StressCovidV1, PascalFrancis, Corpus, bibRecord, 000154

THE HUMAN IMMUNODEFICIENCY VIRUS-1-ASSOCIATED PROTEIN, TAT1-86, IMPAIRS DOPAMINE TRANSPORTERS AND INTERACTS WITH COCAINE TO REDUCE NERVE TERMINAL FUNCTION : A NO-NET-FLUX MICRODIALYSIS STUDY

Identifieur interne : 000154 ( PascalFrancis/Corpus ); précédent : 000153; suivant : 000155

THE HUMAN IMMUNODEFICIENCY VIRUS-1-ASSOCIATED PROTEIN, TAT1-86, IMPAIRS DOPAMINE TRANSPORTERS AND INTERACTS WITH COCAINE TO REDUCE NERVE TERMINAL FUNCTION : A NO-NET-FLUX MICRODIALYSIS STUDY

Auteurs : M. J. Ferris ; D. Frederick-Duus ; J. Fadel ; C. F. Mactutus ; R. M. Booze

Source :

Neuroscience [ 0306-4522 ] ; 2009.

RBID : Francis:09-0199428

Descripteurs français

Pascal (Inist)
- Virus immunodéficience humaine, Protéine transport, Dopamine, Cocaïne, Terminaison nerveuse, Microdialyse.

English descriptors

KwdEn :
- Carrier protein, Cocaine, Dopamine, Human immunodeficiency virus, Microdialysis, Nerve ending.

Abstract

-Injection drug use accounts for approximately one-third of human immunodeficiency virus (HIV) infections in the United States. HIV-associated proteins have been shown to interact with various drugs of abuse to incite concerted neurotoxicity. One common area for their interaction is the nerve terminal, including dopamine transporter (DAT) systems. However, results regarding DAT function and regulation in HIV-infection, regardless of drug use, are mixed. Thus, the present experiments were designed to explicitly control Tat and cocaine administration in an in vivo rat model in order to reconcile differences that exist in the literature to date. We examined Tat plus cocaine-induced alterations using no-net-flux microdialysis, which is sensitive to alterations in DAT function, in order to test the potential for DAT as an early mediator of HIV-induced oxidative stress and neurode-generation in vivo. Within 5 h of intra-accumbal administration of the HIV-associated protein, Tat, we noted a significant reduction in local DAT efficiency with little change in DA overflow/release dynamics. Further, at 48 h post-Tat administration, we demonstrated a concerted effect of the HIV-protein Tat with cocaine on both uptake and release function. Finally, we discuss the extent to which DAT dysfunction may be considered a predecessor to generalized nerve terminal dysfunction. Characterization of DAT dysfunction in vivo may provide an early pharmacotherapeutic target, which in turn may prevent or attenuate downstream mediators of neurotoxicity (i.e., reactive species) to dopamine systems occurring in neuro-AIDS.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

