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Pharmacotherapy of Neurochemical Imbalances
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Rupali Patil, Aman Upaganlawar, Suvarna Ingale
Dynorphins are derived from prodynorphin. Dynorphins are found in hypothalamus, posterior pituitary, and duodenum. Dynorphins are of two types: α- and β-dynorphins (Barrett et al., 2009).
Postulated Physiological and Pathophysiological Roles on Motility
Published in Edwin E. Daniel, Neuropeptide Function in the Gastrointestinal Tract, 2019
Hans-Dieter Allescher, Sultan Ahmad
Proenkephalin B, which is also termed prodynorphin and is expressed in the CNS and in the digestive tract, contains a variety of opioid peptides (α-neoendorphin, β-neoendorphin, dynorphin A [1—17, 1—13, 1—9, 1—8], dynorphin B [1—29, 1—12], and rimorphin).
Selective Post-Translational Processing of Opioid Peptides in Cardioregulatory Mechanisms of the Dorsal Medulla
Published in I. Robin A. Barraco, Nucleus of the Solitary Tract, 2019
William R. Millington, Michael D. Hirsch
Prodynorphin processing is relatively uncomplicated compared to POMC and proenkephalin.27,28 The prohormone contains three copies of leu-enkephalin clustered near its C-terminal, each of which forms the N-terminal of a different set of dynorphin peptides; α-neo-endorphin, dynorphin A (dynorphin-1-17), and dynorphin B-29 (leumorphin). These, in turn, serve as precursors to yet smaller forms. Hence, α-neo-endorphin is converted to β-neo-endorphin through removal of its C-terminal arginine residue, and dynorphin-1-17 undergoes endoproteolytic cleavage at a single arginine residue, forming dynorphin-1-8. Dynorphin B-29 is similarly processed at a single arginine, forming a 13-amino-acid peptide, dynorphin B (rimorphin). Leu-enkephalin may also be a product of prodynorphin processing, at least in certain brain regions.60 Like other opioids, the ratio of dynorphin peptides varies regionally, although dynorphin-18, dynorphin B, and α-neo-endorphin predominate in many brain areas.25,26,28,61
Genetic and epigenetic studies of opioid abuse disorder – the potential for future diagnostics
Published in Expert Review of Molecular Diagnostics, 2023
Sarah Abdulmalek, Gary Hardiman
Ethnicity is a critical factor to account for when it comes to screening for genetic differences. A study in China reported multiple SNPs of the PDYN (prodynorphin) gene that they found to be associated to the increased risk of opioid addiction. Among them were SNPs in the PDYN gene 68 bp (rs35286281), rs1022563 and rs910080 [112]. This was also confirmed by a study on European Americans, which reported the rs1022563 SNP in heroin addicts of both sexes and rs910080, which was found to be more relevant to the female subset of the cohort. However, this finding was not observed in American heroin users of an African descent [113]. The list in genetic screening for SNPs extends to cover all the opioid-associated pathways, the addiction-related neurotransmitters, and their receptors, as well as polymorphisms of numerous growth factors and neuropeptides [101,114].
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
Methamphetamine use has rapidly become widespread in Turkey as well as in the world and poses a serious threat. The development of substance-use disorders following substance use depend on social, psychological and environmental factors, as well as genetic factors. It was reported that genetic factors accounted for 44% of stimulant dependence (Tsuang et al., 1996). It has been suggested that methamphetamine use has a cultural background and use motivations varies interculturally (Evren & Bozkurt, 2018; Li et al., 2004). Prodynorphin (PDYN) is a precursor of dinorphin-related peptides associated with substance dependence. It yields endogeneous k opioid receptor agonists (Schwarzer, 2009). The activation of k opioid receptors within the dopamine terminals results in decreased dopamine release and aversive symptoms such as dysphoria and anhedonia (Pfeiffer et al., 1986).
New concepts in opioid analgesia
Published in Expert Opinion on Investigational Drugs, 2018
Endogenous opioid peptides are derived from the precursors proopiomelanocortin (encoding beta-endorphin), proenkephalin (encoding Met-enkephalin and Leu-enkephalin), and prodynorphin (encoding dynorphins). These peptides contain the common Tyr-Gly-Gly-Phe-Met/Leu sequence at their amino terminals, known as the opioid motif. Beta-endorphin and the enkephalins are antinociceptive agents acting at mu- and delta-opioid receptors. Dynorphins can elicit both pro- and antinociceptive effects via N-methyl-D-aspartate receptors and kappa-opioid receptors, respectively. A fourth group of tetrapeptides (endomorphins) with yet unknown precursors do not contain the pan-opioid motif but bind to mureceptors with high selectivity. Opioid peptides are expressed throughout the central and peripheral nervous systems, in neuroendocrine tissues, and in immune cells [10,11,13,15]. Interactions between immune cell-derived opioid peptides and peripheral opioid receptors have been examined extensively, particularly with regard to the generation of analgesia [9–11].