Involvement of ATP in noxious stimulus-evoked release of glutamate in rat medullary dorsal horn: A microdialysis study |
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| Affiliation: | 1. Department of Environmental Health and Engineering, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, United States of America;2. Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States of America;3. Department of Cell and Molecular Physiology, Loyola University Stritch School of Medicine, Maywood, IL, United States of America;1. Department of Orofacial Pain and Jaw function, Faculty of Odontology, Malmö University, Malmö, Sweden;2. Department of Orofacial Pain and Dysfunction, Academic Centre for Dentistry Amsterdam (ACTA), University of Amsterdam and Vrije Universiteit, Amsterdam, Netherlands;3. School of Dental Sciences, Newcastle University, Newcastle, United Kingdom;4. Newcastle Hospitals’ NHS Foundation Trust, Newcastle, United Kingdom;5. Faculty of Medicine and Health, The University of Sydney, Sydney, Australia;6. Department of Rehabilitation Medicine, Skåne University Hospital, Malmö, Sweden |
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| Abstract: | Our electrophysiological studies have shown that both purinergic and glutamatergic receptors are involved in central sensitization of nociceptive neurons in the medullary dorsal horn (MDH). Here we assessed the effects of intrathecal administration of apyrase (a nucleotide degrading enzyme of endogenous adenosine 5-triphosphate [ATP]), a combination of apyrase and 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, an adenosine A1 receptor antagonist), or 2,3-O-2,4,6-trinitrophenyl-adenosine triphosphate (TNP-ATP, a P2X1, P2X3, P2X2/3 receptor antagonist) on the release of glutamate in the rat MDH evoked by application of mustard oil (MO) to the molar tooth pulp. In vivo microdialysis was used to dialyse the MDH every 5 min, and included 3 basal samples, 6 samples after drug treatment and 12 samples following application of MO. Tooth pulp application of MO induced a significant increase in glutamate release in the MDH. Superfusion of apyrase or TNP-ATP alone significantly reduced the MO-induced glutamate release in the MDH, as compared to vehicle. Furthermore, the suppressive effects of apyrase on glutamate release were reduced by combining it with DPCPX. This study demonstrates that application of an inflammatory irritant to the tooth pulp induces glutamate release in the rat MDH in vivo that may be reduced by processes involving endogenous ATP and adenosine. |
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