Chemical excitation and sensitization in nociceptors

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Abstract
From early psychophysical studies a variety of exogenous and endogenous substances have been found to induce pain and hyperalgesia, that is, to be algogenic. To study the underlying mechanisms several behavioural and reflex models have been developed in animals. However, it has been difficult to differentiate between peripheral and central mechanisms. Single-fibre recordings provided a tool for isolating the contributions of primary afferents. Controlled application of defined mediator concentrations became feasible allowing for the investigation of the direct effects on nociceptive nerve endings. These sensory terminals, however, comprise receptive membrane sections, action potential generator region(s), and conductive zones of the axon, each of which could be the target of a chemical mediator. To differentiate these would require intracellular recording of the membrane potential or currents; this is not achievable due to the submicroscopic size of nociceptive nerve endings and their embedding in the tissue. Considering the cell soma in dissociated sensory ganglion cultures to be a model of its receptive ending, valuable information can be obtained from patch-clamp recordings of chemically mediated membrane effects.

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