Alcohol and Neurotransmitter Interactions
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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. -
Methadone Information Your Safety and the Safety of Everyone
Methadone Information Your Safety and the Safety of Everyone Methadone, when taken as prescribed is safe. Methadone taken by any individual it is NOT prescribed to, can be deadly; and when mixed with other drugs, can be deadly; and in the hands of a child, is most certainly deadly. Why? Because it is often difficult to know what other drugs including prescription medications others are being prescribed including herbal/ natural medications; and because unless you are a pharmacist or an experienced physician who is knowledgeable about METHADONE you truly don’t know what will happen when medications are mixed. Treatment Rules and Regulations clearly state: “It is extremely important that medication (this means METHADONE!) be stored in a VERY secure place away from children once the patient takes it to their home. It is not advisable to store the medication in the refrigerator unless it is in a locked, childproof container.” “Patients are not to give away… (Take) home medications (methadone).”It is clearly stated in Rules and Regulations that “Children cannot be held while dosing.” “…The mixing of chemicals may be harmful or fatal.” This is why Locked boxes must meet stringent criteria; to protect you, and those around you. Methadone is a Central Nervous System (CNS) Depressant. This means that Methadone slows down all your central nervous systems including breathing, heart rate, Some medications should NEVER be taken with methadone because they too are CNS depressants. These include alcohol, Benzodiazepines, Naltrexone, Soma, other Opiates and Barbiturates. These drugs taken together potentiate or add to each other: 1+1 no longer = 2; it equals 5 or more If you are a child or anyone the drug is NOT prescribed for you may not know you are in danger as your heart slows, and your breathing becomes shallower and then you die. -
Distance Learning Program Anatomy of the Human Brain/Sheep Brain Dissection
Distance Learning Program Anatomy of the Human Brain/Sheep Brain Dissection This guide is for middle and high school students participating in AIMS Anatomy of the Human Brain and Sheep Brain Dissections. Programs will be presented by an AIMS Anatomy Specialist. In this activity students will become more familiar with the anatomical structures of the human brain by observing, studying, and examining human specimens. The primary focus is on the anatomy, function, and pathology. Those students participating in Sheep Brain Dissections will have the opportunity to dissect and compare anatomical structures. At the end of this document, you will find anatomical diagrams, vocabulary review, and pre/post tests for your students. The following topics will be covered: 1. The neurons and supporting cells of the nervous system 2. Organization of the nervous system (the central and peripheral nervous systems) 4. Protective coverings of the brain 5. Brain Anatomy, including cerebral hemispheres, cerebellum and brain stem 6. Spinal Cord Anatomy 7. Cranial and spinal nerves Objectives: The student will be able to: 1. Define the selected terms associated with the human brain and spinal cord; 2. Identify the protective structures of the brain; 3. Identify the four lobes of the brain; 4. Explain the correlation between brain surface area, structure and brain function. 5. Discuss common neurological disorders and treatments. 6. Describe the effects of drug and alcohol on the brain. 7. Correctly label a diagram of the human brain National Science Education -
Substance Abuse and Dependence
9 Substance Abuse and Dependence CHAPTER CHAPTER OUTLINE CLASSIFICATION OF SUBSTANCE-RELATED THEORETICAL PERSPECTIVES 310–316 Residential Approaches DISORDERS 291–296 Biological Perspectives Psychodynamic Approaches Substance Abuse and Dependence Learning Perspectives Behavioral Approaches Addiction and Other Forms of Compulsive Cognitive Perspectives Relapse-Prevention Training Behavior Psychodynamic Perspectives SUMMING UP 325–326 Racial and Ethnic Differences in Substance Sociocultural Perspectives Use Disorders TREATMENT OF SUBSTANCE ABUSE Pathways to Drug Dependence AND DEPENDENCE 316–325 DRUGS OF ABUSE 296–310 Biological Approaches Depressants Culturally Sensitive Treatment Stimulants of Alcoholism Hallucinogens Nonprofessional Support Groups TRUTH or FICTION T❑ F❑ Heroin accounts for more deaths “Nothing and Nobody Comes Before than any other drug. (p. 291) T❑ F❑ You cannot be psychologically