5-HT2C Agonists Modulate Schizophrenia-Like Behaviors in Mice
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Serotonin's Role in Alcohol's Effects on the Brain
NEUROTRANSMITTER REVIEW IMPERATO, A., AND DI CHIARA, G. Preferential stimulation of dopamine release in the nucleus accumbens of freely moving rats by ethanol. Journal SEROTONIN’S ROLE IN ALCOHOL’S of Pharmacology and Experimental Therapeutics 239:219–228, 1986. EFFECTS ON THE BRAIN KITAI, S.T., AND SURMEIER, D.J. Cholinergic and dopaminergic modula- tion of potassium conductances in neostriatal neurons. Advances in David M. Lovinger, Ph.D. Neurology 60:40–52, 1993. LE MOINE, C.; NORMAND, E.; GUITTENY, A.F.; FOUQUE, B.; TEOULE, R.; AND BLOCH, B. Dopamine receptor gene expression by enkephalin Serotonin is an important brain chemical that acts as a neurons in rat forebrain. Proceedings of the National Academy of Sciences neurotransmitter to communicate information among USA 87:230–234, 1990. nerve cells. Serotonin’s actions have been linked to al- LE MOINE, C.; NORMAND, E.; AND BLOCH, B. Phenotypical character- cohol’s effects on the brain and to alcohol abuse. ization of the rat striatal neurons expressing the D1 dopamine receptor Alcoholics and experimental animals that consume gene. Proceedings of the National Academy of Sciences USA 88: large quantities of alcohol show evidence of differences 4205–4209, 1991. in brain serotonin levels compared with nonalcoholics. LYNESS, W.H., AND SMITH F.L. Influence of dopaminergic and sero- Both short- and long-term alcohol exposure also affect tonergic neurons on intravenous ethanol self-administration in the rat. the serotonin receptors that convert the chemical sig- Pharmacology and Biochemistry of Behavior 42:187–192, 1992. nal produced by serotonin into functional changes in the signal-receiving cell. -
The Baseline Structure of the Enteric Nervous System and Its Role in Parkinson’S Disease
life Review The Baseline Structure of the Enteric Nervous System and Its Role in Parkinson’s Disease Gianfranco Natale 1,2,* , Larisa Ryskalin 1 , Gabriele Morucci 1 , Gloria Lazzeri 1, Alessandro Frati 3,4 and Francesco Fornai 1,4 1 Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, 56126 Pisa, Italy; [email protected] (L.R.); [email protected] (G.M.); [email protected] (G.L.); [email protected] (F.F.) 2 Museum of Human Anatomy “Filippo Civinini”, University of Pisa, 56126 Pisa, Italy 3 Neurosurgery Division, Human Neurosciences Department, Sapienza University of Rome, 00135 Rome, Italy; [email protected] 4 Istituto di Ricovero e Cura a Carattere Scientifico (I.R.C.C.S.) Neuromed, 86077 Pozzilli, Italy * Correspondence: [email protected] Abstract: The gastrointestinal (GI) tract is provided with a peculiar nervous network, known as the enteric nervous system (ENS), which is dedicated to the fine control of digestive functions. This forms a complex network, which includes several types of neurons, as well as glial cells. Despite extensive studies, a comprehensive classification of these neurons is still lacking. The complexity of ENS is magnified by a multiple control of the central nervous system, and bidirectional communication between various central nervous areas and the gut occurs. This lends substance to the complexity of the microbiota–gut–brain axis, which represents the network governing homeostasis through nervous, endocrine, immune, and metabolic pathways. The present manuscript is dedicated to Citation: Natale, G.; Ryskalin, L.; identifying various neuronal cytotypes belonging to ENS in baseline conditions. -
7 X 11.5 Three Lines.P65
Cambridge University Press 978-0-521-71413-6 - Antipsychotics and Mood Stabilizers: Stahl’s Essential Psychopharmacology, Third Edition Stephen M. Stahl Index More information Index Page numbers followed by ‘f ’ indicate figures; page numbers followed by ‘t ’ indicate tables. 