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Review
. 2004 Mar;53 Suppl 2(Suppl 2):ii9-12.
doi: 10.1136/gut.2003.033423.

Recent advances in understanding molecular mechanisms of primary afferent activation

J N Wood  1
Affiliations
Review

Recent advances in understanding molecular mechanisms of primary afferent activation

J N Wood. Gut. 2004 Mar.

Abstract

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.

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Figures

Figure 1
Figure 1
Cell signalling through the red tyrosine kinase by members of the glial derived neurotrophic factor family. The associated α subunits determine the specificity of the interaction between the various ligands GDNF (α-1), neurturin (α-2), artemin (α-3), and persephin (α-4). GFR, growth factor receptor; GPI, glycophosphoinositol.
Figure 2
Figure 2
Structure of a voltage sodium channel α subunit showing the voltage sensor S4 domains and the accessory subunits that anchor the channel with respect to extracellular signals.
See this image and copyright information in PMC

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