Low-intensity ultrasound stimulation modulates cortical neurovascular coupling in an attention deficit hyperactivity disorder rat model
Mengran Wang, Teng Wang, Xin Li, Yi Yuan
Cerebral Cortex 2023, 33, 11646-11655 · 10.1093/cercor/bhad398
Abstract
Attention deficit hyperactivity disorder is accompanied by changes in cranial nerve function and cerebral blood flow (CBF). Low-intensity ultrasound stimulation can modulate brain neural activity in attention deficit hyperactivity disorder. However, to date, the modulatory effects of low-intensity ultrasound stimulation on CBF and neurovascular coupling in attention deficit hyperactivity disorder have not been reported. To address this question, Sprague-Dawley, Wistar-Kyoto, and spontaneously hypertensive (attention deficit hyperactivity disorder (ADHD) rat model) rats were divided into the control and low-intensity ultrasound stimulation (LIUS) groups. Cortical electrical stimulation was used to induce cortical excitability in different types of rats, and a penetrable laser speckle contrast imaging (LSCI) system and electrodes were used to evaluate the electrical stimulation-induced CBF, cortical excitability, and neurovascular coupling in free-moving rats. The CBF, cortical excitability, and neurovascular coupling (NVC) under cortical electrical stimulation in the attention deficit hyperactivity disorder rats were significantly different from those in the Sprague-Dawley and Wistar-Kyoto rats. We also found that low-intensity ultrasound stimulation significantly interfered with the cortical excitability and neurovascular coupling induced by cortical electrical stimulation in rats with attention deficit hyperactivity disorder. Our findings suggest that neurovascular coupling is a potential biomarker for attention deficit hyperactivity disorder. Furthermore, low-intensity ultrasound stimulation can improve abnormal brain function in attention deficit hyperactivity disorder and lay a research foundation for its application in the clinical treatment of attention deficit hyperactivity disorder.
Abstract via europepmc.
Exposures
Exposure 1: LIUS to prefrontal cortex in SD, WKY and SHR (ADHD model) rats
Target: prefrontal cortex — “prefrontal cortex”
Device: Olympus / Panametrics · Olympus · V301-SU ✓
| Waveform | pulsed | |
|---|---|---|
| Fundamental frequency (kHz) | 500 | ✓✓✓ |
| Pulse duration (ms) | 50 | ✓✓✓⚑ |
| Pulse repetition frequency (Hz) | 1 | ✓✓✓ |
| Duty cycle (%) | 5pulse duration × PRF gives 5% | ✓✓✓ |
| Sonication duration (s) | 900 | ✓✓✓ |
| 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 |
LIUS (500 kHz fundamental frequency, 1 Hz PRF, 5% duty cycle, 50 ms pulse) delivered to the prefrontal cortex for a total stimulation time of 15 min per day, continuously for 7 days; cortical electrical stimulation (15 uA, 3 s, 10 trials at 5-min intervals) was used afterward to probe evoked CBF, LFP and neurovascular coupling on days 1, 4 and 7.
Flags from extraction
exposures[0].timing.pulse_duration_ms— The paper labels 50 ms as 'stimulation duration' rather than explicitly as pulse duration; this was resolved via the burst rule because duty cycle (5%) / PRF (1 Hz) = 0.05 s = 50 ms, matching the stated value exactly, confirming it is the pulse duration rather than a separate sonication-train duration.n_subjects— Paper gives n=7 LIUS-exposed rats per strain (SD, WKY, SHR); a combined total across strains is not explicitly stated.anaesthesia— Rats were anesthetized (2% isoflurane) for surgery, but the recording/LIUS system is explicitly built for 'free-moving rats'; anesthesia status during the LIUS stimulation itself is not explicitly restated, so 'awake' is inferred from the free-moving-rat framing.