3PPP, 134f agitation, benzodiazepines for, 188 AAADC (aromatic amino acid decarboxylase), and receptor conformation, 132f 97, 98f agranulocytosis, clozapine and, 164 ABT089, 203 akathisia acetylcholine (ACh), from aripiprazole, 175 in arousal pathways, 150, 152f nigrostriatal pathway dopamine deficiencies and blocked dopamine receptors, 93f and, 31 overactivity, 95 alanine-serine-cysteine transporter (ASC-T), reciprocal relationship with dopamine, 92f glial, 34 acetylcholine-linked mechanisms, 202 alogia, 5, 6t ACP 103, 200 alpha 1 adrenergic receptors ACP-104, 129, 134f atypical antipsychotic agents and, 139f ACR16, 134f and sedation, 151f adipose tissue, insulin resistance in, 141, alpha-1 receptor, antagonism, 94f 144f alpha-2 adrenergic receptors, atypical adolescence antipsychotic agents and, 139f aggressiveness in, 179 alpha 2 antagonists, 168 removal of synaptic connections, 68 alpha-4 beta-2 nicotinic acetylcholine receptor, risperidone for treating psychotic disorders, 203 166 alpha-7-nicotinic cholinergic agonists, affective blunting, 5 202 affective flattening, as SSRI side effect, 110 alpha amino-3-hydroxy-5-methyl-4- affective symptoms isoxazolepropionic acid (AMPA) dorsal vs. ventral regulation, 76f receptors, 40, 40f, 66f mesolimbic dopamine pathway role -
The Serotonergic System in Migraine Andrea Rigamonti Domenico D’Amico Licia Grazzi Susanna Usai Gennaro Bussone
J Headache Pain (2001) 2:S43–S46 © Springer-Verlag 2001 MIGRAINE AND PATHOPHYSIOLOGY Massimo Leone The serotonergic system in migraine Andrea Rigamonti Domenico D’Amico Licia Grazzi Susanna Usai Gennaro Bussone Abstract Serotonin (5-HT) and induce migraine attacks. Moreover serotonin receptors play an impor- different pharmacological preventive tant role in migraine pathophysiolo- therapies (pizotifen, cyproheptadine gy. Changes in platelet 5-HT content and methysergide) are antagonist of are not casually related, but they the same receptor class. On the other may reflect similar changes at a neu- side the activation of 5-HT1B-1D ronal level. Seven different classes receptors (triptans and ergotamines) of serotoninergic receptors are induce a vasocostriction, a block of known, nevertheless only 5-HT2B-2C neurogenic inflammation and pain M. Leone • A. Rigamonti • D. D’Amico and 5HT1B-1D are related to migraine transmission. L. Grazzi • S. Usai • G. Bussone (౧) syndrome. Pharmacological evi- C. Besta National Neurological Institute, Via Celoria 11, I-20133 Milan, Italy dences suggest that migraine is due Key words Serotonin • Migraine • e-mail: [email protected] to an hypersensitivity of 5-HT2B-2C Triptans • m-Chlorophenylpiperazine • Tel.: +39-02-2394264 receptors. m-Chlorophenylpiperazine Pathogenesis Fax: +39-02-70638067 (mCPP), a 5-HT2B-2C agonist, may The 5-HT receptor family is distinguished from all other 5- Introduction 1 HT receptors by the absence of introns in the genes; in addi- tion all are inhibitors of adenylate cyclase [1]. Serotonin (5-HT) and serotonin receptors play an important The 5-HT1A receptor has a high selective affinity for 8- role in migraine pathophysiology. -
THE USE of MIRTAZAPINE AS a HYPNOTIC O Uso Da Mirtazapina Como Hipnótico Francisca Magalhães Scoralicka, Einstein Francisco Camargosa, Otávio Toledo Nóbregaa
ARTIGO ESPECIAL THE USE OF MIRTAZAPINE AS A HYPNOTIC O uso da mirtazapina como hipnótico Francisca Magalhães Scoralicka, Einstein Francisco Camargosa, Otávio Toledo Nóbregaa Prescription of approved hypnotics for insomnia decreased by more than 50%, whereas of antidepressive agents outstripped that of hypnotics. However, there is little data on their efficacy to treat insomnia, and many of these medications may be associated with known side effects. Antidepressants are associated with various effects on sleep patterns, depending on the intrinsic pharmacological properties of the active agent, such as degree of inhibition of serotonin or noradrenaline reuptake, effects on 5-HT1A and 5-HT2 receptors, action(s) at alpha-adrenoceptors, and/or histamine H1 sites. Mirtazapine is a noradrenergic and specific serotonergic antidepressive agent that acts by antagonizing alpha-2 adrenergic receptors and blocking 5-HT2 and 5-HT3 receptors. It has high affinity for histamine H1 receptors, low affinity for dopaminergic receptors, and lacks anticholinergic activity. In spite of these potential beneficial effects of mirtazapine on sleep, no placebo-controlled randomized clinical trials of ABSTRACT mirtazapine in primary insomniacs have been conducted. Mirtazapine was associated with improvements in sleep on normal sleepers and depressed patients. The most common side effects of mirtazapine, i.e. dry mouth, drowsiness, increased appetite and increased body weight, were mostly mild and transient. Considering its use in elderly people, this paper provides a revision about studies regarding mirtazapine for sleep disorders. KEYWORDS: sleep; antidepressive agents; sleep disorders; treatment� A prescrição de hipnóticos aprovados para insônia diminuiu em mais de 50%, enquanto de antidepressivos ultrapassou a dos primeiros. -
