title: Neuronal NTPDase3 Mediates Extracellular ATP Degradation in Trigeminal Nociceptive Pathway.
abstract: ATP induces pain via activation of purinergic receptors in nociceptive sensory nerves. ATP signaling is terminated by ATP hydrolysis mediated by cell surface-localized ecto-nucleotidases. Using enzymatic histochemical staining, we show that ecto-ATPase activity is present in mouse trigeminal nerves. Using immunofluorescence staining, we found that ecto-NTPDase3 is expressed in trigeminal nociceptive neurons and their projections to the brainstem. In addition, ecto-ATPase activity and ecto-NTPDase3 are also detected in the nociceptive outermost layer of the trigeminal subnucleus caudalis. Furthermore, we demonstrate that incubation with anti-NTPDase3 serum reduces extracellular ATP degradation in the nociceptive lamina of both the trigeminal subnucleus caudalis and the spinal cord dorsal horn. These results are consistent with neuronal NTPDase3 activity modulating pain signal transduction and transmission by affecting extracellular ATP hydrolysis within the trigeminal nociceptive pathway. Thus, disruption of trigeminal neuronal NTPDase3 expression and localization to presynaptic terminals during chronic inflammation, local constriction and injury may contribute to the pathogenesis of orofacial neuropathic pain.
authors.affiliation: Department of Dentistry, Eastman Institute for Oral Health, University of Rochester School of Medicine and Dentistry, Rochester, NY, United States of America.|Department of Dentistry, School of Stomatology, Zhengzhou University, Zhengzhou, China.
authors.forename: Lihua
authors.initials: L
authors.lastname: Ma
authors.affiliation: Department of Dentistry, Eastman Institute for Oral Health, University of Rochester School of Medicine and Dentistry, Rochester, NY, United States of America.
authors.forename: Thu
authors.initials: T
authors.lastname: Trinh
authors.affiliation: Department of Dentistry, Eastman Institute for Oral Health, University of Rochester School of Medicine and Dentistry, Rochester, NY, United States of America.
authors.forename: Yanfang
authors.initials: Y
authors.lastname: Ren
authors.affiliation: Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, Rochester, NY, United States of America.
authors.forename: Robert T
authors.initials: RT
authors.lastname: Dirksen
authors.affiliation: Department of Dentistry, Eastman Institute for Oral Health, University of Rochester School of Medicine and Dentistry, Rochester, NY, United States of America.|Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, Rochester, NY, United States of America.
authors.forename: Xiuxin
authors.initials: X
authors.lastname: Liu
mesh_terms: D000251:Adenosine Triphosphatases / Q000378:metabolism*; D000255:Adenosine Triphosphate / Q000737:chemistry*; D000818:Animals; D005260:Female; D006868:Hydrolysis; D008297:Male; D051379:Mice; D010146:Pain / Q000201:enzymology; D015398:Signal Transduction; D014275:Trigeminal Caudal Nucleus / Q000378:metabolism*
chemical_list: D000255:Adenosine Triphosphate; D000251:Adenosine Triphosphatases; C027201:ectoATPase