Transgene-mediated enkephalin release enhances the effect of morphine and evades tolerance to produce a sustained antiallodynic effect in neuropathic pain
- 1 March 2003
- journal article
- research article
- Published by Wolters Kluwer Health in Pain
- Vol. 102 (1) , 135-142
- https://doi.org/10.1016/s0304-3959(02)00346-9
Abstract
We examined the pharmacologic characteristics of herpes simplex virus (HSV) vector-mediated expression of proenkephalin in the dorsal root ganglion in a rodent model of neuropathic pain. We found that: (i) vector-mediated enkephalin produced an antiallodynic effect that was reversed by naloxKeywords
This publication has 29 references indexed in Scilit:
- Endocytosis of the Mu Opioid Receptor Reduces Tolerance and a Cellular Hallmark of Opiate WithdrawalNeuron, 2001
- Antinociceptive effect of a genomic herpes simplex virus-based vector expressing human proenkephalin in rat dorsal root ganglionGene Therapy, 2001
- Design and application of HSV vectors for neuroprotectionGene Therapy, 2000
- Basal and touch-evoked fos-like immunoreactivity during experimental inflammation in the ratPAIN®, 1996
- Antiallodynic effects of a CCKB antagonist in rats with nerve ligation injury: role of endogenous enkephalinsNeuroscience Letters, 1996
- Systemic and supraspinal, but not spinal, opiates suppress allodynia in a rat neuropathic pain modelNeuroscience Letters, 1995
- An experimental model for peripheral neuropathy produced by segmental spinal nerve ligation in the ratPain, 1992
- Induction of c-fos-like protein in spinal cord neurons following sensory stimulationNature, 1987
- Tolerance and cross tolerance to morphine after chronic spinal D-Ala2-D-Leu5-enkephalin infusionLife Sciences, 1982
- Efficient Analysis of Experimental ObservationsAnnual Review of Pharmacology and Toxicology, 1980