Oxytocin Effects in Mothers and Infants During Breastfeeding
© 2013 SNL All rights reserved REVIEW Oxytocin effects in mothers and infants during breastfeeding Oxytocin integrates the function of several body systems and exerts many effects in mothers and infants during breastfeeding. This article explains the pathways of oxytocin release and reviews how oxytocin can affect behaviour due to its parallel release into the blood circulation and the brain. Oxytocin levels are higher in the infant than in the mother and these levels are affected by mode of birth. The importance of skin-to-skin contact and its association with breastfeeding and mother-infant bonding is discussed. Kerstin Uvnäs Moberg Oxytocin – a system activator increased function of inhibitory alpha-2 3 MD, PhD xytocin, a small peptide of just nine adrenoceptors . Professor of Physiology amino acids, is normally associated The regulation of the release of oxytocin Swedish University of Agriculture O with labour and the milk ejection reflex. is complex and can be affected by different [email protected] However, oxytocin is not only a hormone types of sensory inputs, by hormones such Danielle K. Prime but also a neurotransmitter and a as oestrogen and even by the oxytocin 1,2 molecule itself. This article will focus on PhD paracrine substance in the brain . During Breastfeeding Research Associate breastfeeding it is released into the brain of four major sensory input nervous Medela AG, Baar, Switzerland both mother and infant where it induces a pathways (FIGURES 2 and 3) activated by: great variety of functional responses. 1. Sucking of the mother’s nipple, in which Through three different release pathways the sensory nerves originate in the (FIGURE 1), oxytocin functions rather like a breast. -
MDMA) Cause Selective Ablation of Serotonergic Axon Terminals in Forebrain: Lmmunocytochemical Evidence for Neurotoxicity
The Journal of Neuroscience, August 1988, 8(8): 2788-2803 Methylenedioxyamphetamine (MDA) and Methylenedioxymetham- phetamine (MDMA) Cause Selective Ablation of Serotonergic Axon Terminals in Forebrain: lmmunocytochemical Evidence for Neurotoxicity E. O’Hearn,” G. Battaglia, lab E. B. De Souza,’ M. J. Kuhar,’ and M. E. Molliver Departments of Neuroscience, and Neurology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, and ‘Neuroscience Branch, Addiction Research Center, National Institute on Drug Abuse, Baltimore, Maryland 21224 The psychotropic amphetamine derivatives 3,4-methylene- The synthetic amphetamine derivatives 3,4-methylenedioxy- dioxyamphetamine (MDA) and 3,4-methylenedioxymetham- amphetamine (MDA) and 3,4-methylenedioxymethamphet- phetamine (MDMA) have been used for recreational and amine (MDMA) are potent mood-altering drugs that have at- therapeutic purposes in man. In rats, these drugs cause large tained public interest (Seymour, 1986) due to their widespread, reductions in brain levels of serotonin (5HT). This study self-administration by young adults (e.g., Klein, 1985). These employs immunocytochemistry to characterize the neuro- drugs have also been proposed for medical use in psychotherapy toxic effects of these compounds upon monoaminergic neu- because they produce augmentation of mood and enhanced in- rons in the rat brain. Two weeks after systemic administra- sight (Naranjo et al., 1967; Yensen et al., 1976; Di Leo, 198 1; tion of MDA or MDMA (20 mg/kg, s.c., twice daily for 4 d), Greer and Tolbert, 1986; Grinspoon and Bakalar, 1986). How- there is profound loss of serotonergic (5HT) axons through- ever, concern has been raised about the safety of these com- out the forebrain; catecholamine axons are completely pounds based on evidence that they may be toxic to brain seroto- spared. -
5-HT2A/2C Receptor Modulation of Absence Seizures and Characterization of the GHB-Model
