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Biological Mechanisms and Perinatal Exposure to Drugs

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Biological Mechanisms and Perinatal Exposure to Drugs National Institute on Drug Abuse RESEARCH MONOGRAPH SERIES Biological Mechanisms and Perinatal Exposure to Drugs U.S. Department of Health and Human1 Services 5• Public Health 8Service • National Institutes of Health Biological Mechanisms and Perinatal Exposure to Abused Drugs Editor: Pushpa V. Thadani, Ph.D. NIDA Research Monograph 158 1995 U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES Public Health Service National Institutes of Health National Institute on Drug Abuse Division of Basic Research 5600 Fishers Lane Rockville, MD 20857 ACKNOWLEDGMENT This monograph is based on the papers from a technical review on “Biological Mechanisms and Perinatal Exposure to Abused Drugs” held on May 25-26, 1994. The review meeting was sponsored by the National Institute on Drug Abuse. COPYRIGHT STATUS The National Institute on Drug Abuse has obtained permission from the copyright holders to reproduce certain previously published material as noted in the text. Further reproduction of this copyrighted material is permitted only as part of a reprinting of the entire publication or chapter. For any other use, the copyright holder’s permission is required. All other material in this volume except quoted passages from copyrighted sources is in the public domain and may be used or reproduced without permission from the Institute or the authors. Citation of the source is appreciated. Opinions expressed in this volume are those of the authors and do not necessarily reflect the opinions or official policy of the National Institute on Drug Abuse or any other part of the U.S. Department of Health and Human Services. The U.S. Government does not endorse or favor any specific commercial product or company. Trade, proprietary, or company names appearing in this publication are used only because they are considered essential in the context of the studies reported herein. National lnstitute on Drug Abuse NIH Publication No. 95-4024 Printed 1995 NIDA Research Monographs are indexed in the Index Medicus. They are selectively included in the coverage of American Statistics Index, BioSciences Information Service, Chemical Abstracts, Current Contents, Psychological Abstracts, and Psychopharmacology Abstracts. ii Contents Preface . 1 Pushpa V. Thadani Species-, Gender-, and Pregnancy-Related Differences in the Pharmacokinetics and Pharmacodynamics of Cocaine . 2 Hisayo O. Morishima and Robert A. Whittington Effects of Morphine and Cocaine on Breathing Control in Neonatal Animals: A Minireview . , . 22 George D. Olsen and Laine J. Murphey Cardiovascular Effects of Cocaine in Infant and Juvenile Piglets . 40 Frank M. Scalzo and Lora J. Burge Effects of Cocaine on Fetal Brain Metabolism and Behavioral State in the Sheep Model . 58 David J. Burchfield Fetal Cerebral Vascular Effects of Cocaine Exposure . 67 Michael D. Schreiber Effects of Prenatal Morphine and Cocaine on Postnatal Behaviors and Brain Neurotransmitters . 88 Ilona Vathy Prenatal Cocaine Produces Biochemical and Functional Changes in Brain Serotonin Systems in Rat Progeny . 115 George Battaglia, Theresa M. Cabrera, and Louis D. Van de Kar Ontogeny of Methamphetamine-Induced Neurotoxicity in the Rat Model . 149 Charles V. Vorhees and Cunfeng Pu Ontogeny of Nociception and Antinociception . 172 Gordon A. Barr Perinatal Benzodiazepine Modulation of GABAA Receptor Function: Influence on Adaptive Responses . 202 Carol K. Kellogg iii Preface Pushpa V. Thadani On May 25 and 26, 1994, the National Institute on Drug Abuse held a Technical Review entitled “Biological Mechanisms and Perinatal Exposure to Abused Drugs” to review and discuss state-of-the art findings in this important area, to identify needs and future research opportunities, and to promote interdisciplinary communications. Biomedical researchers discussed the recent advances in the development of innovative animal models and their utilization to monitor drug-induced changes in fetal and neonatal physiological systems under controlled conditions. They also discussed the biological mechanisms responsible for the transient or long-term effects of perinatal exposure to abused substance(s) or the lack of these effects and the relevance of these experimental findings in different animal species to clinical reports/observations. The methodological and paradigmatic issues that need to be considered and integrated in future experimental study designs were also discussed. A conference report summarizing the major findings and the methodological and experimental issues discussed at the meeting (and which lists all conference participants) was published in the March 1995 issue of “Synapse” (Thadani 1995). This monograph consists of the papers presented at the Technical Review meeting. AUTHOR Pushpa V. Thadani, Ph.D. Pharmacologist/Program Officer Division of Basic Research National Institute on Drug Abuse Parklawn Building, Room 10A-19 5600 Fishers Lane Rockville, MD 20857 REFERENCES Thadani, P.V. Conference Report: Biological mechanisms and perinatal exposure to abused drugs. Synapse 19:228-232, 1995. 