A01	`01`	`1`		`@0 0306-4522`
A02	`01`			`@0 NRSCDN`
A03		`1`		`@0 Neuroscience`
A05				`@2 159`
A06				`@2 4`
A08	`01`	`1`	`ENG`	`@1 THE HUMAN IMMUNODEFICIENCY VIRUS-1-ASSOCIATED PROTEIN, TAT_1-86, IMPAIRS DOPAMINE TRANSPORTERS AND INTERACTS WITH COCAINE TO REDUCE NERVE TERMINAL FUNCTION : A NO-NET-FLUX MICRODIALYSIS STUDY`
A11	`01`	`1`		`@1 FERRIS (M. J.)`
A11	`02`	`1`		`@1 FREDERICK-DUUS (D.)`
A11	`03`	`1`		`@1 FADEL (J.)`
A11	`04`	`1`		`@1 MACTUTUS (C. F.)`
A11	`05`	`1`		`@1 BOOZE (R. M.)`
A14	`01`			`@1 Department of Psychology, Program in Behavioral Neuroscience, University of South Carolina @2 Columbia, SC 29208 @3 USA @Z 1 aut. @Z 4 aut. @Z 5 aut.`
A14	`02`			`@1 Department of Pharmacology, Physiology and Neuroscience, University of South Carolina School of Medicine @2 Columbia, SC 29208 @3 USA @Z 2 aut. @Z 3 aut. @Z 5 aut.`
A20				`@1 1292-1299`
A21				`@1 2009`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 17194 @5 354000186798120110`
A44				`@0 0000 @1 © 2009 INIST-CNRS. All rights reserved.`
A45				`@0 1 p.1/4`
A47	`01`	`1`		`@0 09-0199428`
A60				`@1 P`
A61				`@0 A`
A64	`01`	`1`		`@0 Neuroscience`
A66	`01`			`@0 GBR`
C01	`01`		`ENG`	@0 -Injection drug use accounts for approximately one-third of human immunodeficiency virus (HIV) infections in the United States. HIV-associated proteins have been shown to interact with various drugs of abuse to incite concerted neurotoxicity. One common area for their interaction is the nerve terminal, including dopamine transporter (DAT) systems. However, results regarding DAT function and regulation in HIV-infection, regardless of drug use, are mixed. Thus, the present experiments were designed to explicitly control Tat and cocaine administration in an in vivo rat model in order to reconcile differences that exist in the literature to date. We examined Tat plus cocaine-induced alterations using no-net-flux microdialysis, which is sensitive to alterations in DAT function, in order to test the potential for DAT as an early mediator of HIV-induced oxidative stress and neurode-generation in vivo. Within 5 h of intra-accumbal administration of the HIV-associated protein, Tat, we noted a significant reduction in local DAT efficiency with little change in DA overflow/release dynamics. Further, at 48 h post-Tat administration, we demonstrated a concerted effect of the HIV-protein Tat with cocaine on both uptake and release function. Finally, we discuss the extent to which DAT dysfunction may be considered a predecessor to generalized nerve terminal dysfunction. Characterization of DAT dysfunction in vivo may provide an early pharmacotherapeutic target, which in turn may prevent or attenuate downstream mediators of neurotoxicity (i.e., reactive species) to dopamine systems occurring in neuro-AIDS.
C02	`01`	`X`		`@0 770E02 @1 V`
C03	`01`	`X`	`FRE`	`@0 Virus immunodéficience humaine @2 NW @5 01`
C03	`01`	`X`	`ENG`	`@0 Human immunodeficiency virus @2 NW @5 01`
C03	`01`	`X`	`SPA`	`@0 Human immunodeficiency virus @2 NW @5 01`
C03	`02`	`X`	`FRE`	`@0 Protéine transport @5 02`
C03	`02`	`X`	`ENG`	`@0 Carrier protein @5 02`
C03	`02`	`X`	`SPA`	`@0 Proteína transportador @5 02`
C03	`03`	`X`	`FRE`	`@0 Dopamine @2 NK @2 FR @5 03`
C03	`03`	`X`	`ENG`	`@0 Dopamine @2 NK @2 FR @5 03`
C03	`03`	`X`	`SPA`	`@0 Dopamina @2 NK @2 FR @5 03`
C03	`04`	`X`	`FRE`	`@0 Cocaïne @2 NK @2 FR @2 FX @5 04`
C03	`04`	`X`	`ENG`	`@0 Cocaine @2 NK @2 FR @2 FX @5 04`
C03	`04`	`X`	`SPA`	`@0 Cocaína @2 NK @2 FR @2 FX @5 04`
C03	`05`	`X`	`FRE`	`@0 Terminaison nerveuse @5 05`
C03	`05`	`X`	`ENG`	`@0 Nerve ending @5 05`
C03	`05`	`X`	`SPA`	`@0 Terminación nerviosa @5 05`
C03	`06`	`X`	`FRE`	`@0 Microdialyse @5 06`
C03	`06`	`X`	`ENG`	`@0 Microdialysis @5 06`
C03	`06`	`X`	`SPA`	`@0 Microdiálisis @5 06`
C07	`01`	`X`	`FRE`	`@0 Lentivirus @2 NW`
C07	`01`	`X`	`ENG`	`@0 Lentivirus @2 NW`
C07	`01`	`X`	`SPA`	`@0 Lentivirus @2 NW`
C07	`02`	`X`	`FRE`	`@0 Retroviridae @2 NW`
C07	`02`	`X`	`ENG`	`@0 Retroviridae @2 NW`
C07	`02`	`X`	`SPA`	`@0 Retroviridae @2 NW`
C07	`03`	`X`	`FRE`	`@0 Virus @2 NW`
C07	`03`	`X`	`ENG`	`@0 Virus @2 NW`
C07	`03`	`X`	`SPA`	`@0 Virus @2 NW`
C07	`04`	`X`	`FRE`	`@0 Catécholamine @5 20`
C07	`04`	`X`	`ENG`	`@0 Catecholamine @5 20`
C07	`04`	`X`	`SPA`	`@0 Catecolamina @5 20`
C07	`05`	`X`	`FRE`	`@0 Neurotransmetteur @5 21`
C07	`05`	`X`	`ENG`	`@0 Neurotransmitter @5 21`
C07	`05`	`X`	`SPA`	`@0 Neurotransmisor @5 21`
C07	`06`	`X`	`FRE`	`@0 Substance toxicomanogène @5 22`
C07	`06`	`X`	`ENG`	`@0 Drug of abuse @5 22`
C07	`06`	`X`	`SPA`	`@0 Sustancia toxicomanógena @5 22`
C07	`07`	`X`	`FRE`	`@0 Stimulant SNC @5 23`
C07	`07`	`X`	`ENG`	`@0 CNS stimulant @5 23`
C07	`07`	`X`	`SPA`	`@0 Estimulante SNC @5 23`
C07	`08`	`X`	`FRE`	`@0 Psychotrope @2 FX @5 24`
C07	`08`	`X`	`ENG`	`@0 Psychotropic @2 FX @5 24`
C07	`08`	`X`	`SPA`	`@0 Psicotropo @2 FX @5 24`
N21				`@1 145`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