5-HT2A/2C receptor modulation of absence seizures and characterization of the GHB-model A thesis submitted to Cardiff University for the degree of Doctor of Philosophy by Marcello Venzi (MSc) School of Biosciences, Cardiff University, October 2014 Chapter 1 Declaration and Statements This work has not been submitted in substance for any other degree or award at this or any other university or place of learning, nor is being submitted concurrently in candidature for any degree or other award. Signed ………………………………………… (candidate) Date ………………………… STATEMENT 1 This thesis is being submitted in partial fulfillment of the requirements for the degree of PhD . Signed ………………………………………… (candidate) Date ………………………… STATEMENT 2 This thesis is the result of my own independent work/investigation, except where otherwise stated. Other sources are acknowledged by explicit references. The views expressed are my own. Signed ………………………………………… (candidate) Date ………………………… STATEMENT 3 I hereby give consent for my thesis, if accepted, to be available for photocopying and for inter- library loan, and for the title and summary to be made available to outside organisations. Signed ………………………………………… (candidate) Date ………………………… STATEMENT 4: PREVIOUSLY APPROVED BAR ON ACCESS I hereby give consent for my thesis, if accepted, to be available for photocopying and for inter- library loans after expiry of a bar on access previously approved by the Academic Standards & Quality Committee. Signed ………………………………………… (candidate) Date ………………………… II Chapter 1 Summary Absence seizures (ASs) are non-convulsive epileptic events which are common in pediatric and juvenile epilepsies. They consist of EEG generalized spike-and-wave-discharges (SWDs) accompanied by an impairment of consciousness and are expressed within the thalamocortical network. -
Neurotransmitter Actions
Central University of South Bihar Panchanpur, Gaya, India E-Learning Resources Department of Biotechnology NB: These materials are taken/borrowed/modified/compiled from various resources like research articles and freely available internet websites, and are meant to be used solely for the teaching purpose in a public university, and for serving the needs of specified educational programmes. Dr. Jawaid Ahsan Assistant Professor Department of Biotechnology Central University of South Bihar (CUSB) Course Code: MSBTN2003E04 Course Name: Neuroscience Neurotransmitter Actions • Excitatory Action: – A neurotransmitter that puts a neuron closer to an action potential (facilitation) or causes an action potential • Inhibitory Action: – A neurotransmitter that moves a neuron further away from an action potential • Response of neuron: – Responds according to the sum of all the neurotransmitters received at one time Neurotransmitters • Acetylcholine • Monoamines – modified amino acids • Amino acids • Neuropeptides- short chains of amino acids • Depression: – Caused by the imbalances of neurotransmitters • Many drugs imitate neurotransmitters – Ex: Prozac, zoloft, alcohol, drugs, tobacco Release of Neurotransmitters • When an action potential reaches the end of an axon, Ca+ channels in the neuron open • Causes Ca+ to rush in – Cause the synaptic vesicles to fuse with the cell membrane – Release the neurotransmitters into the synaptic cleft • After binding, neurotransmitters will either: – Be destroyed in the synaptic cleft OR – Taken back in to surrounding neurons (reuptake) Excitable cells: Definition: Refers to the ability of some cells to be electrically excited resulting in the generation of action potentials. Neurons, muscle cells (skeletal, cardiac, and smooth), and some endocrine cells (e.g., insulin- releasing pancreatic β cells) are excitable cells. -
5-HT3 Receptor Antagonists in Neurologic and Neuropsychiatric Disorders: the Iceberg Still Lies Beneath the Surface
