Increased Prostaglandin E2Release and Activated Akt/β-Catenin Signaling Pathway Occur after Opioid Withdrawal in Rat Spinal Cord

Abstract

These results suggest that opioid withdrawal activates signaling pathways associated with neuronal survival and transcriptional control, two processes implicated in neuronal development and synaptic plasticity.

Withdrawal-associated injury site pain (WISP): a descriptive case series of an opioid cessation phenomenon

“…13,15,16,22,25,26,39,43,58,86,92,93,98,128,129,145 Among our participants, just one person each named ketamine, phenobarbital, alcohol, and cannabis as relieving WISP. Although these may be coincidental, there is evidence that these or related substances may mitigate OIH, WIH, or other forms of pain through modulation of one of the above mechanisms, some of which are also involved with gabapentinoids.…”

“…6,29,51 Once opioids are stopped, the pain sensitivity can continue or seem to heighten temporarily because any pain-relieving effect opioids may have provided is eliminated, and the drug-opposite effect can take time to subside. 139 Also, in preclinical models, opioid withdrawal induces central changes in neurotransmitters, along with neuroimmune and neuroinflammatory mediators involved in nociception, 43,44 thus potentially intensifying pain beyond OIH. A general increase in pain sensitivity after opioid cessation can occur after acute 4,55 or chronic 66,109,132,144 opioid exposure, referred to by a variety of names including withdrawal-induced hyperalgesia (WIH).…”

Pentazocine Protects SN4741 Cells Against MPP+-Induced Cell Damage via Up-Regulation of the Canonical Wnt/β-Catenin Signaling Pathway

“…Previous studies have indicated that the Wnt/β-catenin signaling pathway is activated after opioids administration in the rat spinal cord and cerebral cortex (Novikova et al, 2005; Dunbar et al, 2006). Furthermore, morphine has been showed to induce the secretion of Wnt signaling proteins (Jaremko et al, 2014).…”

“…As a weak agonist, pentazocine shows less chance of addiction compared to morphine and fentanyl that show robust addiction in response to the agonist treatment. Previous studies have indicated that the Wnt/β-catenin signaling can be activated by treatment with opioids (Dunbar et al, 2006). Besides, the opioids have many beneficial roles against damage inside the central nervous system.…”

Pleiotrophin modulates morphine withdrawal but has no effects on morphine-conditioned place preference

“…As a result of the blockade of the phosphatase activity, PTN increases the tyrosine phosphorylation levels of the different substrates of RPTPβ/ζ, such as β-catenin [24], Fyn [27], β-adducin [28], etc. M a n u s c r i p t 12 Interestingly, morphine treatment has been shown to activate Wnt/β-catenin signaling in cell cultures [26], and more specifically, β-catenin is one of the factors that are induced by morphine withdrawal in the rat [7]. Based on the fact that PTN activates β-catenin via RPTPβ/ζ [24] and the implication of endogenous PTN in naloxone-induced morphine withdrawal demonstrated here, it is reasonable to propose that PTN may function during morphine withdrawal through the activation of β-catenin.…”