Format Inist (serveur)

NO :	FRANCIS 09-0199428 INIST
ET :	THE HUMAN IMMUNODEFICIENCY VIRUS-1-ASSOCIATED PROTEIN, TAT_1-86, IMPAIRS DOPAMINE TRANSPORTERS AND INTERACTS WITH COCAINE TO REDUCE NERVE TERMINAL FUNCTION : A NO-NET-FLUX MICRODIALYSIS STUDY
AU :	FERRIS (M. J.); FREDERICK-DUUS (D.); FADEL (J.); MACTUTUS (C. F.); BOOZE (R. M.)
AF :	Department of Psychology, Program in Behavioral Neuroscience, University of South Carolina/Columbia, SC 29208/Etats-Unis (1 aut., 4 aut., 5 aut.); Department of Pharmacology, Physiology and Neuroscience, University of South Carolina School of Medicine/Columbia, SC 29208/Etats-Unis (2 aut., 3 aut., 5 aut.)
DT :	Publication en série; Niveau analytique
SO :	Neuroscience; ISSN 0306-4522; Coden NRSCDN; Royaume-Uni; Da. 2009; Vol. 159; No. 4; Pp. 1292-1299; Bibl. 1 p.1/4
LA :	Anglais
EA :	-Injection drug use accounts for approximately one-third of human immunodeficiency virus (HIV) infections in the United States. HIV-associated proteins have been shown to interact with various drugs of abuse to incite concerted neurotoxicity. One common area for their interaction is the nerve terminal, including dopamine transporter (DAT) systems. However, results regarding DAT function and regulation in HIV-infection, regardless of drug use, are mixed. Thus, the present experiments were designed to explicitly control Tat and cocaine administration in an in vivo rat model in order to reconcile differences that exist in the literature to date. We examined Tat plus cocaine-induced alterations using no-net-flux microdialysis, which is sensitive to alterations in DAT function, in order to test the potential for DAT as an early mediator of HIV-induced oxidative stress and neurode-generation in vivo. Within 5 h of intra-accumbal administration of the HIV-associated protein, Tat, we noted a significant reduction in local DAT efficiency with little change in DA overflow/release dynamics. Further, at 48 h post-Tat administration, we demonstrated a concerted effect of the HIV-protein Tat with cocaine on both uptake and release function. Finally, we discuss the extent to which DAT dysfunction may be considered a predecessor to generalized nerve terminal dysfunction. Characterization of DAT dysfunction in vivo may provide an early pharmacotherapeutic target, which in turn may prevent or attenuate downstream mediators of neurotoxicity (i.e., reactive species) to dopamine systems occurring in neuro-AIDS.
CC :	770E02
FD :	Virus immunodéficience humaine; Protéine transport; Dopamine; Cocaïne; Terminaison nerveuse; Microdialyse
FG :	Lentivirus; Retroviridae; Virus; Catécholamine; Neurotransmetteur; Substance toxicomanogène; Stimulant SNC; Psychotrope
ED :	Human immunodeficiency virus; Carrier protein; Dopamine; Cocaine; Nerve ending; Microdialysis
EG :	Lentivirus; Retroviridae; Virus; Catecholamine; Neurotransmitter; Drug of abuse; CNS stimulant; Psychotropic
SD :	Human immunodeficiency virus; Proteína transportador; Dopamina; Cocaína; Terminación nerviosa; Microdiálisis
LO :	INIST-17194.354000186798120110
ID :	09-0199428