My Coke” dependent on a drug without also being She had just caught me with cocaine again after I had managed to convince her that physically dependent on it. (p. 295) I hadn’t used in over a month. Of course I had been tooting (snorting) almost every T❑ F❑ More teenagers and young adults die day, but I had managed to cover my tracks a little better than usual. So she said to from alcohol-related motor vehicle accidents me that I was going to have to make a choice—either cocaine or her. Before she than from any other cause. (p. 297) finished the sentence, I knew what was coming, so I told her to think carefully about what she was going to say. It was clear to me that there wasn’t a choice. I love my T❑ F❑ It is safe to let someone who has wife, but I’m not going to choose anything over cocaine. -
Medications to Treat Opioid Use Disorder Research Report
Research Report Revised Junio 2018 Medications to Treat Opioid Use Disorder Research Report Table of Contents Medications to Treat Opioid Use Disorder Research Report Overview How do medications to treat opioid use disorder work? How effective are medications to treat opioid use disorder? What are misconceptions about maintenance treatment? What is the treatment need versus the diversion risk for opioid use disorder treatment? What is the impact of medication for opioid use disorder treatment on HIV/HCV outcomes? How is opioid use disorder treated in the criminal justice system? Is medication to treat opioid use disorder available in the military? What treatment is available for pregnant mothers and their babies? How much does opioid treatment cost? Is naloxone accessible? References Page 1 Medications to Treat Opioid Use Disorder Research Report Discusses effective medications used to treat opioid use disorders: methadone, buprenorphine, and naltrexone. Overview An estimated 1.4 million people in the United States had a substance use disorder related to prescription opioids in 2019.1 However, only a fraction of people with prescription opioid use disorders receive tailored treatment (22 percent in 2019).1 Overdose deaths involving prescription opioids more than quadrupled from 1999 through 2016 followed by significant declines reported in both 2018 and 2019.2,3 Besides overdose, consequences of the opioid crisis include a rising incidence of infants born dependent on opioids because their mothers used these substances during pregnancy4,5 and increased spread of infectious diseases, including HIV and hepatitis C (HCV), as was seen in 2015 in southern Indiana.6 Effective prevention and treatment strategies exist for opioid misuse and use disorder but are highly underutilized across the United States. -
GABA Receptors
D Reviews • BIOTREND Reviews • BIOTREND Reviews • BIOTREND Reviews • BIOTREND Reviews Review No.7 / 1-2011 GABA receptors Wolfgang Froestl , CNS & Chemistry Expert, AC Immune SA, PSE Building B - EPFL, CH-1015 Lausanne, Phone: +41 21 693 91 43, FAX: +41 21 693 91 20, E-mail: [email protected] GABA Activation of the GABA A receptor leads to an influx of chloride GABA ( -aminobutyric acid; Figure 1) is the most important and ions and to a hyperpolarization of the membrane. 16 subunits with γ most abundant inhibitory neurotransmitter in the mammalian molecular weights between 50 and 65 kD have been identified brain 1,2 , where it was first discovered in 1950 3-5 . It is a small achiral so far, 6 subunits, 3 subunits, 3 subunits, and the , , α β γ δ ε θ molecule with molecular weight of 103 g/mol and high water solu - and subunits 8,9 . π bility. At 25°C one gram of water can dissolve 1.3 grams of GABA. 2 Such a hydrophilic molecule (log P = -2.13, PSA = 63.3 Å ) cannot In the meantime all GABA A receptor binding sites have been eluci - cross the blood brain barrier. It is produced in the brain by decarb- dated in great detail. The GABA site is located at the interface oxylation of L-glutamic acid by the enzyme glutamic acid decarb- between and subunits. Benzodiazepines interact with subunit α β oxylase (GAD, EC 4.1.1.15). It is a neutral amino acid with pK = combinations ( ) ( ) , which is the most abundant combi - 1 α1 2 β2 2 γ2 4.23 and pK = 10.43. -
Dynamic Regulation of the GABAA Receptor Function by Redox Mechanisms S
