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McNaughton Lab

About the McNaughton Lab

McNaughton-pain-bannerThe McNaughton Lab's overall research theme is sensory systems – how do we detect the world around us, and how we know about the internal state of our own body? Current research projects focus on the following broad questions: How do we sense pain? What happens to pain sensation in chronic inflammation and following nerve injury – why does pain get worse? How do we sense warmth and cold? How do we sense our body temperature and how do we react in order to maintain body temperature constant? How do cells of the immune system “sniff out” and migrate towards areas of damage and pathogen invasion? 

Pain is initiated when specific pain-sensitive nerve fibres (nociceptors) are activated by painful stimuli such as heat, strong mechanical stimuli and chemical stimuli. Examples of chemical stimuli include acid (e.g. from lemon juice) or capsaicin, the active ingredient of chilli peppers. In the last 10 years much progress has been made in understanding the cellular basis of pain, and in particular in isolating and characterising the membrane ion channels which open in response to these stimuli and thus initiate action potentials in primary pain-sensitive afferent nerve fibres. Our overall aim is to use a range of state-of-the-art cellular and molecular techniques to unravel an age-old problem which lies at the root of much human suffering. 

Pain is unique amongst sensations in that it increases with prolonged exposure, a process known as sensitization, while in other sensory systems adaptation to a prolonged stimulus is observed. Sensitization has obvious protective value for the organism, but it is also responsible for much suffering in chronic pain states. Sensitization is caused by release of inflammatory mediators, such as bradykinin, prostaglandins and nerve growth factor (NGF), which bind to receptors on the neuronal cell membrane and activate cellular signalling pathways, which in turn modify the activity of downstream targets such as TRPV1 and HCN2. 

We still do not have a full picture of the mechanisms which detect warmth and cold in intact animals. Our lab recently discovered that TRPM2, a member of the TRP ion channel family, plays a previously unsuspected role as a sensor of mild warmth in the environment. The mechanisms in the central nervous system which detect and regulate body temperature, however, still remain to be discovered. 

We have recently become interested in how macrophages and neutrophils, cells of the immune system, are directed towards areas of damage or pathogen invasion, where they are needed to engulf pathogens and initiate tissue repair. We think that ion channels of the TRP family may be involved in this critical function. 

We approach these questions about pain and thermal sensation using molecular and cellular techniques to find out about the proteins and cellular signalling systems that underlie sensation. We also use transgenic animals in which specific genes have been deleted to find out how particular genes influence pain and thermal sensation at the level of the whole animal. The main thrust of the work in our lab is basic science, but some of our discoveries have suggested novel “targets” for drugs effective against pain. We have started two drug discovery programmes aimed at developing novel analgesics which will inhibit these targets. 


The main techniques in use in the lab are:

Patch clamp electrophysiology; Calcium imaging; Confocal microscopy; Fluorescence microscopy; Molecular biology; Immunohistochemistry; Cell culture; Creation of transgenic mouse strains; Animal behavioural experiments


Our work is funded by: the Medical Research Council (MRC), the Biotechnology and Biological Sciences Research Council (BBSRC) and the Wellcome Trust. 



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