Links to Exploration step

Francis:09-0199428

Le document en format XML

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<front><div type="abstract" xml:lang="en">-Injection drug use accounts for approximately one-third of human immunodeficiency virus (HIV) infections in the United States. HIV-associated proteins have been shown to interact with various drugs of abuse to incite concerted neurotoxicity. One common area for their interaction is the nerve terminal, including dopamine transporter (DAT) systems. However, results regarding DAT function and regulation in HIV-infection, regardless of drug use, are mixed. Thus, the present experiments were designed to explicitly control Tat and cocaine administration in an in vivo rat model in order to reconcile differences that exist in the literature to date. We examined Tat plus cocaine-induced alterations using no-net-flux microdialysis, which is sensitive to alterations in DAT function, in order to test the potential for DAT as an early mediator of HIV-induced oxidative stress and neurode-generation in vivo. Within 5 h of intra-accumbal administration of the HIV-associated protein, Tat, we noted a significant reduction in local DAT efficiency with little change in DA overflow/release dynamics. Further, at 48 h post-Tat administration, we demonstrated a concerted effect of the HIV-protein Tat with cocaine on both uptake and release function. Finally, we discuss the extent to which DAT dysfunction may be considered a predecessor to generalized nerve terminal dysfunction. Characterization of DAT dysfunction in vivo may provide an early pharmacotherapeutic target, which in turn may prevent or attenuate downstream mediators of neurotoxicity (i.e., reactive species) to dopamine systems occurring in neuro-AIDS.</div>
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<fC01 i1="01" l="ENG"><s0>-Injection drug use accounts for approximately one-third of human immunodeficiency virus (HIV) infections in the United States. HIV-associated proteins have been shown to interact with various drugs of abuse to incite concerted neurotoxicity. One common area for their interaction is the nerve terminal, including dopamine transporter (DAT) systems. However, results regarding DAT function and regulation in HIV-infection, regardless of drug use, are mixed. Thus, the present experiments were designed to explicitly control Tat and cocaine administration in an in vivo rat model in order to reconcile differences that exist in the literature to date. We examined Tat plus cocaine-induced alterations using no-net-flux microdialysis, which is sensitive to alterations in DAT function, in order to test the potential for DAT as an early mediator of HIV-induced oxidative stress and neurode-generation in vivo. Within 5 h of intra-accumbal administration of the HIV-associated protein, Tat, we noted a significant reduction in local DAT efficiency with little change in DA overflow/release dynamics. Further, at 48 h post-Tat administration, we demonstrated a concerted effect of the HIV-protein Tat with cocaine on both uptake and release function. Finally, we discuss the extent to which DAT dysfunction may be considered a predecessor to generalized nerve terminal dysfunction. Characterization of DAT dysfunction in vivo may provide an early pharmacotherapeutic target, which in turn may prevent or attenuate downstream mediators of neurotoxicity (i.e., reactive species) to dopamine systems occurring in neuro-AIDS.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>770E02</s0>
<s1>V</s1>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Virus immunodéficience humaine</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Human immunodeficiency virus</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Human immunodeficiency virus</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Protéine transport</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Carrier protein</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Proteína transportador</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Dopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Dopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Dopamina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Cocaïne</s0>
<s2>NK</s2>
<s2>FR</s2>
<s2>FX</s2>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Cocaine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s2>FX</s2>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Cocaína</s0>
<s2>NK</s2>
<s2>FR</s2>
<s2>FX</s2>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Terminaison nerveuse</s0>
<s5>05</s5>
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<s5>05</s5>
</fC03>
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<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Microdialyse</s0>
<s5>06</s5>
</fC03>
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<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Microdiálisis</s0>
