2016
DOI: 10.1016/j.neuroscience.2015.11.065
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Descending nociceptive inhibition is modulated in a time-dependent manner in a double-hit model of chronic/tonic pain

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Cited by 17 publications
(17 citation statements)
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“…By the visceral hypersensitivity, pain sensation is amplified and sometimes stimuli that normally do not cause pain become painful. As a corollary, the hypersensitivity would promote hyperactivation of descending pain inhibitory pathways . In fact, alteration in the inhibition of spinal nociceptive transmission (ie, descending inhibition pathways) has been reported in patients with IBS .…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…By the visceral hypersensitivity, pain sensation is amplified and sometimes stimuli that normally do not cause pain become painful. As a corollary, the hypersensitivity would promote hyperactivation of descending pain inhibitory pathways . In fact, alteration in the inhibition of spinal nociceptive transmission (ie, descending inhibition pathways) has been reported in patients with IBS .…”
Section: Discussionmentioning
confidence: 99%
“…As a corollary, the hypersensitivity would promote hyperactivation of descending pain inhibitory pathways. 40 In fact, alteration in the inhibition of spinal nociceptive transmission (ie, descending inhibition pathways) has been reported in patients with IBS. [41][42][43][44] Moreover, chronic stress, a risk factor for IBS, increases 5-HT biosynthesis in the rostral ventromedial medulla, which is one of the origins of the descending pain inhibitory pathways.…”
Section: Discussionmentioning
confidence: 99%
“…Animals were randomly allocated to sham or CCI group. Neuropathic pain was induced with CCI as previously described by Bennett and Xie29 with a 5-0 chromic gut suture 30. In brief, after the intraperitoneal injection of sodium pentobarbital (35 mg/kg), the left sciatic nerve was loosely ligated with four sutures distant by 1–1.5 mm at the upstream of the nerve trifurcation of tibial, sural, and the common peroneal nerve.…”
Section: Methodsmentioning
confidence: 99%
“…Furthermore, inflammation showed to increase the excitability in the dorsal horn and the RVM, which later on enhanced descending pain modulation (Schaible et al., ; Ren and Dubner, ; Terayama et al., ). It was hypothesized that the enhanced inhibition would gradually disappear and result in a classical hyperalgesic pain response (Ren and Dubner, ; Parent et al., ). It was assumed that due to a progressive dysfunction of endogenous analgesia this system cannot compensate long‐term painful states (Millan, ).…”
Section: Discussionmentioning
confidence: 99%