1 Species-, Gender-, and Pregnancy-Related Differences in the Pharmacokinetics and Pharmacodynamics of Cocaine Hisayo O. Morishima and Robert A. Whittington INTRODUCTION A great number of studies in cocaine research have expanded researchers’ basic knowledge of the pharmacologic and physiologic effects of cocaine in humans and animals. This chapter will discuss species-, gender-, and pregnancy-related differences in cocaine disposition and how these biological factors may modify the effects of cocaine. The effects of route and mode of drug administration that may likewise influence the pharmacokinetics, pharmacodynamics, and possibly the toxicity of cocaine will also be examined. It is not the authors’ purpose to provide a complete review of the effects of cocaine, but rather to illustrate the importance of these factors in cocaine-associated adverse effects. More specific information regarding perinatal cocaine exposure on the fetus and newborn has been reviewed in other chapters of this research monograph. COCAINE METABOLISM, PHARMACOKINETICS, AND PHARMACODYNAMICS The metabolism of cocaine involves several different pathways (figure 1). In humans, cocaine has an elimination half-life from 42 to 82 minutes (Barnett et al. 1981) and is metabolized rapidly by three major pathways with the resultant formation of two primary metabolites: ecgonine methyl ester and benzoylecgonine. The metabolite ecgonine methyl ester is thought to be formed by hepatic as well as by plasma esterases, while formation of benzoylecgonine occurs by spontaneous, nonenzymatic hydrolysis particularly at physiological pH (Ambre et al. 1991; Stewart et al. 1979; Van Dette and Comish 1989). About 1 to 2 percent of cocaine is biotransferred to a pharmacologically active metabolite, norcocaine, by an N-demethylation reaction catalyzed 2 FIGURE 1. Metabolic pathways of cocaine. by hepatic microsomal enzymes. These enzymes play an important role in drug-induced toxicity. It is suggested that the cocaine-induced hepatotoxicity seen in animals may be due to norcocaine and its metabolite N-hydroxy-norcocaine (Hawks et al. 1975; Nayak et al. 1976). The authors’ comparative toxicity study of norcocaine and cocaine in rats indicates that the lethal dose of norcocaine is smaller. In addition, massive cerebral and hepatic hemorrhages were commonly observed in animals that died from norcocaine (Morishima et al., unpublished data). Data also show that human plasma norcocaine concentrations measured during concomitant alcohol and cocaine use are 2 times higher than those measured in the presence of cocaine alone (Farre et al. 1993). At present, it is unclear whether these increased norcocaine concentrations are a result of alcohol-related changes in either microsomal enzymes or nonspecific esterases. In humans, cocaine metabolites are excreted almost entirely in urine with an elimination half-life of 4.2 hours for ecgonine methyl ester and 5.1 hours for benzoylecgonine (Ambre et al. 1984, 1988; Hamilton et al. 1977; Inaba et al. 1978; Jeffcoat et al. 1989; Jindal et al. 1978; Smith 1984). 3 The pharmacological and toxic effects of cocaine may be potentiated by combined ethanol use. Cocaine in the presence of alcohol abuse is biotransformed into ethyl-benzoylecgonine (cocaethylene) by a nonspecific liver carboxylesterase (Bosron et al. 1991; Boyer and Petersen 1991; Dean et al. 199 1; Elsworth et al. 1990). Concentrations of cocaethylene often exceed the concentration of cocaine in blood, brain, liver, and urine (Hear-n et al. 1991; Jatlow et al. 1991). Moreover, in the brain cocaethylene may be a much more selective dopamine agonist than cocaine (Jatlow 1993). Findings also indicate that cocaine and cocaethylene induce similar psychomotor stimulant effects in mice (Katz et al. 1992). On the other hand, as shown in figure 2, data in rats demonstrate that cocaethylene is more potent than cocaine in producing central nervous system (CNS) and cardiovascular manifestations (Whittington et al. 1995). Furthermore, unlike cocaine, there were no gender- or pregnancy-related differences in the observed cocaethylene toxicity. FIGURE 2. Comparison of the mean (±SE) dose of cocaethylene (CE) and cocaine (COC) necessary to produce major toxic manifestations in awake male, nonpregnant female, and pregnant rats. CE or COC was infused intravenously at a rate of 2 mg/kg/min. 4 SPECIES-RELATED DIFFERENCES IN DISPOSITION OF COCAINE Recent findings show large species-related differences in the pharmacokinetics of cocaine.
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