Supplemental material to this article can be found at: http://molpharm.aspetjournals.org/content/suppl/2016/07/20/mol.116.105205.DC1 1521-0111/90/3/326–333$25.00 http://dx.doi.org/10.1124/mol.116.105205 MOLECULAR PHARMACOLOGY Mol Pharmacol 90:326–333, September 2016 Copyright ª 2016 by The American Society for Pharmacology and Experimental Therapeutics MINIREVIEW—A LATIN AMERICAN PERSPECTIVE ON ION CHANNELS Dynamic Regulation of the GABAA Receptor Function by Redox Mechanisms s Daniel J. Calvo and Andrea N. Beltrán González Laboratorio de Neurobiología Celular y Molecular, Instituto de Investigaciones en Ingeniería Genética y Biología Molecular Downloaded from ¨Dr. Héctor N. Torres¨ (INGEBI), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Ciudad Autónoma de Buenos Aires, Argentina (D.J.C., A.N.B.G.) Received May 15, 2016; accepted July 14, 2016 ABSTRACT molpharm.aspetjournals.org Oxidizing and reducing agents, which are currently involved normally present in neurons and glia or are endogenously in cell metabolism and signaling pathways, can regulate fast generated in these cells under physiologic states or during inhibitory neurotransmission mediated by GABA receptors in the oxidative stress (e.g., hydrogen peroxide, superoxide and hy- nervous system. A number of in vitro studies have shown that droxyl radicals, nitric oxide, ascorbic acid, and glutathione), diverse redox compounds, including redox metabolites and induce potentiating or inhibiting actions on different native and reactive oxygen and nitrogen species, modulate phasic and recombinant GABAA receptor subtypes. Based on these results, it tonic responses mediated by neuronal GABAA receptors through is thought that redox signaling might represent a homeostatic both presynaptic and postsynaptic mechanisms. -
Neonatal Clonazepam Administration Induced Long-Lasting Changes in GABAA and GABAB Receptors
International Journal of Molecular Sciences Article Neonatal Clonazepam Administration Induced Long-Lasting Changes in GABAA and GABAB Receptors Hana Kubová 1,* , Zde ˇnkaBendová 2,3 , Simona Moravcová 2,3 , Dominika Paˇcesová 2,3, Luisa Rocha 4 and Pavel Mareš 1 1 Institute of Physiology, Academy of Sciences of the Czech Republic, 14220 Prague, Czech Republic; [email protected] 2 Faculty of Science, Charles University, 12800 Prague, Czech Republic; [email protected] (Z.B.); [email protected] (S.M.); [email protected] (D.P.) 3 National Institute of Mental Health, 25067 Klecany, Czech Republic 4 Pharmacobiology Department, Center of Research and Advanced Studies, Mexico City 14330, Mexico; [email protected] * Correspondence: [email protected]; Tel.: +420-2-4106-2565 Received: 31 March 2020; Accepted: 28 April 2020; Published: 30 April 2020 Abstract: Benzodiazepines (BZDs) are widely used in patients of all ages. Unlike adults, neonatal animals treated with BZDs exhibit a variety of behavioral deficits later in life; however, the mechanisms underlying these deficits are poorly understood. This study aims to examine whether administration of clonazepam (CZP; 1 mg/kg/day) in 7–11-day-old rats affects Gama aminobutyric acid (GABA)ergic receptors in both the short and long terms. Using RT-PCR and quantitative autoradiography, we examined the expression of the selected GABAA receptor subunits (α1, α2, α4, γ2, and δ) and the GABAB B2 subunit, and GABAA, benzodiazepine, and GABAB receptor binding 48 h, 1 week, and 2 months after treatment discontinuation. Within one week after CZP cessation, the expression of the α2 subunit was upregulated, whereas that of the δ subunit was downregulated in both the hippocampus and cortex. -
Targeting Glycine Reuptake in Alcohol Seeking and Relapse
JPET Fast Forward. Published on January 24, 2018 as DOI: 10.1124/jpet.117.244822 This article has not been copyedited and formatted. The final version may differ from this version. TITLE PAGE Targeting Glycine Reuptake in Alcohol Seeking and Relapse Valentina Vengeliene, Martin Roßmanith, Tatiane T. Takahashi, Daniela Alberati, Berthold Behl, Anton Bespalov, Rainer Spanagel Downloaded from The primary laboratory of origin: Institute of Psychopharmacology, Central Institute of jpet.aspetjournals.org Mental Health, Faculty of Medicine Mannheim, Heidelberg University, Germany; at ASPET Journals on September 30, 2021 VV, MR, TTT, RS: Institute of Psychopharmacology, Central Institute of Mental Health, Faculty of Medicine Mannheim, Heidelberg University, Germany; DA: Roche Pharma Research and Early Development, Neuroscience, Ophthalmology and Rare Diseases, Roche Innovation Center Basel, CH-4070 Basel, Switzerland; BB, AB: Department of Neuroscience Research, AbbVie Deutschland GmbH & Co. KG, Ludwigshafen, Germany; AB: Department of Psychopharmacology, Pavlov Medical University, St Petersburg, Russia JPET #244822 JPET Fast Forward. Published on January 24, 2018 as DOI: 10.1124/jpet.117.244822 This article has not been copyedited and formatted. The final version may differ from this version. RUNNING TITLE GlyT1 in