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  1. Article ; Online: Animal models of nicotine withdrawal: intracranial self-stimulation and somatic signs of withdrawal.

    Bauzo, Rayna M / Bruijnzeel, Adrie W

    Methods in molecular biology (Clifton, N.J.)

    2012  Volume 829, Page(s) 257–268

    Abstract: Tobacco addiction is one of the leading causes of preventable death worldwide. Despite the negative health outcomes of tobacco use and a desire to quit, there is a low success rate of maintaining abstinence. Nicotine, the main psychoactive component of ... ...

    Abstract Tobacco addiction is one of the leading causes of preventable death worldwide. Despite the negative health outcomes of tobacco use and a desire to quit, there is a low success rate of maintaining abstinence. Nicotine, the main psychoactive component of tobacco smoke, is mildly rewarding and maintains smoking behavior. Nicotine withdrawal induces somatic symptoms that may contribute to smoking behavior. However, it has been hypothesized that the negative affective signs are of greater motivational significance in contributing to relapse and continued tobacco use than the somatic symptoms of nicotine withdrawal (Markou and Koob (Eds.) Intracranial self-stimulation thresholds as a measure of reward, Vol. 2, Oxford University Press, New York, 1993; Koob et al. Semin Neurosci 5: 351-358, 1993). Intracranial self-stimulation (ICSS) has been established as a method to assess the bivalent properties of nicotine exposure and withdrawal from acute and chronic nicotine administration. Thus, ICSS provides a means to measure the negative affective aspects of nicotine withdrawal in animal models and may contribute to the understanding of the neurobiological bases of nicotine dependence and the development of effective treatment strategies to facilitate nicotine abstinence.
    MeSH term(s) Animals ; Behavior, Animal ; Deep Brain Stimulation/methods ; Male ; Models, Animal ; Nicotine/administration & dosage ; Nicotine/adverse effects ; Rats ; Self Administration ; Smoking ; Substance Withdrawal Syndrome ; Substance-Related Disorders ; Tobacco Use Disorder
    Chemical Substances Nicotine (6M3C89ZY6R)
    Language English
    Publishing date 2012
    Publishing country United States
    Document type Journal Article
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-61779-458-2_16
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  2. Article ; Online: The cystine-glutamate transporter enhancer N-acetyl-L-cysteine attenuates cocaine-induced changes in striatal dopamine but not self-administration in squirrel monkeys.

    Bauzo, Rayna M / Kimmel, Heather L / Howell, Leonard L

    Pharmacology, biochemistry, and behavior

    2011  Volume 101, Issue 2, Page(s) 288–296

    Abstract: Extrasynaptic glutamate has been shown to regulate dopamine function in the mesocorticolimbic pathway, which plays an important role in the behavioral pharmacology of psychostimulants. Basal levels of glutamate are primarily regulated by the cystine- ... ...

    Abstract Extrasynaptic glutamate has been shown to regulate dopamine function in the mesocorticolimbic pathway, which plays an important role in the behavioral pharmacology of psychostimulants. Basal levels of glutamate are primarily regulated by the cystine-glutamate transporter and provide glutamatergic tone on extrasynaptic glutamate receptors. The present study examined the effects of a cystine-glutamate transporter enhancer on the neurochemical and behavioral effects of cocaine and amphetamine in nonhuman primates. It was hypothesized that augmenting extrasynaptic glutamate release with N-acetyl-L-cysteine (NAC), a cystine prodrug, would attenuate cocaine- or amphetamine-induced increases in extracellular dopamine and their corresponding behavioral-stimulant and reinforcing effects. In vivo microdialysis was used to evaluate cocaine-induced changes in extracellular dopamine (DA) in the caudate nucleus (n=3). NAC significantly attenuated cocaine-induced increases in dopamine but had inconsistent effects on amphetamine-induced increases in dopamine (n=4). Separate groups of subjects were either trained on a fixed-interval schedule of stimulus termination (n=6) or on a second-order schedule of self-administration (n=5) to characterize the behavioral-stimulant and reinforcing effects of psychostimulants, respectively. Systemic administration of NAC did not alter the behavioral-stimulant effects of either cocaine or amphetamine. Furthermore, cocaine self-administration and reinstatement of previously extinguished cocaine self-administration were not altered by pretreatment with NAC. Hence, drug interactions on caudate neurochemistry in vivo were not reflected in behavioral measures in squirrel monkeys. The present results in nonhuman primates do not support the use of NAC as a pharmacotherapy for cocaine abuse, although rodent and clinical studies suggest otherwise.
    MeSH term(s) Acetylcysteine/pharmacology ; Acetylcysteine/therapeutic use ; Amino Acid Transport System y+/agonists ; Amino Acid Transport System y+/metabolism ; Animals ; Behavior, Addictive/drug therapy ; Behavior, Addictive/metabolism ; Cocaine/administration & dosage ; Cocaine/antagonists & inhibitors ; Corpus Striatum/drug effects ; Corpus Striatum/metabolism ; Dopamine/metabolism ; Male ; Saimiri ; Self Administration
    Chemical Substances Amino Acid Transport System y+ ; Cocaine (I5Y540LHVR) ; Dopamine (VTD58H1Z2X) ; Acetylcysteine (WYQ7N0BPYC)
    Language English
    Publishing date 2011-12-31
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 191042-5
    ISSN 1873-5177 ; 0091-3057
    ISSN (online) 1873-5177
    ISSN 0091-3057
    DOI 10.1016/j.pbb.2011.12.018
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  3. Article ; Online: Interactions between the mGluR2/3 agonist, LY379268, and cocaine on in vivo neurochemistry and behavior in squirrel monkeys.

