Amphetamine and methamphetamine differentially affect dopamine transporters in vitro and in vivo.
Open accessAbstract
The psychostimulants d-amphetamine (AMPH) and methamphetamine (METH) release excess dopamine (DA) into the synaptic clefts of dopaminergic neurons. Abnormal DA release is thought to occur by reverse transport through the DA transporter (DAT), and it is believed to underlie the severe behavioral effects of these drugs. Here we compare structurally similar AMPH and METH on DAT function in a heterologous expression system and in an animal model. In the in vitro expression system, DAT-mediated whole-cell currents were greater for METH stimulation than for AMPH. At the same voltage and concentration, METH released five times more DA than AMPH and did so at physiological membrane potentials. At maximally effective concentrations, METH released twice as much [Ca(2+)](i) from internal stores compared with AMPH. [Ca(2+)](i) responses to both drugs were independent of membrane voltage but inhibited by DAT antagonists. Intact phosphorylation sites in the N-terminal domain of DAT were required for the AMPH- and METH-induced increase in [Ca(2+)](i) and for the enhanced effects of METH on [Ca(2+)](i) elevation. Calmodulin-dependent protein kinase II and protein kinase C inhibitors alone or in combination also blocked AMPH- or METH-induced Ca(2+) responses. Finally, in the rat nucleus accumbens, in vivo voltammetry showed that systemic application of METH inhibited DAT-mediated DA clearance more efficiently than AMPH, resulting in excess external DA. Together these data demonstrate that METH has a stronger effect on DAT-mediated cell physiology than AMPH, which may contribute to the euphoric and addictive properties of METH compared with AMPH.
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D-amphetamine and methamphetamine rapidly enter the brain and increase synaptic DA by competitively inhibiting DAT and reversing DAT direction.
“D-amphetamine and methamphetamine enter brain rapidly after administration. They competitively inhibit dopamine transporter (DAT) clearing dopamine (DA), and also release DA via reversing DAT direction, ultimately causing excessive DA accumulation in synaptic cleft ultimately (11).”
From Effects of Lisdexamfetamine, a Prodrug of D-Amphetamine, on Locomotion, Spatial Cognitive Processing and Neurochemical Profiles in Rats: A Comparison With Immediate-Release Amphetamine (2022) · cites this paper as [11]
The Abstract states that D-amphetamine and methamphetamine competitively inhibit DAT-mediated dopamine uptake and release dopamine through reverse transport; the Discussion also describes excess dopamine in synaptic clefts. Our copy does not establish that both drugs enter the brain rapidly after administration, so that part of the attributed claim is unsupported. (LLM, conf=0.88)
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“the action-potential independent release of monoamines [8,74], however, action potentials occur in hippocampal slices independent of electrical stimulation [75,76,77].”
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Raineri, M., González, B., Goitia, B., Garcia-Rill, E., Krasnova, I., Cadet, J., Urbano, F. J., & Bisagno, V. (2012) · PLoS ONE · doi:10.1371/journal.pone.0046599 · Cited by 72
“DA accumulates in the cytoplasm, which alters the concentration gradient and likely serves to favor the reverse transport of DA via the DAT [33].”
BackgroundAlpha-synuclein modulates dopamine neurotransmission
Butler, B., Sambo, D. O., & Khoshbouei, H. (2016) · Journal of Chemical Neuroanatomy · doi:10.1016/j.jchemneu.2016.06.001 · Cited by 71 · see citing works
Self-citationRole of organic cation transporters (OCTs) in the brain.
Couroussé, T., & Gautron, S. (2015) · Pharmacology and Therapeutics · doi:10.1016/j.pharmthera.2014.09.008 · Cited by 71 · see citing works
Psychostimulant addiction treatment
Phillips, K. A., Epstein, D. H., & Preston, K. L. (2014) · Neuropharmacology · doi:10.1016/j.neuropharm.2014.04.002 · Cited by 75 · see citing works
“Methamphetamine is more potent and more efficacious than amphetamine, producing much higher concentrations of synaptic dopamine (Goodwin et al., 2009) and more toxic effects on nerve terminals (Carvalho et al.”
