← Explore

Induction of a torpor-like hypothermic and hypometabolic state in rodents by ultrasound

Yaoheng Yang, Jinyun Yuan, Rachael L. Field, Dezhuang Ye, Zhongtao Hu, Kevin Xu, Lu Xu, Yan Gong, Yimei Yue, Alexxai V. Kravitz, Michael R. Bruchas, Jianmin Cui, Jonathan R. Brestoff, Hong Chen

Nature Metabolism 2023, 5, 789-803 · 10.1038/s42255-023-00804-z

rodentin vitro cellhealthyautonomic physiologybehaviourcellular imaginghistology molecularother mri

Abstract

Torpor is an energy-conserving state in which animals dramatically decrease their metabolic rate and body temperature to survive harsh environmental conditions. Here, we report the noninvasive, precise and safe induction of a torpor-like hypothermic and hypometabolic state in rodents by remote transcranial ultrasound stimulation at the hypothalamus preoptic area (POA). We achieve a long-lasting (>24 h) torpor-like state in mice via closed-loop feedback control of ultrasound stimulation with automated detection of body temperature. Ultrasound-induced hypothermia and hypometabolism (UIH) is triggered by activation of POA neurons, involves the dorsomedial hypothalamus as a downstream brain region and subsequent inhibition of thermogenic brown adipose tissue. Single-nucleus RNA-sequencing of POA neurons reveals TRPM2 as an ultrasound-sensitive ion channel, the knockdown of which suppresses UIH. We also demonstrate that UIH is feasible in a non-torpid animal, the rat. Our findings establish UIH as a promising technology for the noninvasive and safe induction of a torpor-like state.

Abstract via europepmc.

Speciesmouse (C57BL/6NCrl, UCP1-KO); rat (Wistar Han IGS); HEK293T cells (in vitro)
Subjectsnot reported animals
Sessions per subjectnot reported
Randomisedyes
Blindingnot reported
Sham / controlundescribed
Auditory controlramped pulses
Readout timingboth
Anaesthesiaawake
Readoutsautonomic physiology, behaviour, cellular imaging, histology molecular, other mriBody/BAT/tail temperature (thermal imaging, telemetry), VO2/RQ (indirect calorimetry), ECG/heart rate, locomotor activity, fiber photometry (GCaMP6s) in POA and DMH, single-nucleus RNA-sequencing, FISH/immunohistochemistry (Fos, Trpm2, Adcyap1, NeuN, GFAP, Iba1), MRI thermometry
Direction of effectexcitatoryUltrasound stimulation of the POA activated POA and downstream DMH neurons (increased Fos expression and evoked Ca2+ activity), which in turn suppressed BAT thermogenesis and drove systemic hypothermia and hypometabolism; the effect required the ultrasound-sensitive ion channel TRPM2 and was attenuated (not abolished) by TRPM2 knockdown.
Adverse eventsnone observedImmunohistological examination of mouse brains after ultrasound treatment did not find any visible tissue damage or inflammation.

Exposures

Exposure 1: Ultrasound-induced hypothermia/hypometabolism (UIH), mouse POA, 3.2 MHz

Target: hypothalamus — “hypothalamus preoptic area (POA)
Device: custom-built

Pulse timing
Waveformpulsed
Fundamental frequency (kHz)3,200✓✓
Pulse duration (ms)50✓✓
Pulse repetition frequency (Hz)10✓✓
Duty cycle (%)50pulse duration × PRF gives 50%✓✓
Sonication duration (s)2, 10swept✓✓
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 estimatemeasurementsingle value
In-situ pressure (kPa)400, 800, 1,200, 1,600swept✓✓
In-situ Isppa (W/cm²)not reported
In-situ Ispta (W/cm²)not reported
Protocol, in the paper’s words

Default protocol: peak negative in-situ pressure 1.6 MPa, duty cycle 50%, PRF 10 Hz, stimulus duration 10 s, inter-stimulus interval 30 s, 6 stimuli total, via a wearable transducer glued to the mouse skull over the POA. A gaussian envelope was applied to pulse onset/offset to reduce broadband auditory activation. In a parameter study, stimulus duration (2-10 s) and acoustic pressure (0.4, 0.8, 1.2, 1.6 MPa) were varied independently while other parameters were held constant. A closed-loop feedback controller turned ultrasound on/off (same parameters, 20 s inter-stimulus interval) to hold core temperature below 34 degC for approximately 24 h continuously, with pressure increased 10% and stimulus number increased to 8 after 12 h to compensate for gel attenuation.

