Robert Christopher Pierce
University Of Pennsylvania
Project start date: 2002-04-01
Project end date: 2013-01-31
Sponsored Links Excellgen http://Excellgen.com
MPFC, N. Accumbens And Reinstatement Of Cocaine Seeking
Robert Christopher Pierce, Associate Professor
Boston University Medical Campus 715 Albany St, 560 Boston, Ma 021182394
Grant 5R01DA015214-05 from National Institute On Drug Abuse IRG: ZRG1
Abstract: One of the major determinants of reinstatement of cocaine use among human addicts is acute re-exposure to the drug, which often precipitates cocaine craving and relapse. This grant proposal will use an animal model of cocaine relapse in order to determine the anatomical and pharmacological determinants of reinstatement of cocaine-seeking behavior following a priming injection. These experiments will focus on the nucleus accumbens and medial prefrontal cortex (mPFC); two nuclei know to play important roles in cocaine reinforcement. All experiments will be performed in rats. Specific Aims 1 and 2 will examine the role of dopamine in the nucleus accumbens and mPFC in cocaine relapse by administering a priming microinjection of cocaine, selective dopamine reuptake blockers, D1-like or D2-like dopamine agonists into the nucleus accumbens or mPFC. In order to assess further the role of specific dopamine receptors in cocaine relapse, selective dopamine receptor antagonists will be administered directly into the nucleus accumbens or mPFC prior to a systemic priming injection of cocaine. Specific Aim 3 will focus on the role of glutamate in reinstatement of cocaine seeking. Although cocaine does not directly influence the glutamate system, recent evidence indicates that ionotropic glutamate receptor agonists administered into the nucleus accumbens reinstate cocaine-seeking behavior. Since the mPFC sends a major glutamatergic projection to the nucleus accumbens, it will be determined if cocaine microinjections into the mPFC reinstate cocaine-seeking behavior by altering glutamate and/or dopamine transmission in the nucleus accumbens. This will be achieved by microinjecting AMPA, NMDA, D1-like or D2-like antagonists into the nucleus accumbens prior to a priming microinjection of cocaine into the mPFC. Collectively, the proposed research will provide fundamental information on the anatomy and pharmacology of relapse to cocaine-seeking behavior and will facilitate the development of effective pharmacological strategies for relapse prevention.
Keywords: cocaine, craving, nucleus accumbens, prefrontal lobe /cortex, relapse /recurrence, substance abuse related behavior, biological signal transduction, dopamine, dopamine antagonist, dopamine receptor, drug abuse, excitatory aminoacid, glutamate, glutamate receptor, neurobiology, reinforcer, behavior test, behavioral /social science research tag, laboratory rat, microinjection
Project start date: 2003-02-10
Project end date: 2008-01-31
5R01DA015214-05 (2007): $229697
5R01DA015214-04 (2006): $236557
5R01DA015214-03 (2005): $242250
5R01DA015214-02 (2004): $242250
MPFC, N. ACCUMBENS AND AND REINSTATEMENT OF COCAINE SEEKING
Robert Christopher Pierce, Associate Professor
University Of Pennsylvania, 3451 Walnut Street, Philadelphia, Pa 19104
Grant 5R01DA015214-09 from National Institute On Drug Abuse
Keywords: 8-Azabicyclo(3.2.1)octane-2-carboxylic acid, 3-(benzoyloxy)-8-methyl-, methyl ester, (1R-(exo, exo))-; Address; Ammon Horn; Amygdala; Amygdaloid Body; Amygdaloid Nucleus; Amygdaloid structure; Analysis, Data; Animal Welfare; Animals; Behavior; Bibliography; Boston; Budgets; Career Development Awards; Career Development Awards and Programs; Career Development Programs K-Series; Cell Nucleus; Cessation of life; City of Boston; Climate; Cocaine; Collection; Common Rat Strains; Cornu Ammonis; Country; D2 receptor; DA Neuron; DRD2; DRD2 Receptor; Data Analyses; Data Analysis, Statistical; Data Interpretation, Statistical; Death; Deep Brain Stimulation; Dopamine D2 Receptor; Dopamine neuron; Dose; Drugs; Ecological impact; Environment; Environmental Impact; Equipment; Ethics Committees, Research; Euthanasia; Funding; Globus Pallidus; Glutamates; Guidelines; Hippocampus; Hippocampus (Brain); Housing; IACUC; IRBs; ISA; Impact, Environmental; Independent Scientist Award; Individual; Institutional Animal Care and Use Committee; Institutional Review Boards; International; K-Awards; K-Series Research Career Programs; K02 Award; L-Glutamate; Mammals, Rats; Medial; Mediating; Medication; Mental disorders; Mental health disorders; Mercy Killing; Meteorological Climate; Methods; Methods and