    Bauzo, Rayna M / Kimmel, Heather L / Howell, Leonard L

    Pharmacology, biochemistry, and behavior

    2009  Volume 94, Issue 1, Page(s) 204–210

    Abstract: Recent evidence indicates that group II metabotropic glutamate receptors (mGluR2 and mGluR3) may play a role in the pathology of cocaine addiction. The purpose of the current study was to determine the effects of the mGluR2/3 agonist, LY379268, on ... ...

    Abstract Recent evidence indicates that group II metabotropic glutamate receptors (mGluR2 and mGluR3) may play a role in the pathology of cocaine addiction. The purpose of the current study was to determine the effects of the mGluR2/3 agonist, LY379268, on cocaine-induced changes in DA neurochemistry in nonhuman primates. Furthermore, the current study aimed to determine if changes in DA neurochemistry would correlate with LY379268-induced changes in the behavioral effects of cocaine. In vivo microdialysis was conducted in conscious squirrel monkeys (n=4) in order to monitor cocaine-induced changes in extracellular DA in the caudate nucleus. Separate groups of subjects were trained on a fixed-interval schedule of stimulus termination (n=4) or a second-order schedule of cocaine self-administration (n=5) to characterize the behavioral-stimulant and reinforcing effects, respectively. LY379268 significantly attenuated cocaine-induced increases in DA. LY379268 also significantly attenuated cocaine-induced behavioral-stimulant effects following a short pretreatment time, but not following a longer pretreatment time. Cocaine self-administration was significantly attenuated but only at an intermediate pretreatment dose of LY379268. Moreover, reinstatement of previously extinguished cocaine self-administration was not significantly attenuated by LY379268. Hence, drug interactions on neurochemistry did not correlate well with behavioral measures.
    MeSH term(s) Amino Acids/administration & dosage ; Amino Acids/pharmacology ; Animals ; Behavior, Animal/drug effects ; Bridged Bicyclo Compounds, Heterocyclic/administration & dosage ; Bridged Bicyclo Compounds, Heterocyclic/pharmacology ; Caudate Nucleus/drug effects ; Caudate Nucleus/metabolism ; Cocaine/administration & dosage ; Cocaine/pharmacology ; Conditioning, Psychological/drug effects ; Dopamine/metabolism ; Dopamine Uptake Inhibitors/administration & dosage ; Dopamine Uptake Inhibitors/pharmacology ; Dose-Response Relationship, Drug ; Drug Interactions ; Excitatory Amino Acid Agonists/administration & dosage ; Excitatory Amino Acid Agonists/pharmacology ; Extinction, Psychological/drug effects ; Infusions, Intravenous ; Injections, Intramuscular ; Male ; Microdialysis ; Reaction Time/drug effects ; Receptors, Metabotropic Glutamate/agonists ; Reinforcement Schedule ; Saimiri ; Self Administration ; Time Factors
    Chemical Substances Amino Acids ; Bridged Bicyclo Compounds, Heterocyclic ; Dopamine Uptake Inhibitors ; Excitatory Amino Acid Agonists ; LY 379268 ; Receptors, Metabotropic Glutamate ; Cocaine (I5Y540LHVR) ; Dopamine (VTD58H1Z2X)
    Language English
    Publishing date 2009-08-22
    Publishing country United States
    Document type Journal Article
    ZDB-ID 191042-5
    ISSN 1873-5177 ; 0091-3057
    ISSN (online) 1873-5177
    ISSN 0091-3057
    DOI 10.1016/j.pbb.2009.08.011
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  4. Article ; Online: A critical role for the melanocortin 4 receptor in stress-induced relapse to nicotine seeking in rats.

