Resiniferatoxin mediated ablation of TRPV1+ neurons removes TRPA1 as well

László Pecze, Péter Pelsoczi, Miklós Kecskés, Zoltán Winter, András Papp, Krisztián Kaszá, Tamás Letoha, Csaba Vizler, Zoltán Oláh

Research output: Contribution to journalArticle

30 Citations (Scopus)


Objectives: Resiniferatoxin, the most potent agonist of inflammatory pain/vanilloid receptor/cation channel (TRPV1) can be used for neuron subtype specific ablation of pain generating cells at the level of the peripheral nervous system by Ca2+-excytotoxicity. Molecular neurosurgery is an emerging technology either to alleviate severe pain in cancer or treat/prevent different local neuropathies. Our aim was determining sensory modalities that may be lost after resiniferatoxin treatment. Methods: Newborn or adult mice were treated with resiniferatoxin, thenchanges in chemical and heat sensitivity were correlated with alterations of the cell composition of sensory ganglions. Results: Only mice treated at adult age became less sensitive to heat stimuli, while both treatment groups lost sensitivity to specific vanilloid agonists of TRPV1 and, interestingly, to allyl-isothiocyanate, a selective agonist of TRPA1. Our in vivo and post mortem analytical results confirmed that TRPV1 and TRPA1 function together and resiniferatoxin-mediated neurosurgery removes both sensor molecules. Discussion: In adult mice resiniferatoxin causes: i) desensitization to heat and ii) sensitization to cold. Cold hyperalgesia, an imbalance in thermosensation, might be conferred by a prominent cold receptor that is expressed in surviving resiniferatoxin-resistant sensory neurons and compensates for pain signals lost with TRPA1 and TRPV1 double positive cells in the peripheral nervous system.

Original languageEnglish
Pages (from-to)234-241
Number of pages8
JournalCanadian Journal of Neurological Sciences
Issue number2
Publication statusPublished - Jan 1 2009


ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

Cite this