Increased spinal dynorphin contributes to chronic nicotine-induced mechanical hypersensitivity in the rat

Lough, Chris; Young, Tracey; Parker, Renée; Wittenauer, Shannon; Vincler, Michelle

doi:10.1016/j.neulet.2007.06.002

Cited by 9 publications

(6 citation statements)

References 36 publications

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“…67,75,77,78 Compared with nicotine-naïve rats, nicotine-tolerant rats develop greater mechanical hyperalgesia after spinal nerve ligation or sciatic nerve injury. 79,80 The increased mechanical hyperalgesia was associated with increased spinal dynorphin levels 81 as well as increased production of cytokines centrally and peripherally. 79 Thus, when evaluating the behavioral effects of chronic nicotine exposure a complex interplay among receptor desensitization, overexpression, and neural plasticity in associated nociceptive pathways must be considered.…”

Section: Educationmentioning

confidence: 99%

Smoking and Pain

Weingarten²,

et al. 2010

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Cigarette smoke, which serves as a nicotine delivery vehicle in humans, produces profound changes in physiology. Experimental studies suggest that nicotine has analgesic properties. However, epidemiologic evidence shows that smoking is a risk factor for chronic pain. The complex relationship between smoking and pain not only is of scientific interest, but also has clinical relevance in the practice of anesthesiology and pain medicine. This review will examine current knowledge regarding how acute and chronic exposure to nicotine and cigarette smoke affects acute and chronic painful conditions. It will cover the relevant pharmacology of nicotine and other ligands at the nicotinic acetylcholine receptor as related to pain, explore the association of cigarette smoking with chronic painful conditions and potential mechanisms to explain this association, and examine clinical implications for the care of smokers with pain.

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Section: Educationmentioning

confidence: 99%

Smoking and Pain

Weingarten²,

et al. 2010

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“…Many experimental models of pathological pain show significant regional elevations of dynorphin A in the spinal cord. These include inflammatory pain [31], neuropathic pain [17,27,48], bone cancer pain [29], chronic pancreatitis [46], abnormal pain (hyperalgesia) following sustained exposure to morphine [44] or nicotine [25], spinal cord trauma [1,13,39], and arthritis [54]. Elevated levels of dynorphin A are critical for the expression of chronic pain because approaches that inhibit dynorphin A activity consistently normalize the enhanced sensory responses (i.e., diminish hyperalgesia).…”

Section: Introductionmentioning

confidence: 99%

Pronociceptive actions of dynorphin via bradykinin receptors

Lai

Luo

Chen

et al. 2008

Neuroscience Letters

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The endogenous opioid peptide dynorphin A is distinct from other endogenous opioid peptides in having significant neuronal excitatory and neurotoxic effects that are not mediated by opioid receptors. Some of these non-opioid actions of dynorphin contribute to the development of abnormal pain resulting from a number of pathological conditions. Identifying the mechanisms and the sites of action of dynorphin is essential for understanding the pathophysiology of dynorphin and for exploring novel therapeutic targets for pain. This review will discuss the mechanisms that have been proposed and the recent finding that spinal dynorphin may be an endogenous ligand of bradykinin receptors under pathological conditions to promote pain.

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“…Furthermore, knockout of the dynorphin gene prevented development of chronic pain in mice. The use of anti-dynorphin A anti-serum could reduce thermal hyperalgesia [ 35 ], and the application of anti-dynorphin A anti-serum in the nerve sheath could reduce the abnormal pain after spinal cord trauma [ 36 ]. All those have shown the correlation between Dyn and hypersensitivity.…”

Section: Discussionmentioning

confidence: 99%

Dynorphin participates in interaction between depression and non-erosive reflux disease

et al. 2022

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Background To explore the relationships between anxiety/depression and NERD, we focused on dynorphin (Dyn), an important member of visceral hypersensitivity, and its related pathways. Methods Pearson’s correlation analysis on patients with NERD and in vivo experiment on NERD rat model. Part 1: Pearson’s correlation analysis among serum levels of Dyn, clinical symptoms and HADS scores of NERD patients were carried on. Part 2: Wistar rats were randomly divided into 2 groups: control group and model group. The data of pH value, immobility time, serum Dyn concentration, NMDAR1 and SP expression were, respectively, derived from automatic pH recorder, tail suspension test, enzyme-linked immunosorbent assay, immunohistochemistry and immunofluorescence. Results Part 1: Pearson’s correlation analysis showed that there was a linear correlation between Clinical Symptom (CS) score and HADS score (HAD-A, HAD-D), and the correlation coefficients were 0.385 and 0.273 respectively; the correlation coefficient between lg (Dyn) and lg (CS score) was r = 0.441, P = 0.002; the correlation coefficient between lg(Dyn) and lg (HAD-D score) was r = 0.447, P = 0.002. Part 2: The pH value of the lower esophagus in the model group was lower than that in the control group (P < 0.01). The tail suspension immobility time of model group was significantly longer than that of control group (P < 0.01). The serum Dyn concentration and the expression level of NMDAR1 in spinal cord and SP in lower esophageal mucosa of model group were significantly higher than those of control group (P < 0.05). Conclusion Increased serum dynorphin level may be a sign of correlation between depression and NERD.

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Increased spinal dynorphin contributes to chronic nicotine-induced mechanical hypersensitivity in the rat

Cited by 9 publications

References 36 publications

Smoking and Pain

Smoking and Pain

Pronociceptive actions of dynorphin via bradykinin receptors

Dynorphin participates in interaction between depression and non-erosive reflux disease

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