<s5>06</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Lentivirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Lentivirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Lentivirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Retroviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Retroviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Retroviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Catécholamine</s0>
<s5>20</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Catecholamine</s0>
<s5>20</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Catecolamina</s0>
<s5>20</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Neurotransmetteur</s0>
<s5>21</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Neurotransmitter</s0>
<s5>21</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Neurotransmisor</s0>
<s5>21</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Substance toxicomanogène</s0>
<s5>22</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Drug of abuse</s0>
<s5>22</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Sustancia toxicomanógena</s0>
<s5>22</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Stimulant SNC</s0>
<s5>23</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>CNS stimulant</s0>
<s5>23</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Estimulante SNC</s0>
<s5>23</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Psychotrope</s0>
<s2>FX</s2>
<s5>24</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Psychotropic</s0>
<s2>FX</s2>
<s5>24</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Psicotropo</s0>
<s2>FX</s2>
<s5>24</s5>
</fC07>
<fN21><s1>145</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
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<server><NO>FRANCIS 09-0199428 INIST</NO>
<ET>THE HUMAN IMMUNODEFICIENCY VIRUS-1-ASSOCIATED PROTEIN, TAT<sub>1-86</sub>
, IMPAIRS DOPAMINE TRANSPORTERS AND INTERACTS WITH COCAINE TO REDUCE NERVE TERMINAL FUNCTION : A NO-NET-FLUX MICRODIALYSIS STUDY</ET>
<AU>FERRIS (M. J.); FREDERICK-DUUS (D.); FADEL (J.); MACTUTUS (C. F.); BOOZE (R. M.)</AU>
<AF>Department of Psychology, Program in Behavioral Neuroscience, University of South Carolina/Columbia, SC 29208/Etats-Unis (1 aut., 4 aut., 5 aut.); Department of Pharmacology, Physiology and Neuroscience, University of South Carolina School of Medicine/Columbia, SC 29208/Etats-Unis (2 aut., 3 aut., 5 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Neuroscience; ISSN 0306-4522; Coden NRSCDN; Royaume-Uni; Da. 2009; Vol. 159; No. 4; Pp. 1292-1299; Bibl. 1 p.1/4</SO>
<LA>Anglais</LA>
<EA>-Injection drug use accounts for approximately one-third of human immunodeficiency virus (HIV) infections in the United States. HIV-associated proteins have been shown to interact with various drugs of abuse to incite concerted neurotoxicity. One common area for their interaction is the nerve terminal, including dopamine transporter (DAT) systems. However, results regarding DAT function and regulation in HIV-infection, regardless of drug use, are mixed. Thus, the present experiments were designed to explicitly control Tat and cocaine administration in an in vivo rat model in order to reconcile differences that exist in the literature to date. We examined Tat plus cocaine-induced alterations using no-net-flux microdialysis, which is sensitive to alterations in DAT function, in order to test the potential for DAT as an early mediator of HIV-induced oxidative stress and neurode-generation in vivo. Within 5 h of intra-accumbal administration of the HIV-associated protein, Tat, we noted a significant reduction in local DAT efficiency with little change in DA overflow/release dynamics. Further, at 48 h post-Tat administration, we demonstrated a concerted effect of the HIV-protein Tat with cocaine on both uptake and release function. Finally, we discuss the extent to which DAT dysfunction may be considered a predecessor to generalized nerve terminal dysfunction. Characterization of DAT dysfunction in vivo may provide an early pharmacotherapeutic target, which in turn may prevent or attenuate downstream mediators of neurotoxicity (i.e., reactive species) to dopamine systems occurring in neuro-AIDS.</EA>
<CC>770E02</CC>
<FD>Virus immunodéficience humaine; Protéine transport; Dopamine; Cocaïne; Terminaison nerveuse; Microdialyse</FD>
<FG>Lentivirus; Retroviridae; Virus; Catécholamine; Neurotransmetteur; Substance toxicomanogène; Stimulant SNC; Psychotrope</FG>
<ED>Human immunodeficiency virus; Carrier protein; Dopamine; Cocaine; Nerve ending; Microdialysis</ED>
<EG>Lentivirus; Retroviridae; Virus; Catecholamine; Neurotransmitter; Drug of abuse; CNS stimulant; Psychotropic</EG>
<SD>Human immunodeficiency virus; Proteína transportador; Dopamina; Cocaína; Terminación nerviosa; Microdiálisis</SD>
<LO>INIST-17194.354000186798120110</LO>
<ID>09-0199428</ID>
</server>
</inist>
</record>

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THE HUMAN IMMUNODEFICIENCY VIRUS-1-ASSOCIATED PROTEIN, TAT1-86, IMPAIRS DOPAMINE TRANSPORTERS AND INTERACTS WITH COCAINE TO REDUCE NERVE TERMINAL FUNCTION : A NO-NET-FLUX MICRODIALYSIS STUDY

THE HUMAN IMMUNODEFICIENCY VIRUS-1-ASSOCIATED PROTEIN, TAT1-86, IMPAIRS DOPAMINE TRANSPORTERS AND INTERACTS WITH COCAINE TO REDUCE NERVE TERMINAL FUNCTION : A NO-NET-FLUX MICRODIALYSIS STUDY

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