Glen Wotherspoon

TL;DR: It is suggested that under conditions of increased nociception, microglial CatS is responsible for the liberation of neuronal FKN, which stimulates p38 MAPK phosphorylation in microglia, thereby activating neurons via the release of pronociceptive mediators.

TL;DR: It is shown that RNAi can block a pathophysiological pain response and provide relief from neuropathic pain in a rat disease model by down regulating an endogenous, neuronally expressed gene.

TL;DR: Examination of the expression of the sensory neuron‐specific cation channel Vanilloid Receptor 1 (VR1), an important transducer of noxious stimuli, in three models of nerve injury in the rat found that VR1‐IR persisted in the transected sciatic nerve proximal to the lesion, despite its down‐regulation in the damaged neuronal somata.

TL;DR: The induction of bone cancer in the rat by the syngeneic MRMT‐1 mammary tumour cell line provides a valid pre‐clinical model for pain associated with bone metastases and suggests a reasonable time window for evaluation of anti‐nociceptive agents between day 14 and 20 after cancer cell inoculation in this model.

TL;DR: The utility of ASO approaches for validating gene targets in in vivo pain models and evidence for a role of P2X3 receptors in the pathophysiology of chronic pain are provided.