Sensory transduction in peripheral nerve axons elicits ectopic action potentials
Tal Hoffmann1, Susanne K Sauer, Raymund E Horch
1Institute for Physiology and Pathophysiology, University Medical Center, University of Erlangen-Nuremberg, D-91054 Erlangen, Germany. diskin@physiologie1.uni-erlangen.de
Summary
Peripheral nerve axons share heat sensitivity with skin receptors, potentially causing ectopic discharge and pain during inflammation. This study investigated axonal activation and sensory properties in mouse C-fibers.
Area of Science:
- Neuroscience
- Pain Research
- Sensory Physiology
Background:
- Unmyelinated axons release neuropeptides in response to noxious stimuli.
- Inflammatory mediators sensitize axons via the transient receptor potential vanilloid receptor-1 (TRPV1) channel.
- The role of ectopic action potential generation in neuropathic pain remained unclear.
Purpose of the Study:
- To investigate whether axonal sensitization by inflammatory mediators is accompanied by ectopic generation of action potentials.
- To compare sensory properties of peripheral axons with their cutaneous terminals.
- To utilize propagated action potentials as an index of axonal activation.
Main Methods:
- Used an isolated mouse skin-nerve preparation.
- Performed single-fiber recordings from 51 mechanosensitive mouse C-fibers.
- Measured responses to graded heating of cutaneous receptive fields and the saphenous nerve.
Main Results:
- A majority of polymodal nociceptors responded to graded heating of both receptive fields and the nerve.
- Axonal heat responses paralleled receptive field responses in thresholds and discharge rates.
- Axonal mechanosensitivity was poor, and noxious cold sensitivity was rarely encountered.
Conclusions:
- Peripheral nerve axons possess sensory transduction capacities for noxious heat, similar to skin nociceptive terminals.
- Axons do not exhibit similar sensitivity to mechanical and cold stimuli.
- Axonal heat sensitivity may lead to ectopic discharge and pain if the threshold drops to body temperature during inflammation.
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