Techniques; Methods, Other; Minor; NIDA; NIH; National Institute of Drug Abuse; National Institutes of Health; National Institutes of Health (U.S.); Nerve Cells; Nerve Transmitter Substances; Nerve Unit; Nervous System Diseases; Neural Cell; Neurocyte; Neurologic Disorders; Neurological Disorders; Neurons; Neurotransmitters; Nucleus; Nucleus Accumbens; Nucleus tegmentalis pedunculopontinus; Operation; Operative Procedures; Operative Surgical Procedures; Pedunculopontine Tegmental Nucleus; Pharmaceutic Preparations; Pharmaceutical Preparations; Play; Prefrontal Cortex; Principal Investigator; Procedures; Programs (PT); Programs [Publication Type]; Protocol; Protocols documentation; Psychiatric Disease; Psychiatric Disorder; Psychological reinforcement; R01 Mechanism; R01 Program; RPG; Rat; Rattus; Reinforcement; Reinforcement (Psychology); Relative; Relative (related person); Research; Research Career Program; Research Career Programs, K-Series; Research Ethics Committees; Research Grants; Research Project Grants; Research Projects; Research Projects, R-Series; Research Resources; Resources; Role; Salaries; Schools, Medical; Statistical Data Analyses; Statistical Data Interpretation; Study Section; Surgical; Surgical Interventions; Surgical Procedure; Synapses; Synaptic; System; System, LOINC Axis 4; Techniques; Testing; Time; Transmission; United States National Institutes of Health; Universities; Unspecified Mental Disorder; Ventral Tegmental Area; Vertebrate Animals; Vertebrates; Wages; Work; ing; amygdaloid nuclear complex; application in practice; cholinergic; climatic; cost; dopaminergic neuron; drug/agent; experiment; experimental research; experimental study; expiration; graduate student; hippocampal; human subject; medical schools; mental illness; nervous system disorder; neurological disease; neuronal; neuronal circuitry; novel; pallidum; practical application; programs; psychological disorder; research study; social role; surgery; transmission process; ventral tegmentum; vertebrata
Project start date: 2002-04-01
Project end date: 2013-01-31
Budget start date: 1-FEB-2010
Budget end date: 31-JAN-2011
PFA/PA: PA-07-070
5R01DA015214-09 (2010): $311850
Grants awarded to Robert Christopher Pierce
Psychostimulant-Induced Craving And Toxicity
Robert Christopher Pierce, Associate Professor
Boston University Medical Campus 715 Albany Street,m-921 Boston, Ma 021182394
Grant 5K02DA018678-02 from National Institute On Drug Abuse IRG: NIDA
Abstract: This application is a K02 Independent Scientist Career Development Award submitted by R. Christopher Pierce, Ph.D. There are five major goals of the career development plan, which include i) focusing more attention on Dr. Pierce s primary research program (funded by R01 DA15214, R.C. Pierce, PI), which is concentrated on delineating the neurochemical and biochemical changes in various limbic nuclei responsible for the reinstatement of cocaine-induced drug seeking; ii) increasing the scope of these studies to include imaging experiments in non-human primate subjects in order to evaluate changes in the CNS prior to, during and after periods of excessive cocaine intake; iii) learning the technical and methodological details associated with magnetic resonance imaging and magnetic resonance spectroscopy experiments, which will be required to complete the second goal. Goals ii and iii will be done in collaboration with Drs. James Rowlett and Itamar Ronen; iv) expanding Dr. Pierce s research program from a relatively single-minded focus on the behavioral pharmacology of cocaine to include issues related to the neurotoxicity produced by other drugs of abuse. Specifically, he will determine the functional consequences of MDMA-induced damage of central serotonin systems as well as potential toxic interactions between cocaine and MDMA; and v) learning new techniques from Dr. Bryan Yamamoto and Dr. Jean-Jacques Soghomonian related to measures of neurotoxicity (i.e. measures of free radical formation, lipid and protein oxidation, excitoxicity and terminal degradation) in the context of the MDMA-cocaine project. Dr. Pierce currently devotes 60% effort to research and 40% effort to teaching and administrative duties. If this application is funded, he will be released from 25% of his non-research duties such that 85% of his time will be devoted to research. This release time will allow Dr. Pierce to devote more attention to his existing research and also expand his research collaborations with Drs. Rowlett, Ronen, Yamamoto and Soghomonian, which will have a significant positive impact on his career development.
