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Neuropeptide Regulation of Ion Channels and Food Intake
Published in Tian-Le Xu, Long-Jun Wu, Nonclassical Ion Channels in the Nervous System, 2021
A large number of feeding-related neuropeptides modulate the neuronal activity through the opening or closing of the GIRK channels. NPY is a typical inhibitory neuropeptide that decreases neuronal activity when it binds to NPY receptors widely expressed in the brain. The hyperpolarizing effects of NPY are mainly mediated by the increased activity of GIRK channels following the activation of NPY receptors in many areas including the arcuate nucleus, lateral hypothalamus, ventromedial hypothalamus, hippocampus, lateral amygdala, and thalamus (Acuna-Goycolea et al. 2005; Sun, Huguenard, and Prince 2001; Roseberry et al. 2004; Fu, Acuna-Goycolea, and van den Pol 2004). Endogenous opioid peptides are also involved in the control of food intake. Both dynorphin and met-enkephalin are released in the hypothalamus for regulating the activity of feeding-related neural circuits. In the arcuate nucleus, dynorphin inhibits both POMC and dopamine neurons through the opening of GIRK channels after the activation of kappa opioid receptors (Zhang and van den Pol 2013, 2015). In addition to dynorphin, met-enkephalin potentiates GIRK currents in POMC neurons through activating mu opioid receptors (Zhang and van den Pol 2015).
Physiology of the Pain System
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
The limbic system is a set of brain structures on either side of the thalamus that directs emotion, behavior, motivation, long-term memory, and olfaction. The mesolimbic pathway is part of the reward circuit. Dopaminergic neurons in the ventral tegmental area (VTA) of the midbrain project to the forebrain nucleus accumbens (NAc). Burst firing of dopaminergic neurons into the NAc serves as a reward signal and is inhibited by tonic GABA input.15 Opioids inhibit GABAergic tone on these neurons, while pain relief directly engages dopamine circuitry.15 The mesolimbic pathway has been implicated in depression, anxiety, pain sensation, anticipation of analgesia or placebo-induced analgesia, and chronic pain.16 Different types of pain can impact different aspects of the VTA and result in either activation or inhibition. In this way, dopamine release is variable based on various pain signals.16 These dopaminergic pathways are variably altered with stress as well as opioids. Dynorphin and the kappa opioid receptor can play a role in impairing dopamine release in the Na.16
DSM 5 SUD Criterion 11 Withdrawal
Published in Joan Ifland, Marianne T. Marcus, Harry G. Preuss, Processed Food Addiction: Foundations, Assessment, and Recovery, 2017
Joan Ifland, H. Theresa Wright
Koob and Volkow point out that both the hypothalamic–pituitary–adrenal (HPA) axis and brain stress system mediated by CRF are dysregulated by the chronic administration of all major drugs with dependence or abuse potential. There is a common response of elevated adrenocorticotropic hormone, corticosterone, and amygdala CRF during acute withdrawal (Koob et al., 2014; Piazza & Le Moal, 1996). As tolerance and withdrawal develop, brain stress systems, such as CRF, norepinephrine, and dynorphin, are recruited. The dysfunction in stress systems can manifest as negative emotional states in withdrawal and protracted abstinence (Delfs, Zhu, Druhan, & Aston-Jones, 2000; Koob et al., 2014).
Brain site-specific regulation of hedonic intake by orexin and DYN peptides: role of the PVN and obesity
Published in Nutritional Neuroscience, 2022
P. Mattar, S. Uribe-Cerda, C. Pezoa, T. Guarnieri, C. M. Kotz, J. A. Teske, E. Morselli, C. Perez-Leighton
The orexin and dynorphin peptides are part of the neuronal network that regulates hedonic intake, the reward-driven choice and intake of palatable food (tasty food rich in fat, sugar or salt) [1–3]. The orexins (orexin-A, OXA and orexin-B) are excitatory neuropeptides synthesized by neurons in the lateral hypothalamus (LH) and released in several brain sites (ventral tegmental area, VTA; paraventricular thalamic nucleus, PVT; central amygdala, CeA) [4] where they can bind to their receptors (OX1R and OX2R) [5] to enhance hedonic intake and the motivation for reinforcers including palatable food [6–9]. The orexin receptors might have specialized functions with OX1R regulating reward and OX2R regulating the effects of orexin peptides on sleep and energy expenditure [10,11]. The opioid dynorphins are inhibitory neuropeptides synthesized by different neurons and promote depressive states and negative consequences of stress [12]. However, the opioid dynorphin peptide DYN-A1–13, which has a higher affinity for the κ-opioid receptor (KOR) subtype but can bind and activate the μ- (MOR) and δ- (DOR) subtypes [13–15], can enhance hedonic intake through different brain sites including the paraventricular hypothalamic nucleus (PVN) [16–20]. In PVN, individual food and nutrient preference modulates hedonic intake caused by activation of MOR and DOR [16,21–23], but whether food preference modulates the feeding effects of DYN-A1–13 is unknown.
Profiles and Predictors of Treatment-Resistant Opioid Use Disorder (TROUD): A Secondary Data Analysis of Treatment Episode Data Set’s 2017 Admissions
Published in Alcoholism Treatment Quarterly, 2021
David A. Patterson Silver Wolf, Catherine Dulmus, Greg Wilding, Amy Barczykowski, Jihnhee Yu, Sara Beeler-Stinn, Autumn Asher Blackdeer, Steven Harvey, Nicole M. Rodriguez
An understanding of OUD’s impact on the brain and the theory supporting OUD as being a brain disease can be found in the recent consensus report of the National Academies of Science, Engineering, and Medicine, (National Academies of Science, 2019). The altered reward and cognitive processes in combination with the emergence of a chronic stress and negative mood state have been hypothesized to be responsible for a “dark side of addiction” (Koob, 2006), in which the attempts to alleviate negative emotions and the inability to feel pleasure that arise during non-intoxication periods contribute to compulsive drug-taking behavior. A particular component of the brain opioid system—the dynorphin-kappa system—has been strongly implicated in this persistent negative affect which is thought to drive continued drug use, craving, and relapse (Chavkin & Koob, 2016). Moreover, these changes to the brain continue even after an individual discontinues opioid use and no longer has symptoms of acute withdrawal, making long-term recovery more difficult (Leshner, 1997; Volkow, Koob, & McLellan, 2016, p. 30).
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].