Origins, actions and dynamic expression patterns of the neuropeptide VGF in rat peripheral and central sensory neurones following peripheral nerve injury

doi:10.1186/1744-8069-4-62

Molecular Pain

Volume 4

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Moss A
Ingram R
Koch S
Theodorou A
Low L
Baccei M
Hathway GJ
Costigan M
Salton SR
Fitzgerald M

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Moss A
Ingram R
Koch S
Theodorou A
Low L
Baccei M
Hathway GJ
Costigan M
Salton SR
Fitzgerald M
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Research

Origins, actions and dynamic expression patterns of the neuropeptide VGF in rat peripheral and central sensory neurones following peripheral nerve injury

Andrew Moss¹^,4 , Rachel Ingram¹ , Stephanie Koch¹ , Andria Theodorou¹ , Lucie Low¹ , Mark Baccei¹ , Gareth J Hathway¹ , Michael Costigan² , Stephen R Salton³ and Maria Fitzgerald¹

¹UCL Department of Neuroscience, Physiology and Pharmacology, University College London, Gower Street, London, WC1E 6BT, UK

²Neural Plasticity Research Group, Department of Anesthesia & Critical Care, Mass General Hospital & Harvard Medical School, 149 13th Street, Charlestown, MA 02129, USA

³Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY 10029, USA

⁴Pfizer Global Research & Development, Pain Therapeutics, Ramsgate Road, Sandwich, Kent, CT13 9NJ, UK

author email corresponding author email

Molecular Pain 2008, 4:62doi:10.1186/1744-8069-4-62


Published:	10 December 2008

Abstract

Background

The role of the neurotrophin regulated polypeptide, VGF, has been investigated in a rat spared injury model of neuropathic pain. This peptide has been shown to be associated with synaptic strengthening and learning in the hippocampus and while it is known that VGFmRNA is upregulated in dorsal root ganglia following peripheral nerve injury, the role of this VGF peptide in neuropathic pain has yet to be investigated.

Results

Prolonged upregulation of VGF mRNA and protein was observed in injured dorsal root ganglion neurons, central terminals and their target dorsal horn neurons. Intrathecal application of TLQP-62, the C-terminal active portion of VGF (5–50 nmol) to naïve rats caused a long-lasting mechanical and cold behavioral allodynia. Direct actions of 50 nM TLQP-62 upon dorsal horn neuron excitability was demonstrated in whole cell patch recordings in spinal cord slices and in receptive field analysis in intact, anesthetized rats where significant actions of VGF were upon spontaneous activity and cold evoked responses.

Conclusion

VGF expression is therefore highly modulated in nociceptive pathways following peripheral nerve injury and can cause dorsal horn cell excitation and behavioral hypersensitivity in naïve animals. Together the results point to a novel and powerful role for VGF in neuropathic pain.