Keywords: central nervous system stimulant, cocaine, craving, Primate, attention, career, drug abuse, free radical, human, learning, lipid, magnetic resonance imaging, neurotoxicology, oxidation, protein, psychopharmacology, serotonin
Project start date: 2006-04-01
Project end date: 2011-03-31
5K02DA018678-02 (2007): $113605
1K02DA018678-01A2 (2006): $110327
5K02DA018678-06 (2010): $122872
Robert Christopher Pierce, Associate Professor
Boston University Medical Campus 715 Albany St, 560 Boston, Ma 021182394
Grant 5R03DA017166-02 from National Institute On Drug Abuse IRG: MNPS
Abstract: Repeated exposure to psychostimulants, such as cocaine or amphetamine, leads to a progressive and enduring augmentation of locomotor and stereotyped behaviors in rats, a phenomenon known as behavioral sensitization. It has been suggested that the neuronal plasticity underlying behavioral sensitization results in the enhancement of the incentive motivational effects of psychostimulants, which contributes to drug craving. Thus, studies examining the mechanisms underlying behavioral sensitization could provide new insight into plasticity in the central nervous system that may help elucidate the mechanisms underlying the shift to compulsive drug use among human psychostimulant addicts. Growing evidence indicates that the plasma membrane-bound ephrin ligands and their receptors, the Eph tyrosine kinases, play critical roles in synaptic remodeling both during development and in the mature nervous system. Recently, ephrins and their receptors were shown to influence plasticity in the mesotelencephalic dopamine systems, which mediate both the development and long-term expression of behavioral sensitization to psychostimulants. In mammals, eight ephrins (ephrinA1-ephrinA5; ephrinB1-ephrinB3) and thirteen Eph receptors (EphA1-EphA8; EphB1-EphB4, EphB6) have been identified to date. The goal of this grant application is to assess the influence of acute and repeated injections of cocaine on the expression of EphB1 and ephrin-B2 in the neostriatum, core and shell of the nucleus accumbens, substantia nigra and/or ventral termental area. We also will assess the influence of antisense oligonucleotide suppression of EphB1 receptor expression in these nuclei on the development of behavioral sensitization to cocaine. Rats will be used as subjects in all of these experiments.
Keywords: cocaine, drug habituation, ephrin, gene induction /repression, neural plasticity, protein tyrosine kinase, central nervous system stimulant, craving, nucleus accumbens, substantia nigra, tegmentum, antisense nucleic acid, laboratory rat, microinjection, oligonucleotide, western blotting
Project start date: 2005-03-01
Project end date: 2007-02-28
5R03DA017166-02 (2006): $78852
1R03DA017166-01A1 (2005): $80750
MPFC, N. Accumbens And Reinstatement Of Cocaine Seeking
Robert Christopher Pierce, Associate Professor
Boston University Medical Campus 715 Albany St, 560 Boston, Ma 021182394
Grant 1R01DA015214-01A1 from National Institute On Drug Abuse IRG: ZRG1
Abstract: One of the major determinants of reinstatement of cocaine use among human addicts is acute re-exposure to the drug, which often precipitates cocaine craving and relapse. This grant proposal will use an animal model of cocaine relapse in order to determine the anatomical and pharmacological determinants of reinstatement of cocaine-seeking behavior following a priming injection. These experiments will focus on the nucleus accumbens and medial prefrontal cortex (mPFC); two nuclei know to play important roles in cocaine reinforcement. All experiments will be performed in rats. Specific Aims 1 and 2 will examine the role of dopamine in the nucleus accumbens and mPFC in cocaine relapse by administering a priming microinjection of cocaine, selective dopamine reuptake blockers, D1-like or D2-like dopamine agonists into the nucleus accumbens or mPFC. In order to assess further the role of specific dopamine receptors in cocaine relapse, selective dopamine receptor antagonists will be administered directly into the nucleus accumbens or mPFC prior to a systemic priming injection of cocaine. Specific Aim 3 will focus on the role of glutamate in reinstatement of cocaine seeking. Although cocaine does not directly influence the glutamate system, recent evidence indicates that ionotropic glutamate receptor agonists administered into the nucleus accumbens reinstate cocaine-seeking behavior. Since the mPFC sends a major glutamatergic projection to the nucleus accumbens, it will be determined if cocaine microinjections into the mPFC reinstate cocaine-seeking behavior by altering glutamate and/or dopamine transmission in the nucleus accumbens. This will be achieved by microinjecting AMPA, NMDA, D1-like or D2-like antagonists into the nucleus accumbens prior to a priming microinjection of cocaine into the mPFC. Collectively, the proposed research will provide fundamental information on the anatomy and pharmacology of relapse to cocaine-seeking behavior and will facilitate the development of effective pharmacological strategies for relapse prevention.
