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Hyperkinetic Movement Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Morales-Briceno Hugo, Victor S.C. Fung, Annu Aggarwal, Philip Thompson
Immune: Systemic lupus erythematosus.Antiphospholipid antibody syndrome (APS).Anti-N-methyl-d-aspartate receptor antibody-related (NMDAR) encephalitis.Anti-GABAAR antibody encephalitis.Anti-dopamine receptor D2 antibody-associated basal ganglia encephalitis.Paraneoplastic anti-Ma2, CV2/CRMP5, and anti-Ri encephalitis.Anti–myelin oligodendrocyte glycoprotein (MOG) antibody encephalitis.Postinfectious.Hemolytic uremic syndrome.Acute disseminated encephalomyelitis.
The Chemistry of the Brain
Published in Gail S. Anderson, Biological Influences on Criminal Behavior, 2019
Both illegal and therapeutic drugs, such as amphetamines and cocaine, greatly increase dopamine production and sometimes also increase human aggression.4 Although many people smoke, drink alcohol, and even take drugs, only some of these people become addicted. It has been suggested that these people suffer from a reward deficiency syndrome.39 Such people have deficiencies in this normal reward cascade and thus do not receive the normal pleasures from life and hence crave greater stimulation. They are at a much greater risk for addiction than people with normal systems. Because dopamine is the main neurotransmitter in the reward pathway, variants of the genes involved in this pathway are most probably responsible, and some have been identified. Type II alcoholism, which is very strongly influenced by genetics, has also been linked to disruption of several of the genes related to dopamine receptors.39 Obesity, smoking, and pathological gambling have also been linked to variants in the dopamine receptors, in particular dopamine receptor D2 (DRD2).39 However, serotonin, norepinephrine, and other neurotransmitters also regulate dopamine, so variant genes in any of these pathways might contribute to a predisposition for addiction.
Etiology of Geophagia
Published in Anil Gupta, Geophagia, 2019
Further, Beard et al. (1994), Bianco et al. (2008), and Unger et al. (2014) posited that dietary iron deficiency could impair dopaminergic neurotransmission, which could lead to reduced functioning of dopamine transporters and dopamine receptor D2 in the ventral corpus striatum.
What’s new in chronic pain pathophysiology
Published in Canadian Journal of Pain, 2020
Addictive behavior has also been identified as having a strong genetic association, with 43% of the variance in drug abuse due to genetic factors unique to opioid metabolism.20 The dopamine receptor has been a highly active target of study. Dopamine receptor D2 (DRD2) polymorphism is associated with addictive behavior; DRD2 gene Taql RLFP A (rs1800497) was studied in patients with an opioid use disorder versus control. Patients with either A1A1 or A1A2 alleles consumed twice as much heroin as those without the A1 allele.21 This allele is present in 19% of Caucasians with opioid dependence compared to 4.6% of those without drug abuse history.22 Dopamine D3 receptors are prevalent in the reward and reinforcement center of the nucleus accumbens. Opioid-dependent patients with high sensation-seeking scores are more likely to be homozygous for the DRD3 allele compared to patients with lower scores.23
The effect of tramadol on blood glucose concentrations: a systematic review
Published in Expert Review of Clinical Pharmacology, 2020
Samaneh Nakhaee, Jeffrey Brent, Christopher Hoyte, Khadijeh Farrokhfall, Farshad M Shirazi, Masoumeh Askari, Omid Mehrpour
Tramadol hydrochloride is an opioid commonly prescribed for managing moderate to severe pain and whose consumption is growing progressively worldwide [1,2]. Currently, tramadol is widely used worldwide, which has resulted in an increase in the number of cases of adverse effects and death [3,4]. It is often utilized for its antinociceptive analgesic effect and its perception as having a lower risk of dependency and respiratory failure compared with other opioids [5]. The precise mechanism of its action is incompletely understood. Nevertheless, agonism at µ-opioid receptors and inhibition of serotonin and epinephrine reuptake have been shown to be possible mechanisms of its action in animal models [6]. It has also been shown to be a dopamine receptor (D2) agonist and an inhibitor of the release of gamma-aminobutyric acid in the central nervous system. This pharmacodynamic complexity is responsible for a wide spectrum of clinical and toxic effects [7], which are seldom completely predictable. The most common side effects associated with tramadol use are gastrointestinal symptoms (nausea, vomiting, and constipation) and neurotoxic effects (sedation, dizziness, anxiety) [8]. In cases of tramadol overdose, the most common effects are nausea, vomiting, central nervous system depression, tachyarrhythmia, cardiac and respiratory depression, and seizures [9].
MicroRNA-15a, microRNA-15b and microRNA-16 inhibit the human dopamine D1 receptor expression in four cell lines by targeting 3′UTR –12 bp to + 154 bp
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2020
Xue Wu, Feng-ling Xu, Xi Xia, Bao-jie Wang, Jun Yao
The dopamine receptor is G protein-coupled receptor and includes two types: D1-like type and D2-like type. The activation of D1-like receptors increases the cyclic adenosine monophosphate (cAMP) and Ca2+ levels by activating adenylyl cyclase, whereas the activation of D2-like receptors decreases the adenylyl cyclase and cAMP levels [5]. The former includes dopamine receptor D1 (DRD1) and dopamine receptor D5, whereas the later includes dopamine receptor D2, D3 and D4. Dopamine receptor D1 is highly expressed in the basal ganglia and prefrontal cortical region in the brain [6]. It can up-regulate the activity of adenylate cyclase [7]. Dopamine receptor D1 is involved in the regulation of hippocampal synaptic plasticity and memory, motor control and social cognition behaviour [8–10].