Alcohol Seeking and Relapse Corresponding author with complete address: Valentina Vengeliene, Institute of Psychopharmacology, Central Institute of Mental Health (CIMH), J5, 68159 Mannheim, Germany Email: [email protected], phone: +49-621-17036261; fax: +49-621- Downloaded from 17036255 jpet.aspetjournals.org The number of text pages: 33 Number of tables: 0 Number of figures: 6 Number of references: 44 at ASPET Journals on September 30, 2021 Number of words in the Abstract: 153 Number of words in the Introduction: 729 Number of words in the Discussion: 999 A recommended section assignment to guide the listing in the table of content: Drug Discovery and Translational Medicine 2 JPET #244822 JPET Fast Forward. -
Understanding Addiction, Helping Clients and Colleagues
ALABAMA LAWYER ASSISTANCE PROGRAM Understanding Addiction, Helping Clients and Colleagues By Jeanne Marie Leslie rugs change the brain–they according to the American Bar change its structure and how it Association, is 15 to 18 percent.3 D works.1 Many of these changes Lawyers rank high in the incidences of are responsible for the behaviors we see depression compared to other professions in individuals addicted to drugs. and a disproportionate number of Neuroscience has made significant lawyers commit suicide;4 in Alabama advances in our ability to identify and there are about a dozen lawyer suicides understand the mechanisms involved in every year. And these are only the ones the addicted brain. These advancements about which we know. Many lawyers, clearly confirm what many in the addic- including some you know, may be strug- tion medicine field have known for some gling with an addiction or mental health time: the obsession and compulsion to problem when help is readily available use drugs in the addicted brain is instinc- through ALAP. tual and paramount to survival.2 Ignorance and stigma have contributed Addiction Facts to the confusion, moral judgments and Dr. Nora D. Volkow, director of the poor understanding of this destructive National Institute of Drug Abuse and often fatal disease. Our courts are (NIDA), explains how the neuro-chemi- overwhelmed by the behaviors, criminal cal mechanisms of drug abuse catalyze and civil, associated with addiction. and accelerate the onset addiction: Therefore, understanding addiction is “Recognizing drug addiction as a chron- essential for lawyers. Lawyers are in ic, relapsing disease characterized by com- unique positions to initiate change, to pulsive drug seeking and use is critical to advocate for medical treatment over tra- being able to identify and help those who ditional sanctions and to refer individuals have it. -
Molecular Biology of Neuronal Voltage-Gated Calcium Channels
EXPERIMENTAL and MOLECULAR MEDICINE, Vol. 30, No 3, 123-130, September 1998 Molecular biology of neuronal voltage-gated calcium channels Hemin Chin and is capable of directing expression of calcium channel activity in heterologous expression systems. In the central Genetics Research Branch, Division of Basic and Clinical Neuroscience Research, nervous system (CNS), VGCCs are expressed by five National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, distinct a1 subunit genes (α1A, α1B, α1C, α1D and α1E), U.S.A. which exhibit further variations due to alternative splicing of the primary RNA transcripts. The α1C and, α1D su b u n i t Accepted 3 August 1998 genes encode dihydropyridine (DHP)-sensitive L-type channels, while the three other α1 subunit genes (α1A, α1B and α1E) give rise to DHP-insensitive P/Q-, N- and R-type channels, respectively. The α2 and δ s u b u n i t proteins are produced by proteolytic cleavage of a larger precursor produced by the single α2-δ gene (Table 1). Introduction Three alternatively spliced variants of the α2 subunit are expressed in a tissue-specific manner. Two variants Calcium ions are important intracellular messengers have been isolated from the brain and skeletal muscle mediating a number of neuronal functions including neuro- (Kim et al., 1992; Williams et al., 1992), and a distinct transmitter release, neurosecretion, neuronal excitation, third splice variant which is expressed in glial cells has survival of eurons, and regulation of gene expression. been recently identified (Puro et al., 1996). In addition to The entry of calcium across the plasmamembrane in the gene encoding the skeletal muscle β subunit, three response to membrane depolarization or activation of 1 other β subunit genes (β2, β3 and β4) have been isolated neurotransmitter receptors represents a major pathway thus far. -
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.