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Recent advances in understanding molecular mechanisms of primary afferent activation

J N Wood

Correspondence to:
Correspondence to:
J N Wood
Molecular Nociception Group, Department of Biology, University College, London WC1E 6BT, UK; J.Wood{at}ucl.ac.uk

Thermal, mechanical, and chemical stimuli depolarise specialised damage sensing neurons to initiate electrical signals that may ultimately result in a sensation of pain. Over the past decade many of the receptors that transduce these signals have been identified by molecular cloning. In the absence of specific blockers, null mutant mice have proved valuable in exploring the function of these specialised receptors. As well as the mechanisms of signal transduction, the setting of thresholds for excitation and the transmission of electrical signals have also been the focus of intense interest. In vitro studies of dorsal root ganglion sensory neurons have thus facilitated rapid advances in our understanding of the biology of nociceptors. However, the specific properties of visceral afferents are poorly defined, and useful animal models of visceral pain are only now being developed. Visceral neuron receptor subtypes and the consequences of their activation in terms of pain perception and behaviour are thus subjects that still demand a major research effort.

Keywords: pain; primary afferent activation; signal transduction; nociceptors; neurons

Abbreviations: NGF, nerve growth factor; GDNF, glial derived neurotrophic factors; GFR, growth factor receptor; GPI, glycophosphoinositol; IB4, isolectin B4; TrkA, tyrosine kinase A; DRASIC, DRG sensory neurons; TRP, transient receptor potential; TRPV1, TRP-vanilloid receptor 1; CMR1, cold/menthol receptor; ASIC, acid sensing ion channel; ENac, epithelial sodium channel; MDEG, mammalian degenerin; CNS, central nervous system; UTRs, un-translated regions; ATP, adenosine triphosphate; PPK, pickpocket; RPK, ripped pocket; VGSC, voltage gated sodium channels; TTX, tetrodotoxin, Cre-lox-p, cyclase recombinase locus of crossover

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