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Wellcome Trust conference The Challenges of Chronic Pain

11-13 March 2015
Wellcome Trust Genome Campus, Hinxton, Cambridge, UK

Abstract deadline: 30 January 2015
Registration deadline: 16 February 2015

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Archive workshop and seminar slides Professor Peter Karmerman…
Seminar Series There are currently no seminars scheduled.…
 
Past Research
The Mechanisms of Secondary Hyperalgesia
The phenomenon of secondary hyperalgesia provides an excellent experimental tool to examine nociceptive induced changes in central neuronal excitability that are not a simple reflection of increased primary afferent input. By studying neuronal activity in areas of the CNS that do not receive direct input from the injured region, we can concentrate upon the postsynaptic, secondary effects of persistent nociceptive inputs to central spinal circuits. While the phenomenon of primary and secondary hyperlagesia are well-described in man, they have not been adequately modelled in rodents. In addition, in most studies of changes in central excitability in persistent pain models, it is impossible to distinguish the peripheral and central contribution of the effects. Even the formalin test, with its well-described first and second phase, the second being classically ascribed to central processes, may really be a simple response to two phases of primary afferent barrage.
Behavioural models are not appropriate here because of the difficulty in stimulating very carefully defined skin areas in a repeatable manner in freely moving animals. On the other hand dorsal horn cell recording does not provide the neuronal population output measure that we require. We have already successfully set up a rat model of primary and secondary hyperalgesia using the flexion reflex EMG response in response to plantar foot stimulation. Animals are lightly anesthetised with halothane and the EMG activity recorded with a concentric needle electrode in the biceps femoris in response to graded von Frey hair stimulation, heat and cold, capsaicin etc to the plantar skin. The integral of the evoked EMG activity provides a measure of the amplitude and duration of the response (see Figure).


The aim of this project is to
(i) set up a mouse EMG model of secondary hyperalgesia
(ii) describe its latency of onset, magnitude, duration, topographic spread etc
(iii) investigate the role of descending pathways in its onset and maintenance
(iv) investigate the postnatal development and regulation
(v) test the importance of continuing primary hyperalgesia in the maintenance of secondary hyperalgesia.
(vi) design experiments to identify gene expression specifically regulated during the onset and maintenance of secondary hyperalgesia