1521-0081/71/3/383–412$35.00 https://doi.org/10.1124/pr.118.015487 PHARMACOLOGICAL REVIEWS Pharmacol Rev 71:383–412, July 2019 Copyright © 2019 by The Author(s) This is an open access article distributed under the CC BY-NC Attribution 4.0 International license. ASSOCIATE EDITOR: JEFFREY M. WITKIN 5-HT3 Receptor Antagonists in Neurologic and Neuropsychiatric Disorders: The Iceberg Still Lies beneath the Surface Gohar Fakhfouri,1 Reza Rahimian,1 Jonas Dyhrfjeld-Johnsen, Mohammad Reza Zirak, and Jean-Martin Beaulieu Department of Psychiatry and Neuroscience, Faculty of Medicine, CERVO Brain Research Centre, Laval University, Quebec, Quebec, Canada (G.F., R.R.); Sensorion SA, Montpellier, France (J.D.-J.); Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran (M.R.Z.); and Department of Pharmacology and Toxicology, University of Toronto, Toronto, Ontario, Canada (J.-M.B.) Abstract. ....................................................................................384 I. Introduction. ..............................................................................384 II. 5-HT3 Receptor Structure, Distribution, and Ligands.........................................384 A. 5-HT3 Receptor Agonists .................................................................385 B. 5-HT3 Receptor Antagonists. ............................................................385 Downloaded from 1. 5-HT3 Receptor Competitive Antagonists..............................................385 2. 5-HT3 Receptor -
WO 2012/148799 Al 1 November 2012 (01.11.2012) P O P C T
(12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date WO 2012/148799 Al 1 November 2012 (01.11.2012) P O P C T (51) International Patent Classification: (81) Designated States (unless otherwise indicated, for every A61K 9/107 (2006.01) A61K 9/00 (2006.01) kind of national protection available): AE, AG, AL, AM, A 61 47/10 (2006.0V) AO, AT, AU, AZ, BA, BB, BG, BH, BR, BW, BY, BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, DO, (21) International Application Number: DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, HN, PCT/US2012/034361 HR, HU, ID, IL, IN, IS, JP, KE, KG, KM, KN, KP, KR, (22) International Filing Date: KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, ME, 20 April 2012 (20.04.2012) MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, OM, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SC, SD, (25) Filing Language: English SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, TR, (26) Publication Language: English TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. (30) Priority Data: (84) Designated States (unless otherwise indicated, for every 61/480,259 28 April 201 1 (28.04.201 1) US kind of regional protection available): ARIPO (BW, GH, GM, KE, LR, LS, MW, MZ, NA, RW, SD, SL, SZ, TZ, (71) Applicant (for all designated States except US): BOARD UG, ZM, ZW), Eurasian (AM, AZ, BY, KG, KZ, MD, RU, OF REGENTS, THE UNIVERSITY OF TEXAS SYS¬ TJ, TM), European (AL, AT, BE, BG, CH, CY, CZ, DE, TEM [US/US]; 201 West 7th St., Austin, TX 78701 (US). -
货号 英文名称 规格 D50673 A66 2.5Mg,5Mg,100Ul(10Mm/DMSO
货号 英文名称 规格 D50673 A66 2.5mg,5mg,100ul(10mM/DMSO) D50690 Acadesine 25mg,50mg,1ml(10mM/DMSO) D50691 Acadesine phosphate 10mg,25mg,1ml(10mM/DMSO) D50580 Acemetacin 500mg D50669 Acetohexamide 25mg,50mg,1ml(10mM/DMSO) D50574 Acrivastine 10mg D50409 Actinomycin D 1mg D50409s Actinomycin D (10mM in DMSO) 100ul D50553 Adavosertib 5mg D50619 Adenosine 5'-monophosphate monohydrate 100mg,250mg,1ml(10mM/DMSO) D50412 Adriamycin 10mg,50mg D50412s Adriamycin (10mM in DMSO) 200ul D50381 AEBSF 10mg,100mg D50381s AEBSF solution (10mM) 100ul D50600 Afloqualone 10mg,50mg,1ml(10mM/DMSO) D50575 Alcaftadine 5mg D50556 Alosetron 2.5mg D50557 Alosetron Hydrochloride 100mg D50675 Alpelisib 5mg,10mg,200ul(10mM/DMSO) D50616 Alvelestat 1mg,2mg,200ul(10mM/DMSO) D50577 Alvimopan dihydrate 1mg,5mg D50581 Amfenac Sodium Hydrate 100mg D50653 AMG 208 2.5mg,200ul(10mM/DMSO) D50645 AMG319 2mg,5mg,100ul(10mM/DMSO) D50547 Amonafide 5mg D50614 Anacetrapib 5mg,10mg,200ul(10mM/DMSO) D50670 Anethole trithione 100mg,500mg,1ml(10mM/DMSO) D50667 Anhydroicaritin 5mg,10mg,1ml(10mM/DMSO) D52001 Anisomycin 5mg,10mg D50578 Antineoplaston A10 1mg,5mg D50530 Antipain dihydrochloride 1mg,5mg D50671 Antipyrine 10mg,50mg,1ml(10mM/DMSO) D50627 Apararenone 5mg,200ul(10mM/DMSO) D50624 Apixaban 10mg,50mg,1ml(10mM/DMSO) D10360 Aprotinin (5400 KIU/mg) 10mg,25mg,100mg D50507 Arbidol hydrochloride 10mg D50508 Arbidol Hydrochloride Hydrate 500mg D50620 ATP 5g,10g,1ml(10mM/DMSO) D50621 ATP disodium salt hydrate 1g,10g,1ml(10mM/H2O) D50635 Baicalein 100mg,1ml(10mM in DMSO) D50400 b-AP15 5mg D50400s b-AP15