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The Journal of Neurophysiology Vol. 81 No. 4 April 1999, pp. 1966-1969
Copyright ©1999 by the American Physiological Society
RAPID COMMUNICATION
Department of Oral Physiology, Faculty of Dentistry, University of Toronto, Toronto M5G 1G6 Canada
Cairns, Brian E.,
Barry J. Sessle, and
James W. Hu.
Activation of peripheral GABAA receptors inhibits
temporomandibular joint-evoked jaw muscle activity. We have
previously shown that injection of mustard oil or glutamate into rat
temporomandibular joint (TMJ) tissues, an experimental model of acute
TMJ injury, can reflexly induce a prolonged increase in the activity of
both digastric (jaw-opener) and masseter (jaw-closer) muscles. In this study, GABA was applied to the TMJ region by itself or in combination with glutamate, and the magnitude of evoked jaw muscle
electromyographic (EMG) activity was measured. Application of GABA
alone to the TMJ region did not evoke significant jaw muscle EMG
activity when compared with normal saline controls. In contrast,
co-application of GABA and glutamate into the TMJ region decreased the
magnitude of glutamate-evoked EMG activity. This GABA-mediated
inhibition of glutamate-evoked EMG activity followed an inverse
dose-response relationship with an estimated median inhibitory dose
(ID50) of 0.17 ± 0.05 (SE) µmol and
0.031 ± 0.006 µmol for the digastric and masseter muscles,
respectively. Co-administration of the GABAA receptor
antagonist bicuculline (0.05 µmol) but not the GABAB receptor antagonist phaclofen (0.05 or 0.15 µmol) reversed the suppressive actions of GABA, indicating that this action of GABA may be
mediated by peripheral GABAA receptors located within the TMJ region. Our results suggest that activation of peripheral GABAA receptors located within the TMJ region could act to
decrease the transmission of nociceptive information.
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