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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
Psychoneuroimmunology, Stress and Infection
Published in Herman Friedman, Thomas W. Klein, Andrea L. Friedman, Psychoneuroimmunology, Stress, and Infection, 2020
Currently, the major mechanism by which the central nervous system is thought to influence immune function is by chemical messengers: various hormones from the pituitary, and the secretion of catecholamines and peptides from nerve terminals of the autonomic nervous system (Figure 3). The pituitary hormones with known effects on the immune system include ACTH, β-endorphin, prolactin, growth hormone and thyroid-stimulating hormone (TSH). The adrenal medulla secretes enkephalins and dynorphins. Endorphins are also secreted by the sympathetic nervous system along with other neuropeptides (see below).
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).
Identifying molecular mechanisms of acute to chronic pain transition and potential drug targets
Published in Expert Opinion on Therapeutic Targets, 2022
Kannan Aravagiri, Adam Ali, Hank C Wang, Kenneth D Candido, Nebojsa Nick Knezevic
Besides peripheral and central sensitization/priming, the dysregulation of inhibitory interneurons and descending neurons in the spinal cord and brain, specifically in the periaqueductal gray, rostral ventromedial medulla (RVM), and reticular formation, has also been known to be another contributing factor in the transition from acute to chronic pain. An example of dysregulated descending control that has been identified involves the RVM. In models of nerve and mechanical injury, it was found that activation of the RVM with the delivery of substance P to Neurokinin-1 (NK1) reduces inhibitory descending function and therefore maintains the pain state [24,25]. Another process in which this is done is through the production of dynorphin, an endogenous opioid that interacts with NMDA receptors to produce a prolonged pain-state [26]. Initially intended to activate opioid receptors and reduce pain in the short term, ongoing dynorphin release can cause opioid tolerance and therefore opioid-induced hyperalgesia (OIH). Another example of dysregulated descending control that has been identified involves the locus coeruleus (LCL). Activation of the LCL with noxious stimuli prompts the delivery of noradrenergic neurotransmitters and activation of α-2 receptors, allowing for the reduced release of activating neurotransmitters [27]. Both these areas become dysregulated and are implicated when discussing the transition from acute to chronic pain.
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).