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Resiniferatoxin Mediated Ablation of TRPV1+ Neurons Removes TRPA1 as Well

Published online by Cambridge University Press:  02 December 2014

László Pecze
Affiliation:
Institute of Biochemistry, University of Szeged
Péter Pelsőczi
Affiliation:
Institute of Biochemistry, University of Szeged
Miklós Kecskés
Affiliation:
Institute of Biochemistry, University of Szeged
Zoltán Winter
Affiliation:
Institute of Biochemistry, University of Szeged
András Papp
Affiliation:
Biological Research Center of the Hungarian Academy of Sciences, Department of Public Health, University of Szeged
Krisztián Kaszás
Affiliation:
Institute of Biochemistry, University of Szeged
Tamás Letoha
Affiliation:
Institute of Biochemistry, University of Szeged Department of Medical Chemistry, University of Szeged
Csaba Vizler*
Affiliation:
Institute of Biochemistry, University of Szeged
Zoltán Oláh
Affiliation:
Institute of Biochemistry, University of Szeged Acheuron Hungary Ltd., Szeged, Hungary
*
BRC of HAS, Szeged, Hungary-6726, Temesvári krt 62
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Abstract

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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, then changes 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.

Type
Original Article
Copyright
Copyright © The Canadian Journal of Neurological 2009

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