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The Opioid Epidemic
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
Tonic activation of descending bulbospinal (medulla to spinal cord) pain facilitatory loops from the rostral ventromedial medulla (RVM) to the spinal cord play a role in opioid-induced hyperalgesia. Opioid exposure in the RVM can lead to an increased descending facilitation of pain.16 Upregulation of spinal dynorphin has been implicated.1 An increase in dynorphin enhances primary afferent neurotransmitter release.1 Dynorphin has also been shown to potentiate NMDA receptors.17 Upregulated spinal dynorphin is pronociceptive and is required for the maintenance of persistent neuropathic pain.18 Lesioning the dorsolateral funiculus prevents the increase of dynorphin and the presence of the excitatory neuropeptide calcitonin gene-related protein (CGRP).19 In the same vein, treatment with a selective k-opioid receptor antagonist also reduced established opioid-induced hyperalgesia.20
Fibromyalgia Syndrome: Canadian Clinical Working Case Definition, Diagnostic and Treatment Protocols–A Consensus Document
Published in I. Jon Russell, The Fibromyalgia Syndrome: A Clinical Case Definition for Practitioners, 2020
Anil Kumar Jain, Bruce M. Carruthers, Maijorie I. van de Sande, Stephen R. Barron, C. C. Stuart Donaldson, James V. Dunne, Emerson Gingrich, Dan S. Heffez, Y.-K. Frances Leung, Daniel G. Malone, Thomas J. Romano, I. Jon Russell, David Saul, Donald G. Seibel
Dynorphin A: Recent data from animal systems has led one author to hypothesis a very important role for CSF dynorphin A in FMS (179) that must be followed-up with a prospective study. When high concentrations of dynorphin A were administered intrathecally to rats, the animals developed a flaccid paralysis. Intermediate concentrations of dynorphin A were less damaging but caused a persistent allodynia (310). The mechanism responsible for these effects appeared to involve N-methyl-D-aspartate [NMDA] receptors rather than the expected kappa-opioid receptors. Increased production of dynorphin A has been known to occur in animal experiments in which the spinal cord was constricted or otherwise injured. Under those circumstances, administered antibodies to dynorphin A reduced the severity of the deficit resulting from such injury. On the other hand, when dynorphin A was allowed to induce spinal cord injury, the damage appeared to be irreversible.
Miscellaneous Neuropeptides
Published in Paul V. Malven, Mammalian Neuroendocrinology, 2019
A large body of knowledge about opioid receptors has developed in the years since their discovery (Goldstein and Naidu, 1989). Based on comparisons of activity in various bioassays and binding affinities for many synthetic opioid- related drugs, a number of subtypes of the opioid receptor have been identified. Some of these subtypes may represent altered forms of a single receptor, or they may be different molecules (Wollemann, 1990). The selectivity of each subtype for any given EOP or antagonist is never absolute, so that selectivity of binding always depends on dosage (Goldstein and Naidu, 1989). For example, naloxone can antagonize most subtypes if the dosage is sufficiently high. The three primary subtypes are known as mu, delta, and kappa, with an additional one called epsilon. In some of the early literature, there was another one called sigma, but that receptor is probably not opioid in nature. The mu subtype was named for the prototypic opioid drug, morphine, but an endogenous ligand specific for only mu opioid receptors has not been established. Subdivisions of the mu and kappa receptor subtypes, which will not be considered here, have also been characterized. The delta opioid receptor is preferentially selective for endogenous enkephalin-related EOP, although exogenous enkephalin-related compounds can be synthesized which react preferentially with mu receptors. Kappa opioid receptors react preferentially with endogenous dynorphin-related EOP. The epsilon opioid receptor is defined as being specific for β-endorphin, but there is some question about the separate existence of epsilon receptors because β-endorphin binds readily to both mu and delta receptors.
The role of kisspeptin/neurokinin B/dynorphin neurons in pathomechanism of vasomotor symptoms in postmenopausal women: from physiology to potential therapeutic applications
Published in Gynecological Endocrinology, 2018
Anna Szeliga, Adam Czyzyk, Agnieszka Podfigurna, Andrea R. Genazzani, Alessandro D. Genazzani, Blazej Meczekalski
Noteworthy is fact that after menopause changes in KNDy neurons are expressed also by changes in dynorphin secretion. In healthy premenopausal women, dynorphin plays an inhibitory role on reproductive axis by acting on kappa opioid receptor [59]. After menopause, in infundibular nucleus, there is a hypertrophy of dynorphin neurons associated with reduction in number of these neurons. Described changes cause overall decrease in dynorphin synthesis, thus decreasing in dynorphin action [60]. Taking into consideration fact, that dynorphin, also synthesized in hypothalamus by KNDy neurons, plays inhibitory role on GnRH secretion, previously demonstrated increase in gonadotropins secretion after menopause may be related to decreased amount of neurons expressing prodynorphin in infundibular nucleus, thus decreased dynorphin mRNA expression by KNDy neurons of preoptic area, and decreased dynorphin activity [61].
Prodynorphin (PDYN) gene polymorphisms in Turkish patients with methamphetamine use disorder, changes in PDYN serum levels in withdrawal and the relationship between PDYN, temperament and depression
Published in Journal of Ethnicity in Substance Abuse, 2022
Güliz Şenormancı, Çetin Turan, Sevim Karakaş Çelik, Aycan Çelik, Tuba Gökdoğan Edgünlü, Dilek Akbaş, Ayşe Semra Demir Akca, Ömer Şenormancı
In a study conducted in the postmortem period, it was shown that dynorphin mRNA levels and dynorphin protein increased in chronic cocaine users (Frankel et al., 2008). Preclinical studies have evidenced that dynorphin peptides attenuate the extracellular dopamine increase in nucleus accumbens (Zhang et al., 2005). It has been suggested that the dynorphin K opioid system is a regulatory system that reverses substance-induced dopaminergic stimulation and may play a role in the development of dependence (Koob & Kreek, 2007). Chronic methamphetamine exposure stimulates dopamine receptors in nucleus accumbens, leading to an increase in PDYN, which results in the emergence of withdrawal symptoms by decreasing dopamine through k opioid receptors (Nomura et al., 2006).
Can pharmacotherapy improve treatment outcomes in people with co-occurring major depressive and cocaine use disorders?
Published in Expert Opinion on Pharmacotherapy, 2021
Gustavo A. Angarita, Hasti Hadizadeh, Ignacio Cerdena, Marc N. Potenza
Another possible target is the kappa-opioid receptor (KOR)/dynorphin system. Chronic cocaine exposure is associated with upregulation of KORs and its endogenous ligand dynorphin [86]. Increased levels of dynorphin in the NAc inhibit dopamine release [87] and may influence negative emotional states, termed hyperkatifeia, following withdrawal (i.e. dysphoria/anhedonia, aversion and depression/anxiety) [88]. A negative reinforcement cycle, in which individuals find themselves experiencing undesirable emotional states and see drug use as a short-term option to decrease them, has been termed the ‘Dark Side of Addiction’ [89], and the dynorphin/KOR system contributes to this antireward/stress system[88] .