Involvement of the VGF-derived peptide TLQP-62 in nerve injury induced hypersensitivity and spinal neuroplasticity

Alexander G.J. Skorput, Xijing Zhang, Jonathan J. Waataja, Cristina D. Peterson, Maureen S Riedl, Kelley F Kitto, Hai Truong, Cecilia Huffman, Stephen R. Salton, Carolyn A Fairbanks, Christopher N. Honda, Lucy Vulchanova

Research output: Contribution to journalArticlepeer-review

4 Scopus citations


Neuroplasticity in the dorsal horn after peripheral nerve damage contributes critically to the establishment of chronic pain. The neurosecretory protein VGF (nonacronymic) is rapidly and robustly upregulated after nerve injury, and therefore, peptides generated from it are positioned to serve as signals for peripheral damage. The goal of this project was to understand the spinal modulatory effects of the C-Terminal VGF-derived peptide TLQP-62 at the cellular level and gain insight into the function of the peptide in the development of neuropathic pain. In a rodent model of neuropathic pain, we demonstrate that endogenous levels of TLQP-62 increased in the spinal cord, and its immunoneutralization led to prolonged attenuation of the development of nerve injury induced hypersensitivity. Using multiphoton imaging of submaximal glutamate-induced Ca21 responses in spinal cord slices, we demonstrate the ability of TLQP-62 to potentiate glutamatergic responses in the dorsal horn. We further demonstrate that the peptide selectively potentiates responses of high-Threshold spinal neurons to mechanical stimuli in singe-unit in vivo recordings. These findings are consistent with a function of TLQP-62 in spinal plasticity that may contribute to central sensitization after nerve damage.

Original languageEnglish (US)
Pages (from-to)1802-1813
Number of pages12
Issue number9
StatePublished - Sep 1 2018

Bibliographical note

Funding Information:
Supported by PHS Grant R01 DE021996 (L.V. and S.R.S.), R01 NS088518 (L.V.), T32 DA007097 (A.G.J.S.), and F32 NS100438 (A.G.J.S.).

Publisher Copyright:
© 2018 Lippincott Williams and Wilkins. All rights reserved.


  • Nerve injury
  • Neuropeptide
  • Spinal neuroplasticity


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