Abstract
BackgroundDiffuse noxious inhibitory controls (DNIC) can be produced by different types of conditioning stimuli, but the analgesic properties and underlying mechanisms remain unclear. The aim of this study was to differentiate the induction of DNIC analgesia between noxious electrical and inflammatory conditioning stimuli.MethodsFirst, rats subjected to either a supramaximal electrical stimulation or an injection of high-dose formalin in the hind limb were identified to have pain responses with behavioral evidence and spinal Fos-immunoreactive profiles. Second, suppression of tail-flick latencies by the two noxious stimuli was assessed to confirm the presence of DNIC. Third, an opioid receptor antagonist (naloxone) and an α2-adrenoreceptor antagonist (yohimbine) were injected, intraperitoneally and intrathecally respectively, before conditioning noxious stimuli to test the involvement of descending inhibitory pathways in DNIC-mediated analgesia.ResultsAn intramuscular injection of 100 μl of 5% formalin produced noxious behaviors with cumulative pain scores similar to those of 50 μl of 2% formalin in the paw. Both electrical and chemical stimulation significantly increased Fos expression in the superficial dorsal horns, but possessed characteristic distribution patterns individually. Both conditioning stimuli prolonged the tail-flick latencies indicating a DNIC response. However, the electrical stimulation-induced DNIC was reversed by yohimbine, but not by naloxone; whereas noxious formalin-induced analgesia was both naloxone- and yohimbine-reversible.ConclusionsIt is demonstrated that DNIC produced by different types of conditioning stimuli can be mediated by different descending inhibitory controls, indicating the organization within the central nervous circuit is complex and possibly exhibits particular clinical manifestations.
Highlights
Diffuse noxious inhibitory controls (DNIC) can be produced by different types of conditioning stimuli, but the analgesic properties and underlying mechanisms remain unclear
Supramaximal electrical stimulation was noxious It is apparent that noxious behaviors were shown in the halothane-anesthetized rats subjected to the supramaximal electrical stimulation
The results proved that the a2-adrenergic pathway is involved in DNIC produced by either noxious electrical or formalin stimulation
Summary
Diffuse noxious inhibitory controls (DNIC) can be produced by different types of conditioning stimuli, but the analgesic properties and underlying mechanisms remain unclear. Diffuse noxious inhibitory controls (DNIC), among the networks, occur when a painful stimulus (i.e., a conditioning stimulus) in one body region suppresses another noxious response (i.e., a test stimulus) in a remote body region [1,2], and is an important. DNIC effects differ depending on the types of conditioning stimuli, and on the quality, magnitude, and activated nerve fibers [1,2]. Intense electrical stimulation sufficient to activate Aδ and C fibers or to induce pain showed heterotopic analgesia in animals [11,12,13,14] and humans [15,16]. It was intriguing to investigate whether analgesic quality is differential between high-intensity (noxious) electrical stimulation and low-intensity EA-like stimulation
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