Suspended animation a step closer? Scientists uncover mammals' 'snooze button'

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Peer-reviewed: This work was reviewed and scrutinised by relevant independent experts.

Experimental study: At least one thing in the experiment was changed to see if it had an impact on the subjects (often people or animals) – eg: changing the amount of time mice spend on an exercise wheel to find out what impact it has on weight loss.

Animals: This is a study based on research on whole animals.

Suspended animation may be a step closer after Japanese scientists identified brain changes in mice that trigger a naturally occurring temporary hibernation-like state called 'torpor', and then successfully induced the same state in rats, who do not usually naturally hibernate or undergo torpor. In a related study, US scientists identified a population of brain cells that control topor and showed that stimulating these brain cells in mice induces torpor, while blocking them prevents torpor. The researchers say it may be possible to induce synthetic hibernation in humans if we have the same set of brain cells, which could be useful in reducing tissue damage or preserving organs for transplantation.

Journal/conference: Nature

DOI: 10.1038/s41586-020-2163-6

Organisation/s: University of Tsukuba, Japan, Harvard Medical School, USA

Funder: Paper 1: This study was supported by a JSPS KAKENHI Grant-in-Aid for Scientific Research (B) (JP 18H02595) (T.S.); a JSPS KAKENHI Grant-in-Aid for Scientific Research on Innovative Areas ‘Willdynamics’ (16H06401); JSPS KAKENHI grant number JP19K22465 (T.S.); JST CREST grant number JPMJCR1655 Japan (T.S.); the RIKEN Special Postdoctoral Researcher program (G.A.S.); a JSPS KAKENHI Grant-in-Aid for Scientific Research on Innovative Areas ‘Thermal Biology’ (18H04706) (G.A.S.); a JSPS KAKENHI Grant-in-Aid for Scientific Research (A) (19H01066) (G.A.S.); a research grant from the Astellas Foundation for Research on Metabolic Disorders (G.A.S.); and JSPS KAKENHI grant number 19J20876 (T.M.T.). Paper 2: This work was supported by National Institutes of Health grants R01 NS028829 and BRAIN Initiative grant R01 MH114081 to M.E.G., R01 DK107717 to A.S.B. and the Warren Alpert Distinguished Scholar Award to S.H.

Media release

Identifying a mammalian ‘snooze button’

Neuronal circuits that can trigger a state similar to hibernation in rodents are identified in two studies published in Nature this week. Artificial induction of a hibernation-like state could eventually have potential medical applications for humans, although this effect has not been tested in people.

Hibernating animals can lower their body temperature to reduce energy expenditure during times of limited food availability, such as the winter. Previous research has implicated the central nervous system in the regulation of hibernation, but the precise mechanisms involved have been unclear.

To learn more about what drives hibernation, Takeshi Sakurai and colleagues study laboratory mice (which do not hibernate, but exhibit a similar temporary hypometabolic state called torpor). Their experiments identify a distinct set of neurons in the hypothalamus — named Q neurons — that can induce long-lasting (more than 48 hours) reductions in body temperature and metabolism, similar to hibernation. The authors show that these neurons can be activated synthetically with chemicals or light, and uncover the wider circuit of neurons involved in this effect. No adverse effects on mouse behaviour or damage to tissues and organs were observed following the induced hibernation-like state. To determine whether the induced state was distinct from torpor, the authors repeated their experiments in rats, which undergo neither torpor nor hibernation. Once again they found that activation of Q neurons induced a hibernation-like hypometabolic state.

In an independent study, Michael Greenberg and colleagues identify a population of neurons within the hypothalamus that regulate torpor in mice. They demonstrate that stimulating these neurons can drive a mouse to the torpor state, even when there is no shortage of food. The role of these neurons is confirmed by blocking their activity, which prevents natural torpor from being initiated.

These findings help us to understand the neuronal processes that regulate hibernation-like states. Sakurai and colleagues suggest that these neuronal circuits may be conserved in a broad range of mammals, even in non-hibernating species, and posit that it might be possible to selectively manipulate Q neurons. Inducing a state of synthetic hibernation in humans could have the potential to reduce tissue damage after illness or preserve organs for transplantation, although this is currently speculative.


  • Springer Nature
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  • Springer Nature
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    Paper 2: The URL will go live after the embargo ends

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