scholarly journals Dissociable Effects of Kappa-Opioid Receptor Activation on Impulsive Phenotypes in Wistar Rats

2013 ◽  
Vol 38 (11) ◽  
pp. 2278-2285 ◽  
Author(s):  
Brendan M Walker ◽  
Jessica L Kissler
Keyword(s):  
Opioid Receptor ◽  
Wistar Rats ◽  
Receptor Activation ◽  
Kappa Opioid Receptor ◽  
Kappa Opioid

scholarly journals Kappa opioid receptor activation in the amygdala disinhibits CRF neurons to generate pain-like behaviors

2021 ◽  
Vol 185 ◽  
pp. 108456
Author(s):  
Matthew Hein ◽  
Guangchen Ji ◽  
Dalton Tidwell ◽  
Preston D'Souza ◽  
Takaki Kiritoshi ◽  
...  
Keyword(s):  
Opioid Receptor ◽  
Receptor Activation ◽  
Kappa Opioid Receptor ◽  
Kappa Opioid ◽  
Crf Neurons

scholarly journals Analgesic Activity of the Kappa Opioid Receptor Agonist RU-1205 in Rats

2018 ◽  
Vol 3 (2) ◽  
pp. 13 ◽  
Author(s):  
AA Spasov ◽  
OY Grechko ◽  
DM Shtareva ◽  
AI Raschenko ◽  
Natalia Eliseeva ◽  
...  
Keyword(s):  
Opioid Receptor ◽  
Analgesic Activity ◽  
Analgesic Effect ◽  
Physical Dependence ◽  
Receptor Activation ◽  
Kappa Opioid Receptor ◽  
Kappa Opioid ◽  
Hot Plate ◽  
Hot Plate Test ◽  
Plate Test

Introduction: Opioid analgesics are the most efficient and widely used drugs for the management of moderate to severe pain. However, side effects associated with mu receptor activation, such as respiratory depression, tolerance and physical dependence severely limit their clinical application. Currently, the kappa-opioid system is the most attractive in terms of the clinical problem of pain, because kappa-agonists do not cause euphoria and physical dependence. The purpose of this study was to evaluate the antinociceptive effect of the novel compound - RU-1205. Methods: The analgesic activity of RU-1205 was studied on nociceptive models that characterize the central and peripheral pathways of pain sensitivity (hot plate test, electrically induced vocalisation, formalin test, writhing test). Results: RU-1205 exhibited highly potent antinociceptive effects in rodent models of acute pain with ED50 values of 0.002 - 0.49 mg /kg. Pretreatment with the κ-opioid receptor antagonist norBinaltorphimine significantly attenuated the analgesic activity of investigated substance in a hot plate test. Conclusions: It was established that the compound shows a significant dose-dependent central and peripheral analgesic effect. It was assumed kappa-opioidergic mechanism of analgesic effect of RU-1205.

scholarly journals Relative Timing Between Kappa Opioid Receptor Activation and Cocaine Determines the Impact on Reward and Dopamine Release

2015 ◽  
Vol 41 (4) ◽  
pp. 989-1002 ◽  
Author(s):  
Elena H Chartoff ◽  
Shayla R Ebner ◽  
Angela Sparrow ◽  
David Potter ◽  
Phillip M Baker ◽  
...  
Keyword(s):  
Opioid Receptor ◽  
Dopamine Release ◽  
Receptor Activation ◽  
Kappa Opioid Receptor ◽  
Relative Timing ◽  
Kappa Opioid ◽  
The Impact

scholarly journals nor-BNI Antagonism of Kappa Opioid Agonist-Induced Reinstatement of Ethanol-Seeking Behavior

