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2020, Journal of PainCitation Excerpt :When release slows, more dynorphin peptide is made than is secreted, leading to the late accumulation of peptide. Importantly, the measurements in the present report are indicative of accumulation, which begins in the resolution phase, whereas other endpoints such as transcription and peptide release have shown engagement early in the pain process.18,60 Dynorphin induction tracks the hyperalgesia in several pain models including peripheral inflammation, chronic constriction injury, painful peripheral neuropathy, and surgical incision.19,31,32,38,55,59,62
The histology, physiology, neurochemistry and circuitry of the substantia gelatinosa Rolandi (lamina II) in mammalian spinal cord
2018, Progress in NeurobiologyCitation Excerpt :Initial localization studies in cat reported that, differently from ENK, DYN was mainly detected in laminae I and V of the spinal cord and not in SGR (Cruz and Basbaum, 1985). In keeping with this observation, antibodies microprobes detected local release of IR DYN A1-8 in rat laminae I and IV-V (Riley et al., 1996). DYN A and prodynorphin were more recently reported to be present in some SGR neurons (Marvizón et al., 2009).
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2009, International Review of NeurobiologyCitation Excerpt :Another set of evidence supports the notion on the pronociceptive functions of dynorphin A in the spinal cord. Behavioral hyperalgesia as a result of inflammation or tissue injury is accompanied by elevations in spinal dynorphin content (Draisci et al., 1991; Dubner and Ruda, 1992; Iadarola et al., 1988; Kajander et al., 1990; Malan et al., 2000; Riley et al., 1996; Ruda et al., 1988; Wagner and Deleo, 1996). This increase is considered as causative of hyperalgesia and allodynia.
Intrathecally administered cholera toxin blocks allodynia and hyperalgesia in persistent pain models
2001, Journal of PainCitation Excerpt :The opioid peptide and opioid receptor mediating IT cholera toxin's antiallodynic and antihyperalgesic actions are not known. Acute nociception studies have shown the release of enkephalin, dynorphin, and endomorphin in the spinal cord.41-46 Yet, in persistent nociception studies, dynorphin release remained elevated, whereas enkephalin release was suppressed.3