• Perivagal application of capsaicin (1% solution) is considered to cause selective degeneration of vagal afferent (sensory) C fibres and has been used extensively to examine the site of action of many gastrointestinal (GI) neuropeptides. • The actions of both capsaicin and GI neuropeptides may not be restricted to vagal afferent fibres, however, as other non‐sensory neurones displayed sensitivity to capsaicin and brainstem microinjections of these neuropeptides induce GI effects similar to those obtained upon systemic application. • The present study used immunohistochemical, biophysical and functional approaches to test the hypothesis that perivagal capsaicin induces degeneration of vagal efferents controlling GI functions. • Our data indicate that perivagal application of capsaicin induces degeneration of vagal efferent motoneurones and decreased vagal motor responses. Treatment with perivagal capsaicin cannot therefore be considered selective for vagal afferent C fibres and, consequently, care is needed when using perivagal capsaicin to assess the mechanism of action of GI neuropeptides. Abstract Perivagal application of capsaicin (1% solution) is considered to cause a selective degeneration of vagal afferent C fibres and has been used extensively to examine the site of action of many gastrointestinal (GI) neuropeptides. The actions of both capsaicin and GI neuropeptides may not be restricted to vagal afferent fibres, however, as other non‐sensory neurones have displayed sensitivity to capsaicin and brainstem microinjections of these neuropeptides induce GI effects similar to those obtained upon systemic application.

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The aim of the present study was to test the hypothesis that perivagal capsaicin induces degeneration of vagal efferents controlling GI functions. Experiments were conducted 7–14 days after 30 min unilateral perivagal application of 0.1–1% capsaicin. Immunohistochemical analyses demonstrated that, as following vagotomy, capsaicin induced dendritic degeneration, decreased choline acetyltransferase but increased nitric oxide synthase immunoreactivity in rat dorsal motor nucleus of the vagus (DMV) neurones. Electrophysiological recordings showed a decreased DMV input resistance and excitability due, in part, to the expression of a large conductance calcium‐dependent potassium current and the opening of a transient outward potassium window current at resting potential. Furthermore, the number of DMV neurones excited by thyrotrophin‐releasing hormone and the gastric motility response to DMV microinjections of TRH were decreased significantly.

Our data indicate that perivagal application of capsaicin induced DMV neuronal degeneration and decreased vagal motor responses. Treatment with perivagal capsaicin cannot therefore be considered selective for vagal afferent C fibres and, consequently, care is needed when using perivagal capsaicin to assess the mechanism of action of GI neuropeptides.

Introduction Capsaicin (CAP), applied systemically or perivagally, has been used for many years to induce a supposedly selective degeneration of sensory neurones and fibres, including vagal afferents, via actions at TRPV1 receptors (;; ). In particular, perivagal application of CAP is considered to cause selective degeneration of vagal afferent C fibres and has been used extensively to examine the site of action of many gastrointestinal (GI) neuropeptides. Using this approach, the ability of several GI neuropeptides and neurohormones to exert vagally mediated effects upon GI functions via paracrine actions on vagal afferent fibres has been explored, namely, loss of effect following CAP administration was indicative of a vagal afferent site and mechanism of action (;;;;;;;;; ). One must keep in mind, however, that even a localized, brief perineural application involves using very high concentrations of CAP (usually 1% solution, i.e. ∼33 m m) for 30 min) raising the possibility that the observed effects are due at least in part to non‐selective actions on ion channels or receptors other than CAP‐sensitive TRPV1 receptors. In fact, it has been shown that systemic administration of CAP induces degeneration of central nervous system neurones and fibres that do not express TRPV1 receptors and even involves neuronal areas that do not receive sensory inputs from the periphery (; ). These effects occur despite the transient nature of CAP effects on ionic conductances (;;;;; ).