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Adrenergic Agonists
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Cl−-dependent transporters, norepinephrine transporter (NET) which concentrates noradrenaline in the neuronal cytoplasm in the presence of Na+ ions. This further reduces the binding of noradrenaline to postsynaptic neurons producing pharmacological responses (Golan, 2012).
Anxiolytics: Predicting Response/Maximizing Efficacy
Published in Mark S. Gold, R. Bruce Lydiard, John S. Carman, Advances in Psychopharmacology: Predicting and Improving Treatment Response, 2018
Another way to establish a relationship between molecular mechanisms and therapeutic effects is to consider the concentrations at which a variety of drugs which bind to a given receptor exhibit therapeutic effects. If the correlation of minimum effective concentrations for therapeutic effects of a set of drugs and the K1s of those drugs for binding to a receptor is high, then that result is consistent with the conclusion that the therapeutic effect of the drug is by binding to that receptor. This sort of information has been elicited, and it demonstrates the neuronal mechanisms of action of a number of psychotropic drugs: barbiturates bind to the chloride channel of the GABA receptor, benzodiazepines bind to the benzodiazepine receptor, opiates bind to encephalin or endorphin receptors, neuroleptics bind to dopamine receptors, tricyclics and their descendants bind to the serotonin transporter receptor and/or to the norepinephrine transporter receptor and/or to the histamine receptor, clonidine binds to alpha-2 receptors on adrenergic or noradrenergic neurons, propranolol and similar drugs bind to beta adrenergic receptors.100–108
Uptake Mechanisms
Published in Stephen W. Carmichael, Susan L. Stoddard, The Adrenal Medulla 1986 - 1988, 2017
Stephen W. Carmichael, Susan L. Stoddard
Bönisch and Harder (1986) characterized the binding of tritiated desipramine, an uptake inhibitor, to the norepinephrine transporter of PC12 cell plasma membranes and compared the characteristics of binding with those of transport of norepinephrine in PC12 cells. They found and studied a specific binding site for desipramine. The desipramine binding site appears to be the neuronal norepinephrine transporter. This binding site was further characterized by Schmoig and Bonisch (1986). They solubilized the binding sites with the nonionic detergent digitonin. The binding characteristics were essentially unaltered by solubilization, allowing characterization of the binding site.
Psychiatric and non-psychiatric drugs causing false-positive amphetamines urine test in psychiatric patients: a pharmacovigilance analysis using FAERS
Published in Expert Review of Clinical Pharmacology, 2023
Vera Battini, Giovanna Cirnigliaro, Luca Giacovelli, Maria Boscacci, Silvia Massara Manzo, Giulia Mosini, Greta Guarnieri, Michele Gringeri, Beatrice Benatti, Emilio Clementi, Bernardo Dell’Osso, Carla Carnovale
Agents commonly used to treat ADHD, including dextroamphetamine, lisdexamphetamine, and atomoxetine, were among the most frequently reported in the FAERS. Indeed, the second most frequent diagnosis was ADHD. Dextroamphetamine and lisdexamfetamine are psychostimulant agents derived from amphetamine and represent the first-line therapy for ADHD [79,80]. Atomoxetine inhibits the presynaptic norepinephrine transporter (NET), reducing the norepinephrine reuptake, and at the same time is a dopamine reuptake inhibitor in the prefrontal cortex. On the other hand, methylphenidate inhibits the dopamine reuptake by increasing prefrontal, striatal, and accumbal dopamine levels. Since adolescents and adults with ADHD are at high risk for SUD [81], the UDS is crucial in this specific clinical setting; it is therefore of paramount importance for clinicians to consider the possible cross-reactivity of these agents with other substances of abuse.
Evaluation of dystonia in children and adolescents treated with atomoxetine within the Truven MarketScan database: a retrospective cohort study
Published in Expert Opinion on Drug Safety, 2018
Kristin J. Meyers, Himanshu P. Upadhyaya, Robert Goodloe, Ludmila A. Kryzhanovskaya, Marie A. Liles-Burden, Nicole A. Kellier-Steele, Michele Mancini
Attention-deficit/hyperactivity disorder (ADHD) is a common neurodevelopmental disorder in children and adolescents and is characterized by developmentally inappropriate levels of inattention, hyperactivity, or both [1,2]. A meta-analysis conducted in 2015 estimated the prevalence of ADHD worldwide to be 3.4% (95% confidence interval [CI]: 2.6–4.5) [3]. A study of parent reports in the USA between 2003 and 2011 estimated that approximately 11% of children aged 4–17 years had been diagnosed with ADHD at least once [2]. Medications approved to treat ADHD are classified as either stimulants (methylphenidates and amphetamines) [4] or non-stimulants (atomoxetine, guanfacine, and clonidine) [5]. Atomoxetine, a selective inhibitor of the presynaptic norepinephrine transporter, was the first non-stimulant approved for treatment of ADHD by the US Food and Drug Administration (FDA) in 2002 and is indicated in children aged ≥6 years, adolescents, and adults [6,7]. Guanfacine and clonidine were approved for ADHD by the FDA in 2010 [8].
Exploring longitudinal course and treatment-baseline severity interactions in secondary outcomes of smoking cessation treatment in individuals with attention-deficit hyperactivity disorder
Published in The American Journal of Drug and Alcohol Abuse, 2018
Sean X. Luo, Melanie Wall, Lirio Covey, Mei-Chen Hu, Jennifer M. Scodes, Frances R. Levin, Edward V. Nunes, Theresa Winhusen
Methylphenidate is a commonly prescribed centrally acting psychostimulant (9). It acts primarily as a norepinephrine-dopamine reuptake inhibitor, binds to and blocks dopamine transporters and norepinephrine transporter, and increases the concentration of dopamine and norepinephrine in the striatum and the prefrontal cortex at therapeutic doses (10). Osmotic-release oral systems methylphenidate (OROS-MPH) has a longer half-life and is an FDA approved once daily medication for the treatment of ADHD (11). A multi-center, randomized controlled trial was conducted in the National Drug Abuse Treatment Clinical Trials Network (NIDA-CTN-0029) to evaluate whether OROS-MPH, relative to placebo, would increase smoking-cessation rates in smokers with ADHD (12). Prolonged abstinence, the primary outcome, did not differ between placebo and OROS-MPH groups. Subsequent subgroup analyses showed that there was a substantial degree of treatment-response heterogeneity, with significant predictors such as ethnicity (13), baseline motivation (14), history of previous diagnosis of substance use disorders (15), and ADHD subtype (in a three-way interaction with baseline smoking severity and treatment) (16). Baseline ADHD severity emerged as a unique moderator that showed an interaction effect (17): patients with higher baseline ADHD, defined as a score ≥ 36 on the ADHD Symptoms Rating Scale (ADHD-RS), had better smoking abstinence outcomes with OROS-MPH than placebo; in contrast, participants with lower severity baseline ADHD (<36 on the ADHD-RS) had worse smoking-abstinence outcomes with OROS-MPH than with placebo. This interaction effect was also detected using unbiased subgroup analysis methods such as Best Approximating Model (15).