For this round, we are delighted to announce that Dr Michael Ambler, Clinical Lecturer in the School of Physiology, Pharmacology and Neuroscience, was successful. Mike completed his GW4 Wellcome PhD fellowship under Tony Pickering, graduating in 2021.
Alongside his academic duties, Mike is a doctor working in intensive care medicine; this experience allowed him to realise that life-supporting interventions, designed to increase delivery of oxygen and nutrients to vital organs, frequently cause significant harm. He wanted to develop an approach that redresses imbalanced supply and demand of oxygen and nutrients by reducing demand, which might allow patients to better tolerate reduced cardiorespiratory function without the need for invasive organ support. Essentially, he wanted to mimic torpor in critically ill patients, but in order to do this, needed to understand the mechanisms by which torpor is naturally induced.
Having started alone as a PhD student studying torpor, and based on the work presented in this paper, Mike was awarded two grant applications: one, funded by the BBSRC, will study neural mechanisms of torpor and the interaction between torpor and circadian rhythms; the second, funded by the MRC, will study the role of analogous circuits in non-hibernators such as the rat, and investigate the potential protective effects of synthetic torpor states in rodent models of critical illness. These grants are worth ~£550,000 each and will employ two post-doctoral research associates full-time for three years.
Paper: Ambler M, Hitrec T, Wilson A, Cerri M & Pickering A (2022). Neurons in the dorsomedial hypothalamus promote, prolong, and deepen torpor in the mouse. The Journal of Neuroscience.
Daily heterotherms, such as mice, use torpor to cope with environments in which the supply of metabolic fuel is not sufficient for the maintenance of normothermia. Daily torpor involves reductions in body temperature, as well as active suppression of heart rate and metabolism. How the CNS controls this profound deviation from normal homeostasis is not known, but a projection from the preoptic area to the dorsomedial hypothalamus has recently been implicated. We demonstrate that the dorsomedial hypothalamus contains neurons that are active during torpor. Activity in these neurons promotes torpor entry and maintenance, but their activation alone does not appear to be sufficient for torpor entry.
The award was made with the support of the Elizabeth Blackwell Institute.