title: Paraventricular oxytocinergic hypothalamic prevention or interruption of long-term potentiation in dorsal horn nociceptive neurons: electrophysiological and behavioral evidence.
abstract: Spinal long-term potentiation (LTP) elicited by noxious stimulation enhances the responsiveness of dorsal horn nociceptive neurons to their normal input, and may represent a key mechanism of central sensitization by which acute pain could turn into a chronic pain state. This study investigated the electrophysiological and behavioral consequences of the interactions between LTP and descending oxytocinergic antinociceptive mechanisms mediated by the hypothalamic paraventricular nucleus (PVN). PVN stimulation or intrathecal oxytocin (OT) reduced or prevented the ability of spinal LTP to facilitate selectively nociceptive-evoked responses of spinal wide dynamic range (WDR) neurons recorded in anesthetized rats. In a behavioral model developed to study the effects of spinal LTP on mechanical withdrawal thresholds in freely moving rats, the long-lasting LTP-mediated mechanical hyperalgesia was transiently interrupted or prevented by either PVN stimulation or intrathecal OT. LTP mediates long-lasting pain hypersensitivity that is strongly modulated by endogenous hypothalamic oxytocinergic descending controls.
authors.affiliation: Departamento de Neurobiología del Desarrollo y Neurofisiología, Instituto de Neurobiología, Universidad Nacional Autónoma de México. Campus UNAM-Juriquilla, Querétaro, Mexico INSERM/CPN, U.894, Site Pitié Salpêtrière, Paris, France.
authors.forename: Salvador
authors.initials: S
authors.lastname: DeLaTorre
authors.forename: Gerardo
authors.initials: G
authors.lastname: Rojas-Piloni
authors.forename: Guadalupe
authors.initials: G
authors.lastname: Martínez-Lorenzana
authors.forename: Javier
authors.initials: J
authors.lastname: Rodríguez-Jiménez
authors.forename: Luis
authors.initials: L
authors.lastname: Villanueva
authors.forename: Miguel
authors.initials: M
authors.lastname: Condés-Lara
mesh_terms: D000698:Analgesia / Q000379:methods; D000700:Analgesics / Q000378:metabolism / Q000494:pharmacology; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects / Q000502:physiology; D004195:Disease Models, Animal; D004525:Efferent Pathways / Q000378:metabolism / Q000502:physiology; D004599:Electric Stimulation Therapy / Q000379:methods; D006930:Hyperalgesia / Q000188:drug therapy / Q000503:physiopathology*; D007278:Injections, Spinal; D017774:Long-Term Potentiation / Q000187:drug effects / Q000502:physiology*; D008297:Male; D009619:Nociceptors / Q000187:drug effects / Q000378:metabolism*; D010121:Oxytocin / Q000378:metabolism* / Q000494:pharmacology; D010147:Pain Measurement / Q000187:drug effects; D017288:Pain Threshold / Q000187:drug effects / Q000502:physiology; D010286:Paraventricular Hypothalamic Nucleus / Q000378:metabolism*; D020671:Posterior Horn Cells / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D013133:Spinothalamic Tracts / Q000187:drug effects / Q000502:physiology
chemical_list: D000700:Analgesics; D010121:Oxytocin