    Qi, Xiaoli / Yamada, Hidetaka / Corrie, Lu W / Ji, Yue / Bauzo, Rayna M / Alexander, Jon C / Bruijnzeel, Adrie W

    Addiction biology

    2015  Volume 20, Issue 2, Page(s) 324–335

    Abstract: Tobacco addiction is characterized by a lack of control over smoking and relapse after periods of abstinence. Smoking cessation leads to a dysphoric state that contributes to relapse to smoking. After the acute withdrawal phase, exposure to stressors ... ...

    Abstract Tobacco addiction is characterized by a lack of control over smoking and relapse after periods of abstinence. Smoking cessation leads to a dysphoric state that contributes to relapse to smoking. After the acute withdrawal phase, exposure to stressors increases the risk for relapse. Blockade of melanocortin 4 (MC4 ) receptors has anxiolytic and antidepressant-like effects in animal models. The aim of these studies was to investigate the role of MC4 receptors in the dysphoria associated with nicotine withdrawal and stress-induced reinstatement of nicotine seeking. To study stress-induced reinstatement, rats self-administered nicotine for 16 days and then nicotine seeking was extinguished by substituting saline for nicotine. Nicotine seeking was reinstated by intermittent footshock stress. The intracranial self-stimulation (ICSS) procedure was used to assess the negative mood state associated with nicotine withdrawal. Elevations in the ICSS thresholds are indicative of a dysphoric state. The selective MC4 receptor antagonists HS014 and HS024 prevented stress-induced reinstatement of extinguished nicotine seeking. Drug doses that prevented stress-induced relapse did not affect responding for food pellets, which indicates that the drugs did not induce sedation or motor impairments. In the ICSS experiments, the nicotinic acetylcholine receptor antagonist mecamylamine elevated the ICSS thresholds of the nicotine-dependent rats. Pre-treatment with HS014 or HS024 did not prevent the elevations in ICSS thresholds. These studies indicate that MC4 receptors play a critical role in stress-induced reinstatement of nicotine seeking, but these receptors may not play a role in the dysphoria associated with acute nicotine withdrawal.
    MeSH term(s) Animals ; Drug-Seeking Behavior/drug effects ; Drug-Seeking Behavior/physiology ; Nicotine/administration & dosage ; Nicotine/adverse effects ; Nicotinic Agonists/administration & dosage ; Nicotinic Agonists/adverse effects ; Peptides, Cyclic/pharmacology ; Rats ; Receptor, Melanocortin, Type 4/antagonists & inhibitors ; Receptor, Melanocortin, Type 4/metabolism ; Recurrence ; Stress, Psychological/metabolism ; Substance Withdrawal Syndrome/etiology ; Substance Withdrawal Syndrome/metabolism ; Tobacco Use Disorder/metabolism
    Chemical Substances HS 024 ; HS014 cyclic peptide ; Nicotinic Agonists ; Peptides, Cyclic ; Receptor, Melanocortin, Type 4 ; Nicotine (6M3C89ZY6R)
    Language English
    Publishing date 2015-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1324314-7
    ISSN 1369-1600 ; 1355-6215
    ISSN (online) 1369-1600
    ISSN 1355-6215
    DOI 10.1111/adb.12129
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    Zs.A 4586: Show issues Location:
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  5. Article ; Online: Effects of histamine H(3) receptor activation on the behavioral-stimulant effects of methamphetamine and cocaine in mice and squirrel monkeys.