Exposure 2: Ultrasound-induced hypothermia (UIH), rat POA, 1.5 MHz

Target: hypothalamus — “hypothalamus preoptic area (POA)
Device: custom-built

Pulse timing
Waveformpulsed
Fundamental frequency (kHz)1,500✓✓
Pulse duration (ms)50✓✓
Pulse repetition frequency (Hz)10✓✓
Duty cycle (%)50pulse duration × PRF gives 50%✓✓
Sonication duration (s)10✓✓
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 estimatemeasurementsingle value
In-situ pressure (kPa)1,400✓✓
In-situ Isppa (W/cm²)not reported
In-situ Ispta (W/cm²)not reported
Protocol, in the paper’s words

Same wearable-transducer protocol as in mice (duty cycle 50%, PRF 10 Hz, stimulus duration 10 s, inter-stimulus interval 30 s), scaled to a 1.5 MHz transducer and a peak negative in-situ pressure of 1.4 MPa, with 20 stimuli delivered to freely-moving rats.

Exposure 3: In vitro TRPM2 activation by ultrasound in HEK293T cells

Target: other — “HEK293T cells overexpressing TRPM2 (in vitro)
Device: custom-built

Pulse timing
Waveformpulsed
Fundamental frequency (kHz)1,700✓✓
Pulse duration (ms)not reportedimplied by duty cycle ÷ PRF: 40 ms (not stated by the paper)
Pulse repetition frequency (Hz)10✓✓
Duty cycle (%)40✓✓
Sonication duration (s)60✓✓
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 applicable
In-situ pressure (kPa)not applicable
In-situ Isppa (W/cm²)not applicable
In-situ Ispta (W/cm²)not applicable
Pressure, domain unspecified (kPa)1,000✓✓
Protocol, in the paper’s words

Cultured HEK293T cells overexpressing TRPM2 were sonicated with a customized in vitro US setup (different transducer from the in vivo experiments) 30 s after the start of Ca2+ imaging, to test direct ultrasound sensitivity of the TRPM2 channel; a subset of wells received the TRPM2 blocker 2-APB before sonication.

Flags from extraction

  • n_subjectsDozens of separate cohorts (mice, UCP1-KO mice, rats, in vitro cells) with different, non-overlapping n reported per assay across the paper; no single study-wide total of subjects exposed to ultrasound is given.
  • n_sessions_per_subjectMost animals received a single acute stimulation session, but the closed-loop feedback experiment delivered many intermittent stimuli continuously over ~24 h; no single value applies across the study.
  • exposures[1].timing.pulse_duration_msThe 50 ms pulse duration is explicitly stated only in the context of the mouse experiment (Fig. 1c); it is assumed to also apply to rats because duty cycle (50%) and PRF (10 Hz) are stated to be identical for mice and rats, but this is not separately confirmed in the text for rats.
  • exposures[2].timing.pulse_duration_msPulse duration for the in vitro TRPM2 experiment is not stated directly; only duty cycle (40%) and PRF (10 Hz) are given, and pulse duration was not computed from these per instructions.
  • anaesthesiaUltrasound stimulation itself was delivered to awake, freely-moving animals; brief isoflurane anaesthesia (1-1.5%) was used only for surgery and daily transducer attachment (<=15 min), not during stimulation/testing.
  • sham_typeThe exact mechanism of the 'US-' (no ultrasound) control condition (e.g., whether a transducer was worn but inactive) is not explicitly described.