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British Pharmacology Society Winter Meeting: focus on neuropharmacology Expert Rev. Clin. Pharmacol. 2(2), 163–167 (2009)

Stephanie Burroughs*, Natasha Lethbridge* and Paul L Chazot† † Author for correspondence Integrative Neuroscience, School of Biological and Biomedical, Durham University, Durham, DH1 3L, UK Tel.: +44 191 334 1305 Fax: +44 191 334 1201 [email protected]

Both authors contributed equally to this article

*

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British Pharmacology Society Winter Meeting: focus on neuropharmacology Brighton, UK, 15–17 December 2008 This report covers a range of communications delivered at the Winter Meeting of the British Pharmacology Society, held at the Brighton Metropole Hotel on the 15–17th December 2008, which reported new findings in basic and clinical neuropharmacology. The report is subdivided into aspects of analgesia, neurological and psychological disorders. Analgesia

Chronic pain presents a huge economic and social burden, with existing treatments largely unable to satisfy medical needs [1] . Physical insults, including nerve damage, inflammation, visceral pathologies and cancer, can generate long-lasting pain, commonly referred to as chronic pain [2] . Pain is a complex signaling process involving a combination of peripheral innate immune and CNS responses, as well as activation of the hypothalamic–pituitary– adrenal axis [3] . The peripheral innate immune response to injury involves the rapid production and local release of proinflammatory cytokines, such TNF-α, IL-1 and IL-6 [2] . Recent studies into the CNS response to peripheral chronic inflammatory pain strongly implicate a role for glia and local synthesis of proinflammatory cytokines and growth factors [4] . TNF-α-induced thermal hyperalgesia is an animal model of inflammatory pain and has been shown to induce the release of the pro­i nf lammatory cytokine IL-1β. Russel and Brain (King’s College, London, UK) determined whether or not IL-1β release is essential for TNF-α-induced hyperalgesia in mice. Both ipsilateral and contralateral paws displayed elevated levels of IL-1β following intra­planar injections of TNF-α or vehicle in female CD-1 mice. Coadministration of IL-1 receptor antagonist (IL-1ra) and TNF-α prevented thermal hyperalgesia in the ipsilateral paw. Furthermore, injection of the vehicle in 10.1586/17512433.2.2.163

the contralateral paw, in the absence or presence of IL-1ra, caused no thermal hyperalgesia in that paw, and injection of IL-1ra into the vehicle-treated paw did not effect the ipsilateral paw in which TNF-α was administered alone (p 

British Pharmacology Society Winter Meeting: focus on neuropharmacology.

This report covers a range of communications delivered at the Winter Meeting of the British Pharmacology Society, held at the Brighton Metropole Hotel...
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