    Banks, Matthew L / Manvich, Daniel F / Bauzo, Rayna M / Howell, Leonard L

    Pharmacology

    2009  Volume 83, Issue 3, Page(s) 164–169

    Abstract: Background: Cocaine and methamphetamine (METH) are two commonly abused drugs that have behavioral-stimulant properties. These stimulant effects are partially mediated by the dopaminergic system. Recent evidence has suggested that the histamine H(3) ... ...

    Abstract Background: Cocaine and methamphetamine (METH) are two commonly abused drugs that have behavioral-stimulant properties. These stimulant effects are partially mediated by the dopaminergic system. Recent evidence has suggested that the histamine H(3) receptor (H(3)R) may modulate the release of dopamine induced by METH. The aim of the present study was to examine the role of H(3)R in the behavioral-stimulant effects of cocaine and METH in mice and monkeys.
    Methods: Nonhabituated, experimentally naïve mice (n = 5-6) were pretreated with the H(3)R agonist imetit 30 min before METH or cocaine, and activity was measured for 90 min. The behavioral-stimulant effects of METH and cocaine were also studied in squirrel monkeys (n = 3) under a fixed-interval schedule of stimulus termination. Monkeys were pretreated with imetit 30 min before the peak behavioral-stimulant doses of METH or cocaine derived from individual subjects.
    Results: Pretreatment with imetit did not affect basal activity in mice. Imetit significantly attenuated the behavioral-stimulant effects of METH, but not cocaine. In monkeys, no dose of imetit tested significantly altered the behavioral-stimulant effects of METH or cocaine.
    Conclusion: These results suggest a role of H(3)R in the behavioral-stimulant effects of METH, but not cocaine, in mice and no role in monkeys.
    MeSH term(s) Animals ; Behavior, Animal/drug effects ; Central Nervous System Stimulants/pharmacology ; Cocaine/pharmacology ; Conditioning, Operant/drug effects ; Dose-Response Relationship, Drug ; Drug Interactions ; Histamine Agonists/pharmacology ; Imidazoles/pharmacology ; Male ; Methamphetamine/pharmacology ; Mice ; Motor Activity/drug effects ; Receptors, Histamine H3/physiology ; Reinforcement Schedule ; Saimiri ; Thiourea/analogs & derivatives ; Thiourea/pharmacology
    Chemical Substances Central Nervous System Stimulants ; Histamine Agonists ; Imidazoles ; Receptors, Histamine H3 ; Methamphetamine (44RAL3456C) ; imetit (677MJ4VPZC) ; Thiourea (GYV9AM2QAG) ; Cocaine (I5Y540LHVR)
    Language English
    Publishing date 2009-01-15
    Publishing country Switzerland
    Document type Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 206671-3
    ISSN 1423-0313 ; 0031-7012
    ISSN (online) 1423-0313
    ISSN 0031-7012
    DOI 10.1159/000191473
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  6. Article ; Online: Repeated pre-exposure to tobacco smoke potentiates subsequent locomotor responses to nicotine and tobacco smoke but not amphetamine in adult rats.

    Bruijnzeel, Adrie W / Rodrick, Gene / Singh, Rajendra P / Derendorf, Hartmut / Bauzo, Rayna M

    Pharmacology, biochemistry, and behavior

    2011  Volume 100, Issue 1, Page(s) 109–118

    Abstract: These studies investigated if pre-exposure to tobacco smoke affects the locomotor response to tobacco smoke, nicotine, and amphetamine in adult rats. The rats were habituated to an open field for 3-4 days and then exposed to tobacco smoke for 2h/day for ... ...