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Erin Harshberger ◽  
Emily A. Gilson ◽  
Kelli Gillett ◽  
Jasmine H. Stone ◽  
Laila El Amrani ◽  
...  
Keyword(s):  
Opioid Receptor ◽  
Wistar Rats ◽  
Ethanol Solution ◽  
Kappa Opioid Receptor ◽  
Opioid Agonist ◽  
Kappa Opioid ◽  
Seeking Behavior ◽  
Male Wistar Rats ◽  
Kappa Opioid Agonist ◽  
Time Point

Recent work suggests that the dynorphin (DYN)/kappa opioid receptor (KOR) system may be a key mediator in the behavioral effects of alcohol. The objective of the present study was to examine the ability of the KOR antagonist norbinaltorphimine (nor-BNI) to attenuate relapse to ethanol seeking due to priming injections of the KOR agonist U50,488 at time points consistent with KOR selectivity. Male Wistar rats were trained to self-administer a 10% ethanol solution, and then responding was extinguished. Following extinction, rats were injected with U50,488 (0.1–10 mg/kg, i.p.) or saline and were tested for the reinstatement of ethanol seeking. Next, the ability of the nonselective opioid receptor antagonist naltrexone (0 or 3.0 mg/kg, s.c.) and nor-BNI (0 or 20.0 mg/kg, i.p.) to block U50,488-induced reinstatement was examined. Priming injections U50,488 reinstated responding on the previously ethanol-associated lever. Pretreatment with naltrexone reduced the reinstatement of ethanol-seeking behavior. nor-BNI also attenuated KOR agonist-induced reinstatement, but to a lesser extent than naltrexone, when injected 24 hours prior to injections of U50,488, a time point that is consistent with KOR selectivity. While these results suggest that activation of KORs is a key mechanism in the regulation of ethanol-seeking behavior, U50,488-induced reinstatement may not be fully selective for KORs.

scholarly journals EXPRESS: Functional bias of morphine and oliceridine under conditions of minor injury

2021 ◽  
pp. 174480692098844
Author(s):  
Chinwe Nwaneshiudu ◽  
Xiao-You Shi ◽  
Peyman Sahbaie ◽  
J. David Clark
Keyword(s):  
Prefrontal Cortex ◽  
Nucleus Accumbens ◽  
Opioid Receptor ◽  
Medial Prefrontal Cortex ◽  
Receptor Activation ◽  
Kappa Opioid Receptor ◽  
Opioid Antagonist ◽  
Opioid Agonist ◽  
Kappa Opioid ◽  
Mu Opioid

Recent reports suggest pain from surgical injury may influence the risks associated with exposure to opioids. In mice, hind-paw incision attenuates morphine-primed reinstatement due to kappa opioid receptor activation by dynorphin. In this focused group of studies, we examined the hypotheses that kappa-opioid receptor activation in the nucleus accumbens mediates attenuated drug- primed reinstatement after incisional surgery, and the G-protein biased mu-opioid agonist, oliceridine, leads to less priming of the dynorphin effect in comparison to morphine. To address these hypotheses, adult C57BL/6 male mice underwent intracranial cannulation for administration of the selective kappa-opioid antagonist norBNI directly into the nucleus accumbens. After recovery, they were conditioned with morphine or oliceridine after hind-paw incisional injury, then underwent extinction followed by opioid-primed reinstatement. Intra-accumbal administration of norBNI was carried out prior to testing. The nucleus accumbens and medial prefrontal cortex were extracted and analyzed for expression of prodynorphin. We observed that animals conditioned with morphine in the setting of incisional injury demonstrated blunted responses to opioid-primed reinstatement, and that the blunted responses were reversed with intra-accumbal norBNI administration. Persistently elevated levels of prodynorphin expression in the medial prefrontal cortex and nucleus accumbens were observed in the incised morphine-treated animals. However, both behavioral and molecular changes were absent in animals with incisional injury conditioned with oliceridine. These findings suggest a role for prodynorphin expression in the nucleus accumbens with exposure to morphine after surgery that may protect individuals from relapse not shared with biased mu- opioid receptor agonists.

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