Keywords: cocaine, craving, nucleus accumbens, prefrontal lobe /cortex, relapse /recurrence, substance abuse related behavior, biological signal transduction, dopamine, dopamine antagonist, dopamine receptor, drug abuse, excitatory aminoacid, glutamate, glutamate receptor, neurobiology, reinforcer, behavior test, behavioral /social science research tag, laboratory rat, microinjection
Project start date: 2003-02-10
Project end date: 2008-01-31
1R01DA015214-01A1 (2003): $267250
R03--DOPAMINE, CALCIUM AND REPEATED COCAINE
Robert Christopher Pierce, Associate Professor
Pharmacology And Experimental Therapeuticsboston University Medical Campus
85 East Newton Street, M-921
boston, Ma 021182394
Grant 5R03DA011168-03 from National Institute On Drug Abuse IRG: NIDA
Abstract: Applicant´s ) The abuse of amphetamine-like psychostimulants is a medical and social problem throughout the world. The rewarding properties of amphetamine-like stimulants are linked to the capacity of these drugs to increase extracellular concentrations of dopamine in the forebrain, notably in the nucleus accumbens. Despite the advances in our understanding of the cellular and molecular actions of psychostimulants, effective pharmacological treatments for amphetamine and cocaine addition remain elusive. However, several preclinical studies report that calcium channel antagonists influence psychostimulant self-administration and conditioned place preference in rodents in a manner similar to dopamine antagonists. These results suggest that drugs acting on calcium conductances and associated transduction pathways may be potentially effective therapeutic agents for treating psychostimulant abuse. Interestingly, repeated injections of amphetamine-like psychostimulants results in an enhancement in the ability of these drugs to increase extracellular dopamine in the nucleus accumbens, and calcium appears to play an important role in this process. The studies outlined in this proposal will i)identify the mechanisms that underlie the influence of calcium and calcium-stimulated kinases on the enhanced increase in dopamine in the nucleus accumbens of cocaine-pretreated rats and ii) assess the behavioral relevance of these changes in dopamine neuronal function. Since the enhanced increase in dopamine in the nucleus accumbens is observed in both rats that self-administer or receive daily systemic injections of cocaine, the identification of novel mechanisms underlying this neurochemical adaptation to repeated cocaine may have direct clinical significance. Thus, by outlining the role of calcium in the cellular and molecular effects of psychostimulant drugs, the results of the experiments outlined in this proposal could guide the development of novel treatment strategies for amphetamine and cocaine addiction
Keywords: amphetamine, biological signal transduction, calcium channel, calcium channel blocker, calmodulin dependent protein kinase, cocaine, dopamine, psychopharmacology calcium, dopamine agonist, drug addiction, drug tolerance, messenger RNA, nucleus accumbens, protein kinase A, protein kinase C, synapsin behavior test, behavioral /social science research tag, laboratory rat, microdialysis, microinjection, polymerase chain reaction
Project start date: 1997-08-05
Project end date: 1999-10-31
5R03DA011168-03 (1998): $83750
NEUROTROPHINS AND REPEATED COCAINE
Robert Christopher Pierce, Associate Professor
Pharmacology And Experimental Therapeuticsboston University Medical Campus
85 East Newton Street, M-921
boston, Ma 021182394
Grant 3R01DA012171-02S1 from National Institute On Drug Abuse IRG: ZRG1
Abstract: Adapted From ´s ) The abuse of amphetamine-like psychostimulants is a global medical and social problem. The rewarding property of psychostimulants is linked, at least in part, to the capacity of these drugs to increase extracellular dopamine in the basal forebrain, notably in the nucleus accumbens. Despite the advances in our understanding of the cellular and molecular actions of psychostimulants, effective pharmcological treatments for amphetamine and cocaine addiction remain elusive. One paradigm, known as behavioral sensitization, models psychostimulant-induced adaptations in the addict brain by assessing changes in rodent neuronal function