    Abstract These studies investigated if pre-exposure to tobacco smoke affects the locomotor response to tobacco smoke, nicotine, and amphetamine in adult rats. The rats were habituated to an open field for 3-4 days and then exposed to tobacco smoke for 2h/day for 13-14 days. The effect of exposure to tobacco smoke on locomotor activity was investigated after 1, 7, and 14 days of smoke exposure and after one 2-hour exposure session that followed a 3-week off period. The effects of tobacco smoke on the locomotor responses to nicotine (0.04 and 0.4 mg/kg, base) and amphetamine (0.1 and 0.5mg/kg) were investigated on day 14, one day after the last smoke exposure session. The locomotor response to tobacco smoke was increased after 7 and 14 days of smoke exposure and after one exposure session after the 3-week off-period. The acute administration of the high dose of nicotine (0.4 mg/kg) led to a brief period of hypoactivity that was followed by a period of hyperactivity. Pre-exposure to tobacco smoke attenuated the nicotine-induced hypoactivity and potentiated the nicotine-induced hyperactivity. The low dose of nicotine (0.04 mg/kg) did not affect locomotor activity in the control rats but increased the total distance traveled in the tobacco smoke exposed rats. Exposure to tobacco smoke did not affect the locomotor response to amphetamine. These findings indicate that exposure to tobacco smoke leads to tolerance to the depressant effects of nicotine and potentiates the stimulant effects of nicotine and tobacco smoke.
    MeSH term(s) Age Factors ; Amphetamine/administration & dosage ; Animals ; Dose-Response Relationship, Drug ; Drug Administration Schedule ; Drug Synergism ; Inhalation Exposure/adverse effects ; Male ; Motor Activity/drug effects ; Motor Activity/physiology ; Nicotine/administration & dosage ; Rats ; Rats, Wistar ; Smoking/adverse effects ; Nicotiana
    Chemical Substances Nicotine (6M3C89ZY6R) ; Amphetamine (CK833KGX7E)
    Language English
    Publishing date 2011-08-17
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 191042-5
    ISSN 1873-5177 ; 0091-3057
    ISSN (online) 1873-5177
    ISSN 0091-3057
    DOI 10.1016/j.pbb.2011.08.005
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  7. Article ; Online: Methods in tobacco abuse: proteomic changes following second-hand smoke exposure.

    Guingab-Cagmat, Joy / Bauzo, Rayna M / Bruijnzeel, Adrie W / Wang, Kevin K / Gold, Mark S / Kobeissy, Firas H

    Methods in molecular biology (Clifton, N.J.)

    2012  Volume 829, Page(s) 329–348

    Abstract: Smoking is one of the leading preventable causes of disease, disability, and death in the USA and leads to more than 400,000 preventable deaths per year. Nicotine is the major alkaloid present in tobacco smoke, and many of the negative effects of smoking ...

    Abstract Smoking is one of the leading preventable causes of disease, disability, and death in the USA and leads to more than 400,000 preventable deaths per year. Nicotine is the major alkaloid present in tobacco smoke, and many of the negative effects of smoking are attributed to nicotine. Nicotine is not only the addictive component of tobacco smoke, but also highly associated with carcinogenesis and induces oxidative stress. Furthermore, the administration of nicotine via subcutaneous mini-osmotic pumps or by injection is an established method in preclinical studies for this area of research. Thus, preclinical research on the negative effects of tobacco smoke and tobacco addiction has focused primarily on the effects of nicotine. However, there are over 4,500 components found in tobacco smoke, many of which are highly toxic. Other components may also contribute to the addictive properties of tobacco smoke. Furthermore, the negative effects of tobacco smoke are not isolated to the smoker but can have negative effects to those exposed to the secondhand smoke (SHS) stream. SHS exposure is the third leading cause of preventable death. Approximately 38,000 deaths per year are attributed to SHS exposure in the USA. SHS exposure increases the risk of heart disease by approximately 30% and is associated with increased risk of stroke, cancer, type II diabetes, as well as pulmonary disease. Thus, methods of administering tobacco smoke in a controlled environment will further our understanding of tobacco addiction and the role tobacco smoke in other disease states. Moreover, combining smoke exposure with proteomics can lead to the discovery of biomarkers that can be potentially useful tools in screening, early diagnosis, prevention, and treatment of diseases caused by SHS.
    MeSH term(s) Animals ; Environmental Exposure ; Male ; Models, Animal ; Nicotine/administration & dosage ; Nicotine/adverse effects ; Oxidative Stress ; Proteomics/methods ; Rats ; Rats, Sprague-Dawley ; Smoke/adverse effects ; Smoking ; Tandem Mass Spectrometry/methods ; Tobacco Smoke Pollution/adverse effects ; Tobacco Use Disorder/mortality
    Chemical Substances Smoke ; Tobacco Smoke Pollution ; Nicotine (6M3C89ZY6R)
    Language English
    Publishing date 2012
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-61779-458-2_22
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  8. Article ; Online: Tobacco smoke diminishes neurogenesis and promotes gliogenesis in the dentate gyrus of adolescent rats.

