Dr Carole Torsney
Our main research focus is investigation of the altered sensory processing or ‘plasticity’ that occurs in chronic pain conditions with the aim of identifying novel therapies.
- 2012 - present: Lecturer, University of Edinburgh
- 2009 - 2012: Senior Academic Fellowship, University of Edinburgh
- 2006 - 2009: Caledonian Research Fellowship, University of Edinburgh
- 2002 - 2005: Postdoctoral position with Professor Amy MacDermott, Columbia University
- 1998 - 2002: Wellcome Trust Neuroscience four-yr PhD with Professor Maria Fitzgerald, University College London
Chronic pain can arise following tissue damage or injury to the nervous system and is characterised by spontaneous pain, allodynia (touch evoked pain) and hyperalgesia (exaggerated pain). Treatment options for this debilitating condition are frequently ineffective or are limited by adverse side effects. An understanding of the mechanisms underlying chronic pain is key to generating novel therapeutic targets, and is urgently required.
Following injury intense activity in pain sensing ‘C’ nerve fibres leads to or initiates an increase in spinal excitability (central sensitization). As a result of this increase in spinal excitability touch sensing ‘Ab’ nerve fibres are able to gain access to spinal circuits and mediate the sensation of mechanical allodynia. Similarly, pain sensing ‘Aδ’ nerve fibres are able to gain access to spinal circuits and mediate the sensation of mechanical hyperalgesia.
My previous research has identified spinal circuits that may mediate these sensations of allodynia (Figure 1) and hyperalgesia (Figure 2). My current research focusses on the C fibres that initiate this altered spinal sensory processing using electrophysiological, neuroanatomical and behavioural approaches.
We are currently investigating our interesting observation that the temporal relay of pain signals, by C fibres to the spinal cord, is altered in a sex and injury dependent manner. This sex difference in C fibre function is of significant interest given that it increasingly recognised that there are sex differences in pain sensitivity but there is poor understanding of the underlying basis. This lack of understanding is not surprising given that the vast majority of basic science studies of pain have been conducted upon male subjects, leading to mechanism-based development and assessment of therapies which may not be relevant for female subjects. This highlights the need for our future studies of chronic pain mechanisms and circuitry in both sexes to facilitate gender specific tailoring of analgesia.
As part of the University of Edinburgh Translational Pain Research Programme we collaborate with clinical colleagues from the Edinburgh Cancer Research Centre to study chemotherapy-induced neuropathic pain. Notably, this neuropathic pain is so poorly managed that some cancer patients stop life prolonging chemotherapy. We are currently exploring interventions to reduce the oxidative stress and mitochondrial damage that is thought to underlie these conditions with the future aim of limiting the development of this debilitating condition in patients undergoing chemotherapy.
- Kirsten Wilson (PhD student)
- Atanaska Velichkova (PhD student)
- Simona Gulbinaite (Postdoctoral Fellow)
- Dr Lesley Colvin, Edinburgh Cancer Research Centre, University of Edinburgh
- Professor Marie Fallon, Edinburgh Cancer Research Centre, University of Edinburgh
- Dr Sandrine Geranton, University College London
- Prof Helen Galley, University of Aberdeen
Galley HF, Barry McCormick B,Wilson KL, Lowes DA, Colvin, L, Torsney C. Melatonin limits paclitaxel-induced mitochondrial dysfunction in vitro and protects against paclitaxel-induced neuropathic pain in the rat. J. Pineal Res. 2017;e12444
Dickie AC, McCormick B, Lukito V, Wilson KL, Torsney C. Inflammatory Pain Reduces C Fibre Activity-Dependent Slowing in a Sex-Dependent Manner, Amplifying Nociceptive Input to the Spinal Cord. J Neurosci. 2017 Jul 5;37(27):6488-6502
Dickie AC, McCormick B, Lukito V, Wilson KL and Torsney C. Inflammatory pain reduces C fibre activity-dependent slowing in a sex dependent manner, amplifying nociceptive input to the spinal cord. J Neurosci
McCormick B, Lowes DA, Colvin L, Torsney C, Galley HF. MitoVitE, a mitochondria-targeted antioxidant, limits paclitaxel-induced oxidative stress and mitochondrial damage in vitro, and paclitaxel-induced mechanical hypersensitivity in a rat pain model. Br J Anaesth. 2016 Nov;117(5):659-666.
Dickie AC and Torsney C. The chemerin receptor 23 agonist, chemerin, attenuates monosynaptic C-fibre input to lamina I neurokinin 1 receptor expressing rat spinal cord neurons in inflammatory pain. Mol Pain. 2014 Apr 9;10(1):24.
Torsney C (2011) Inflammatory pain unmasks heterosynaptic facilitation in lamina l neurokinin 1 receptor-expressing neurons in rat spinal cord. J Neurosci 31(13):5158-68
Geranton SM, Jimenez-Diaz L, Torsney C, Tochiki KK, Stuart SA, Leith JL, Lumb BM, Hunt SP. A rapamycin-sensitive signalling pathway is essential for the full expression of persistent pain states. J Neurosci Nov 25 2009;29(47):15017-27
Torsney C, Anderson RL, Ryce-Paul K-AG and MacDermott AB. Characterization of sensory neuron subpopulations selectively expressing green fluorescent protein in phosphodiesterase 1C BAC transgenic mice. Molecular Pain. 2006 May 8;2(1):17
Torsney C and MacDermott AB. Disinhibition opens the gate to pathological pain signaling in superficial neurokinin 1 receptor-expressing neurons in rat spinal cord. J Neurosci 2006 Feb 8:26(6):1833-43.
Torsney C and Fitzgerald M. Spinal dorsal horn cell receptive field size is increased in adult rats following neonatal hindpaw skin injury. J Physiol 550(1): 255-61, 2003
Torsney C and Fitzgerald M. Age-dependent effects of peripheral inflammation upon the electrophysiological properties of neonatal rat dorsal horn neurons. J Neurophysiol 87(3):1311-7, 2002