction

  • exposures[0].unspecified_domain.isppa_w_cm2 — Intensity stated without domain; hydrophone used to assess the field with the collimator but the 8.92 W/cm2 is not explicitly free-field.
  • exposures[0].timing.duty_cycle_pct — Duty cycle not stated; not computed.
  • n_subjects — Sample size is 20 rats, 10 per group; analyses in the text use F(1,18).
  • anaesthesia — Cranial window under isoflurane 6 h before; recordings and TUS under isoflurane anaesthesia.