    Bruijnzeel, Adrie W / Bauzo, Rayna M / Munikoti, Vikram / Rodrick, Gene B / Yamada, Hidetaka / Fornal, Casimir A / Ormerod, Brandi K / Jacobs, Barry L

    Brain research

    2011  Volume 1413, Page(s) 32–42

    Abstract: Brain disorders and environmental factors can affect neurogenesis and gliogenesis in the hippocampus. These studies investigated the effects of chronic exposure to tobacco smoke on progenitor cell proliferation and the survival and phenotype of new cells ...

    Abstract Brain disorders and environmental factors can affect neurogenesis and gliogenesis in the hippocampus. These studies investigated the effects of chronic exposure to tobacco smoke on progenitor cell proliferation and the survival and phenotype of new cells in the dentate gyrus of adolescent rats. The rats were exposed to tobacco smoke for 4h/day for 14 days. To investigate cell proliferation, the exogenous marker 5-bromo-2'-deoxyuridine (BrdU, 200mg/kg, ip) was administered 2h into the 4-h smoke exposure session on day 14. The rats were sacrificed 2-4h after the administration of BrdU. To investigate cell survival, the same dose of BrdU was administered 24h before the start of the 14-day smoke exposure period. These rats were sacrificed 24h after the last smoke exposure session. Tobacco smoke exposure decreased both the number of dividing progenitor cells (-19%) and the number of surviving new cells (-20%), labeled with BrdU in the dentate gyrus. The decrease in cell proliferation was not associated with an increase in apoptotic cell death, as shown by TUNEL analysis. Colocalization studies indicated that exposure to tobacco smoke decreased the number of new immature neurons (BrdU/DCX-positive) and transition neurons (BrdU/DCX/NeuN-positive) and increased the number of new glial cells (BrdU/GFAP-positive). These findings demonstrate that exposure to tobacco smoke diminishes neurogenesis and promotes gliogenesis in the dentate gyrus of adolescent rats. These effects may play a role in the increased risk for depression and cognitive impairment in adolescent smokers.
    MeSH term(s) Age Factors ; Animals ; Cell Proliferation/drug effects ; Dentate Gyrus/cytology ; Dentate Gyrus/drug effects ; Dentate Gyrus/physiology ; Male ; Neural Inhibition/drug effects ; Neural Inhibition/physiology ; Neural Stem Cells/cytology ; Neural Stem Cells/drug effects ; Neural Stem Cells/physiology ; Neurogenesis/drug effects ; Neurogenesis/physiology ; Neuroglia/cytology ; Neuroglia/drug effects ; Neuroglia/physiology ; Rats ; Rats, Wistar ; Smoking/adverse effects ; Smoking/pathology
    Language English
    Publishing date 2011-09-21
    Publishing country Netherlands
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1200-2
    ISSN 1872-6240 ; 0006-8993
    ISSN (online) 1872-6240
    ISSN 0006-8993
    DOI 10.1016/j.brainres.2011.07.041
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  9. Article: Effects of Histamine H ; Receptor Activation on the Behavioral-Stimulant Effects of Methamphetamine and Cocaine in Mice and Squirrel Monkeys

    Banks, Matthew L. / Manvich, Daniel F. / Bauzo, Rayna M. / Howell, Leonard L.

    Pharmacology

    2009  Volume 83, Issue 3, Page(s) 164–169

    Abstract: Background: Cocaine and methamphetamine (METH) are two commonly abused drugs that have behavioral-stimulant properties. These stimulant effects are partially mediated by the dopaminergic system. Recent evidence has suggested that the histamine H3 ... ...

