Lecture by Dr. Kirsty Bannister, Lecturer, Pharmacology
King’s College London
Descending controls and considerations: a noradrenergic view
Biography (basic research):
Kirsty Bannister graduated from UCL in 2003 with a BSc in Pharmacology (first class honours) before completing a Master of Research and subsequent PhD in Epigenetics at Imperial College London. In 2008 Kirsty began a post-doctoral placement back at UCL in the Neuropharmacology of Pain laboratory, investigating neural and pharmacological systems that sub-serve pain transmission and modulation in the spinal cord and brain. Kirsty joined King’s College London in the autumn of 2017 on a permanent basis as a Lecturer in Pharmacology and Principal Investigator. Her interests remain investigating how pain can be controlled in both normal and pathological conditions, and how to translate basic science to the patient.
Descending controls comprise pathways that originate in midbrain and brainstem regions and project onto the spinal cord, interacting to produce the overall pain experience. I begin by discussing diffuse noxious inhibitory controls (DNIC), a unique form of endogenous descending inhibitory pathway. Previously we researched the spinal pharmacology of pathways that sub-serve DNIC and showed that, in the normal situation, DNIC produce a final inhibitory effect through the actions of noradrenaline at spinal α2 -adrenoceptors, although serotonin, acting on facilitatory spinal 5-HT3receptors, influences the final expression also.
My current and future research interests remain focused on DNIC and also on mechanisms of gabapentin/pregabalin mediated analgesia. I will highlight our most recent research demonstrating that gabapentin mediated analgesia involves inhibition of injury-induced spinal neuronal excitability and evoked hypersensitivity amongst other factors. My future research interests include understanding precisely what conditioning stimuli can evoke DNIC and whether pregabalin-mediated analgesia at supra-spinal sites interacts with or influences DNIC expression, possibly via spinal 2 adrenoceptor mediated mechanisms.
Professor Thomas Graven-Nielsen, DMSc, PhD
Center for Neuroplasticity and Pain (CNAP)