A Snapshot seminar hosted by the School of Physiology, Pharmacology and Neuroscience

OLM interneurons regulate hippocampal placecell stability: The Hippocampus is well known for harboring neurons that process and store spatial information about the physical environments we inhabit. These ‘place cells’ encode for specific locations in our environment and at the population level enabling us to create spatial memories of new places we have visited and store information about familiar locations visited in the past. 

These place cells, formed via synaptic plasticity, hang in a fine balance between being both stable and robust so information about familiar locations is not lost but also adaptable so that new information can be incorporated when aspects of our environment change. 

We have been investigating this trade-off using in vivo miniscope calcium imaging in mice to measure the activity of place cells and OLM inhibitory interneurons whilst mice explore novel and familiar environments. We show that OLM interneurons exhibit specific activity patterns during exploration. Via optogenetic perturbation of this activity, we show these interneurons enable the formation of new place cells whilst stabilising existing place cells.  

When the going gets tough, the smart switch off: hijacking the hypothalamus to protect the heart: As an intensive care clinician, I am always looking for ways to do less work - both for me and my patients. Torpor is a naturally occurring hypothermic, hypometabolic protective state, which can be brief (in daily heterotherms such as mice), or prolonged (in seasonal hibernators). I have identified some of the brain regions involved in inducing torpor in the mouse. I have been using targeted recombination of activate populations (TRAP) to drive transgene expression in neurons that are active during natural torpor in the mouse.  Using this technique, I have shown that the preoptic area of the hypothalamus (POA) contains neurons that are sufficient for at least some of the features of torpor. Rats do not naturally enter torpor, but I will present data to demonstrate that activating the corresponding regions in the rat POA induces a synthetic torpor state. Finally, I will show some recent data that indicates synthetic torpor in the rat is protective in an ex-vivo cardiac ischaemia-reperfusion model.