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Vol. 282, Issue 2, 928-938, 1997
-Aminobutyric AcidA
Receptors in Formalin-Induced Nociception in the Rat1
Department of Anesthesia and Critical Care, The University of
Chicago, Chicago, Illinois
This study investigated the role of 
-aminobutyric acid (GABA) and
GABAA receptors in the spinal cord in the
expression of pain behaviors evoked by injection of formalin in
concentrations ranging from 0.25 to 2.5% in the hindpaw of the rat.
Two approaches were used. The first approach compared the effect of
drug treatment to saline at each concentration of formalin. The second
approach examined the effect of drug treatment on the
concentration-response functions of formalin, i.e., its
EC50. Intrathecal (i.t.) pretreatment with 0.03 to 0.3 µg of bicuculline, a GABAA receptor
antagonist, dose-dependently increased the number of flinches and
weighted pain scores in the interphase and phase 2, but did not alter
responses in phase 1. In the interphase, the EC50
values of formalin for number of flinches or weighted pain score in
bicuculline-pretreated rats were decreased to one-third or one-fourth,
respectively, of their values in saline-pretreated rats. In phase 2, the EC50 values of formalin for number of
flinches or weighted pain score in bicuculline-pretreated rats were
similarly decreased to one-half of their value in saline-pretreated
rats. These results suggest that formalin was a significantly more
noxious stimulus in the presence of bicuculline. Pretreatment with the
GABAA receptor agonists, muscimol (0.3 µg) or
isoguvacine (10 or 30 µg i.t.), significantly decreased the number of
flinches in phase 1 and phase 2, but produced only a marginal decrease
in the weighted pain score at the highest doses. These findings suggest
that there is little tonic activation of GABAA
receptors by GABA in the spinal cord before or immediately after the
injection of formalin. However, approximately 10 min after the
induction of injury by formalin, there is a release of GABA and
activation of GABAA receptors in the spinal cord
that 1) contributes to the period of quiescence between phase 1 and
phase 2 and 2) coincidentally diminishes the magnitude of pain
behaviors in phase 2, possibly by limiting the development of central
sensitization in the spinal cord.
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