    Institution Yerkes National Primate Research Center and Department of Psychiatry and Behavioral Sciences, Emory University, Atlanta, Ga., USA
    Abstract Background: Cocaine and methamphetamine (METH) are two commonly abused drugs that have behavioral-stimulant properties. These stimulant effects are partially mediated by the dopaminergic system. Recent evidence has suggested that the histamine H3 receptor (H3R) may modulate the release of dopamine induced by METH. The aim of the present study was to examine the role of H3R in the behavioral-stimulant effects of cocaine and METH in mice and monkeys. Methods: Nonhabituated, experimentally naïve mice (n = 5–6) were pretreated with the H3R agonist imetit 30 min before METH or cocaine, and activity was measured for 90 min. The behavioral-stimulant effects of METH and cocaine were also studied in squirrel monkeys (n = 3) under a fixed-interval schedule of stimulus termination. Monkeys were pretreated with imetit 30 min before the peak behavioral-stimulant doses of METH or cocaine derived from individual subjects. Results: Pretreatment with imetit did not affect basal activity in mice. Imetit significantly attenuated the behavioral-stimulant effects of METH, but not cocaine. In monkeys, no dose of imetit tested significantly altered the behavioral-stimulant effects of METH or cocaine. Conclusion: These results suggest a role of H3R in the behavioral-stimulant effects of METH, but not cocaine, in mice and no role in monkeys.
    Keywords Methamphetamine ; Cocaine ; Histamine H ; receptor ; Locomotor behavior, mice ; Fixed-interval schedule, monkeys
    Language English
    Publishing date 2009-01-15
    Publisher S. Karger AG
    Publishing place Basel, Switzerland
    Document type Article
    Note Short Communication
    ZDB-ID 206671-3
    ISSN 1423-0313 ; 0031-7012
    ISSN (online) 1423-0313
    ISSN 0031-7012
    DOI 10.1159/000191473
    Database Karger publisher's database

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  10. Article: Structure-activity relationships of the melanocortin tetrapeptide Ac-His-DPhe-Arg-Trp-NH2 at the mouse melanocortin receptors. Part 3: modifications at the Arg position.

    Holder, Jerry Ryan / Xiang, Zhimin / Bauzo, Rayna M / Haskell-Luevano, Carrie

    Peptides

    2003  Volume 24, Issue 1, Page(s) 73–82

    Abstract: The melanocortin pathway is involved in the regulation of several physiological functions including skin pigmentation, steroidogenesis, obesity, energy homeostasis, and exocrine gland function. This melanocortin pathway consists of five known G-protein ... ...

    Abstract The melanocortin pathway is involved in the regulation of several physiological functions including skin pigmentation, steroidogenesis, obesity, energy homeostasis, and exocrine gland function. This melanocortin pathway consists of five known G-protein coupled receptors, endogenous agonists derived from the proopiomelanocortin (POMC) gene transcript, the endogenous antagonists Agouti and the Agouti-related protein (AGRP) and signals through the intracellular cAMP signal transduction pathway. The melanocortin-3 receptor (MC3R) and melanocortin-4 receptor (MC4R) located in the brain are implicated as participating in the metabolic and food intake aspects of energy homeostasis and are stimulated by melanocortin agonists such as alpha-melanocyte stimulation hormone (alpha-MSH). All the endogenous (POMC-derived) melanocortin agonists contain the putative message sequence "His-Phe-Arg-Trp." Herein, we report 12 tetrapeptides, based upon the template Ac-His(6)-DPhe(7)-Arg(8)-Trp(9)-NH(2) (alpha-MSH numbering) that have been modified at the Arg(8) position by neutral, basic, or acidic amino acid side chains. These peptides have been pharmacologically characterized for agonist activity at the mouse melanocortin receptors MC1R, MC3R, MC4R, and MC5R. The most notable results of this study include the observation that removal of the guanidinyl side chain moiety results in decreased melanocortin receptor potency, but that this Arg(8) side chain is not critical for melanocortin receptor agonist activity. Additionally, incorporation of the homoArg(8) residue results in 56-fold MC4R versus MC3R selectivity, and the Orn(8) residue results in 123-fold MC4R versus MC5R and 63-fold MC5R versus MC3R selectivity.
    MeSH term(s) Animals ; Arginine/chemistry ; Cell Line ; Humans ; Mice ; Oligopeptides/chemistry ; Oligopeptides/drug effects ; Receptor, Melanocortin, Type 3 ; Receptors, Corticotropin/classification ; Receptors, Corticotropin/drug effects ; Receptors, Melanocortin ; Structure-Activity Relationship
    Chemical Substances Mc3r protein, mouse ; Oligopeptides ; Receptor, Melanocortin, Type 3 ; Receptors, Corticotropin ; Receptors, Melanocortin ; acetyl-histidyl-phenylalanyl-arginyl-tryptophanamide ; Arginine (94ZLA3W45F)
    Language English
    Publishing date 2003-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 769028-9
    ISSN 1873-5169 ; 0196-9781
    ISSN (online) 1873-5169
    ISSN 0196-9781
    DOI 10.1016/s0196-9781(02)00278-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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