Partial sciatic nerve ligation leads to an upregulation of Ni2+ -resistant T-type Ca2+ currents in capsaicin-responsive nociceptive dorsal root ganglion neurons

Journal of Pain Research
Monika JeubHeinz Beck

Abstract

Neuropathic pain resulting from peripheral nerve lesions is a common medical condition, but current analgesics are often insufficient. The identification of key molecules involved in pathological pain processing is a prerequisite for the development of new analgesic drugs. Hyperexcitability of nociceptive DRG-neurons due to regulation of voltage-gated ion-channels is generally assumed to contribute strongly to neuropathic pain. There is increasing evidence, that T-type Ca2+-currents and in particular the Cav3.2 T-type-channel isoform play an important role in neuropathic pain, but experimental results are contradicting. To clarify the role of T-type Ca2+-channels and in particular the Cav3.2 T-type-channel isoform in neuropathic pain. The effect of partial sciatic nerve ligation (PNL) on pain behavior and the properties of T-type-currents in nociceptive DRG-neurons was tested in wild-type and Cav3.2-deficient mice. In wild-type mice, PNL of the sciatic nerve caused neuropathic pain and an increase of T-type Ca2+-currents in capsaicin-responsive neurons, while capsaicin-unresponsive neurons were unaffected. Pharmacological experiments revealed that this upregulation was due to an increase of a Ni2+-resistant Ca2+-current compone...Continue Reading

Methods Mentioned

BETA
antisense oligonucleotides
antisense oligodeoxynucleotides

Software Mentioned

Clampfit
pCLAMP8
Graphpad Prism
Excel
Clampex

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