A model of virus-induced hyperalgesia in rats
Date
2008-03-03T08:32:44Z
Authors
Skosana, Musi Thabang
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Abstract
ABSTRACT
The link between infection and hyperalgesia has been determined using mainly
lipopolysaccharide, which is a bacterial antigen. The relationship between viral infection
and hyperalgesia has yet to be fully characterized, with current models of virus-induced
hyperalgesia being based on infections by specific neurotrophic viruses. Therefore, the
aim of this series of studies was to develop a general model of virus-induced hyperalgesia
by injecting a pyrogenic and non-pyrogenic dose of Poly I:C, a synthetic, double-stranded
ribonucleotide that is similar to the double-stranded ribonucleotides produced by almost
all viruses, into rats’ tails.
To identify a pyrogenic and non-pyrogenic dose of Poly I:C, male Sprague Dawley rats
were injected subcutaneously in the tail either with saline (n=8) or 100 μg.kg-1 (n=8) or
1000 μg.kg-1 (n=8) Poly I:C. Only rats that received 1000 μg.kg-1 Poly I:C developed
fever. Subsequently, in a separate experiment, tail withdrawal latencies to noxious
thermal (49° water) and mechanical stimuli (4N blunt force) were recorded for six days
after subcutaneous injection of 100 μg.kg-1 or 1000 μg.kg-1 Poly I:C or saline in male
Sprague Dawley rats. I also took skin tissue samples from the site of injection to
determine the histological changes that occur after Poly I:C injection. Thermal
hyperalgesia was not elicited by Poly I:C injection. However, biphasic mechanical
hyperalgesia developed in the animals receiving 100 μg.kg-1 Poly I:C, and sustained
mechanical hyperalgesia, that lasted for four days, was evident in animals injected with
1000 μg.kg-1 Poly I:C. Mild sustained inflammation, at the injection site of both doses of
Poly I:C, was present even after the hyperalgesia had subsided.
This study provides evidence for a novel model of virus-induced hyperalgesia that is
applicable to most cutaneous viral infections. More importantly, this model can be used
to further our understanding of the mechanisms that underlie virus-induced pain.