and behavior following repeated, daily injections of cocaine. Recent data suggests that the neurotrophins promote neural plasticity in the mesoaccumbens dopamine system and may contribute to behavioral sensitization. This grant proposal will expand on these initial findings by assessing potential cellular and molecular mechanisms whereby neurtrophins and neurotrophin-stimulated second messenger systems influence the ability of psychostimulants to promote behavioral sensitization. These experiments will assess i) the effects of repeated intra-cranial microinjections of neurotrophins on the behavioral activation induced by a subsequent challenge injection of cocaine, ii) changes in neurotrophin mRNA in the mesolimbic/nigrostriatal dopamine system following acute and repeated cocaine, and iii) alterations in extracellular neurotrophins and dopamine in the cell body and terminal regions of mesotelencephalic dopamine projections. Further characterization of the role of the neurotrophins in the behavioral plasticity associated with repeated cocaine injections will provide valuable new information that may be relevant to the pharmacological treatment of the intense drug craving associated with pscyhostimulant withdrawal
Keywords: behavioral habituation /sensitization, cocaine, neurotrophic factor, substance abuse related behavior biological model, dopamine, messenger RNA, neurochemistry, neuropharmacology Rodentia, behavioral /social science research tag
Project start date: 1999-09-30
Project end date: 2003-07-31
3R01DA012171-02S1 (2001): $1773
5R01DA012171-03 (2001): $188338
Sponsored Links Excellgen http://Excellgen.com
5R01DA012171-02 (2000): $159041
1R01DA012171-01A1 (1999): $190407
D1 DOPAMINE RECEPTOR SIGNALING AND COCAINE REINSTATEMENT
Robert Christopher Pierce, Associate Professor
University Of Pennsylvania, 3451 Walnut Street, Philadelphia, Pa 19104
Grant 5R01DA022339-04 from National Institute On Drug Abuse
Abstract: A growing body of evidence indicates that increases in dopamine and glutamate transmission in the nucleus accumbens independently promote the reinstatement of cocaine seeking, an animal model of relapse. The preliminary data presented in the current application demonstrate for the first time that cocaine reinstatement depends on interactions between accumbal shell dopamine and glutamate that are mediated by calcium/calmodulin-dependent protein kinase II (CaM-KII). Stimulation of D1-like (i.e. D1/D5) dopamine receptors in the nucleus accumbens shell reinstated cocaine seeking via the activation of L-type calcium channels. Reinstatement of cocaine seeking also was attenuated by injection of a CaM-KII inhibitor into the accumbens shell. Cocaine reinstatement was associated with increases in pCaM-KII and enhanced phosphorylation of GluR1 AMPA glutamate receptor subunits at S831, a site linked to CaM-KII-dependent trafficking of AMPA receptors to surface membranes. Finally, cocaine reinstatement was attenuated by intra- accumbal shell administration of a membrane-permeable form of Pep2-EVKI, a peptide that impairs AMPA receptor trafficking. Collectively, these results indicate that CaM-KII is a critical link between nucleus accumbens shell dopamine and glutamate systems involved in the neuronal plasticity underlying cocaine priming-induced reinstatement of drug seeking in rats. The current application will further examine the hypothesis that cocaine priming-induced reinstatement of cocaine seeking depends on the serial activation of D1-like dopamine receptors, PKA, L-type calcium channels and CaM-KII as well as the CaM-KII-dependent trafficking of AMPA receptor subunits to the synapse in the nucleus accumbens shell. Moreover, we propose to determine if similar or identical processes underlying cue-induced reinstatement of cocaine seeking. The experiments outlined in this proposal will define fundamental changes in D1-like dopamine receptor signaling that are associated with the reinstatement of cocaine seeking. The ultimate goal of these experiments is to identify novel targets for the development of pharmacotherapies for cocaine addiction. Our preliminary data indicate that L-type calcium channel and CaM-KII inhibitors as well as drugs that specifically influence AMPA receptor trafficking may be appropriate candidates for the treatment of cocaine addiction.The ultimate goal of these experiments is to identify novel targets for the development of drug therapies for cocaine craving and addiction. Using an animal model of cocaine craving, our preliminary data reveal that several classes of therapeutic drugs, including those that modulate dopamine and glutamate transmission in the brain, may be appropriate candidates for the treatment of cocaine addiction
Keywords: 1, 5-Benzothiazepin-4(5H)-one, 3-(acetyloxy)-5-(2-(dimethylamino)ethyl)-2, 3-dihydro-2-(4-methoxyphenyl)-, (2S-cis)-; 3, 4-Dihydroxyphenethylamine; 4-(2-Aminoethyl)-1, 2-benzenediol; 8-Azabicyclo(3.2.1)octane-2-carboxylic acid, 3-(benzoyloxy)-8-methyl-, methyl ester, (1R-(exo, exo))-; AMPA Receptors; ATP-protein phosphotransferase; Addiction, Cocaine; Adenosine Cyclic Monophosphate-Dependent Protein Kinases; Animal Model; Animal Models and Related Studies; Attenuated; Behavior; Behavioral; Blood Coagulation Factor IV; Brain; CNS plasticity; Ca++ element; CaM KII; CaM PK II; CaM kinase II; CaMK; CaMKII; Calcium; Calcium Channel Activators; Calcium Channel Agonists; Calcium Channels, L-Type; Calcium/calmodulin-dependent protein kinase; Coagulation Factor IV; Cocaine; Cocaine Dependences; Common Rat Strains; Cues; Cyclic AMP-Dependent Protein Kinases; D(1B) Dopamine Receptor; D(5) Dopamine Receptor; D1Beta Dopamine Receptor; DBDR; DRD1B; DRD1L2; DRD5; DRD5 Protein; Data; Dependences, Cocaine; Development; Diltiazem; Dopamine; Dopamine Antagonists; Dopamine Receptor; Dopamine Receptor Antagonists; Dopamine Receptor D1B; Dopaminergic Antagonists; Drug Therapy; Drugs; Encephalon; Encephalons; Factor IV; Family; Fore-Brain; Forebrain; Glutamate Receptor; Glutamates; Goals; Hydroxytyramine; Infusion; Infusion procedures; Injection of therapeutic agent; Injections; L-Glutamate; L-Type Calcium Channels; L-Type VDCC; L-Type Voltage-Dependent Calcium Channels; Link; Long-Lasting Calcium Channels; Maintenance; Maintenances; Mammals, Rats; Mediating; Medication; Membrane; Mice, Transgenic; Microinjections; Nerve Cells; Nerve Unit; Nervous System, Brain; Neural Cell; Neurocyte; Neuronal Plasticity; Neurons; Nucleus Accumbens; PKA; Peptides; Pharmaceutic Preparations; Pharmaceutical Preparations; Pharmacotherapy; Phosphorylation; Play; Process; Prosencephalon; Protein Kinase; Protein Kinase A; Protein Phosphorylation; Rat; Rattus; Receptor Protein; Receptor Signaling; Receptors, AMPA; Relapse; Role; Saline; Saline Solution; Self Administration; Self-Administered; Site; Surface; Synapses; Synaptic; System; System, LOINC Axis 4; Therapeutic; Time; Transgenic Mice; Transmission; Work; addiction; cAMP-Dependent Protein Kinases; calcium-calmodulin-dependent PK; calcium-calmodulin-dependent PK type II; calcium-dependent CaM kinase II; calmodulin dependent protein kinase; calmodulin-dependent protein kinase II; craving; design; designing; dopamine D5 receptor; drug seeking behavior; drug/agent; experiment; experimental research; experimental study; glycogen synthase a kinase; hydroxyalkyl protein kinase; inhibitor; inhibitor/antagonist; membrane structure; microtubule associated protein 2 kinase; model organism; neural plasticity; neuronal; neuroplasticity; novel; phosphorylase b kinase kinase; protein kinase II; receptor; research study; social role; trafficking; transmission process
Project start date: 2008-05-15
Project end date: 2013-04-30
Budget start date: 1-MAY-2010
Budget end date: 30-APR-2011
PFA/PA: PA-07-070
5R01DA022339-04 (2010): $352378
5R01DA022339-03 (2009): $355938
Robert Christopher Pierce
University Of Pennsylvania
Project start date: 2012-04-01
Project end date: 2017-02-28
NEUROBIOLOGY OF COCAINE-INDUCED BEHAVIORAL SENSITIZATION
Robert Christopher Pierce, Associate Professor
Washington State University 423 Neill Hall Pullman, Wa 99164
Grant 5F32DA005589-03 from National Institute On Drug Abuse IRG: DABR
5F32DA005589-03 (1995): $28600
NEUROBIOLOGY OF COCAINE-INDUCED BEHVRL SENSITIZATION
Robert Christopher Pierce, Associate Professor
Vet & Comp Anat, Pharm, And Physiol (vcapp)washington State University
423 Neill Hall
pullman, Wa 99164
Grant 1F32DA005589-01 from National Institute On Drug Abuse IRG: DABR
1F32DA005589-01 (1993): $21600