BackgroundReddy, P. K. V., Ng, T. M. H., Oh, E. E., Moady, G., & Elkayam, U. (2020) · Journal of the American Heart Association · doi:10.1161/jaha.120.016704 · Cited by 98 · see citing works
Sambo, D. O., Lebowitz, J. J., & Khoshbouei, H. (2018) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2018.01.009 · Cited by 75 · see citing works
“structures and cellular effects (Goodwin et al., 2009; Saha et al., 2014), and METH is more commonly associated with recreational use and drug addiction.”
Self-citationBranch, S. Y., & Beckstead, M. J. (2012) · Journal of Neurophysiology · doi:10.1152/jn.00094.2012 · Cited by 67 · see citing works
“Data obtained using expression systems and cell culture later identified DAT-mediated excitation produced by dopamine, D-amphetamine, and methamphetamine, including one report in cultured dopamine neurons (Erreger et al. 2008; Goodwin et al. 2009; Ingram et al. 2002; Sonders et al. 1997).”
BackgroundInfluentialMembrane potential shapes regulation of dopamine transporter trafficking at the plasma membrane
Richardson, B. D., Saha, K., Krout, D., Cabrera, E. A., Felts, B., Henry, L. K., Swant, J., Zou, M., Newman, A. H., & Khoshbouei, H. (2016) · Nature Communications · doi:10.1038/ncomms10423 · Cited by 62 · see citing works
Self-citationDopamine Transporter Activity Is Modulated by α-Synuclein*
Butler, B., Saha, K., Rana, T., Becker, J., Sambo, D. O., Davari, P., Goodwin, J., & Khoshbouei, H. (2015) · Journal of Biological Chemistry · doi:10.1074/jbc.m115.691592 · Cited by 65 · see citing works
Self-citationMackie, P. M., Lebowitz, J., Saadatpour, L., Nickoloff, E., Gaskill, P. J., & Khoshbouei, H. (2018) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2018.03.020 · Cited by 70 · see citing works
Self-citationHIV, Tat and dopamine transmission
Gaskill, P. J., Miller, D. R., Gamble‐George, J., Yano, H., & Khoshbouei, H. (2017) · Neurobiology of Disease · doi:10.1016/j.nbd.2017.04.015 · Cited by 77 · see citing works
Self-citationCotter, R., Pei, Y., Mus, L., Harmeier, A., Gainetdinov, R., Hoener, M., & Canales, J. (2015) · Frontiers in Neuroscience · doi:10.3389/fnins.2015.00039 · Cited by 63 · see citing works
“ORIGINAL RESEARCH ARTICLE published: 13 February 2015 doi: 10.3389/fnins.2015.00039 The trace amine-associated receptor 1 modulates methamphetamine’s neurochemical and behavioral effects”
BackgroundInfluentialPsychostimulants and Movement Disorders
Asser, A., & Taba, P. (2015) · Frontiers in Neurology · doi:10.3389/fneur.2015.00075 · Cited by 62 · see citing works
“They induce dopamine release into the synaptic cleft by affecting synaptic vesicular release, more specifically vesicular monoamine transporter type 2 (VMAT2) (60), and altering DAT function by acting as substrates for the transporter (61).”
BackgroundProline-directed phosphorylation of the dopamine transporter N-terminal domain
Gorentla, B. K., Moritz, A. E., Foster, J., & Vaughan, R. (2009) · Biochemistry · doi:10.1021/bi801696n · Cited by 62 · see citing works
“The precise mechanisms by which most of these effects occur remain unknown, although DAT N-terminal phosphorylation has been reported to be required for AMPH-induced efflux and AMPH/METHinduced increases in intracellular Ca2+ (29) but not for PKC orAMPH-inducedDATendocytosisanddown-regulation(18,30).”
BackgroundMethamphetamine Regulation of Firing Activity of Dopamine Neurons
Lin, M., Sambo, D. O., & Khoshbouei, H. (2016) · Journal of Neuroscience · doi:10.1523/jneurosci.1392-16.2016 · Cited by 61 · see citing works
“The cell culture and maintenance have been described previously (Goodwin et al., 2009; Saha et al., 2014).”
BackgroundMethodSelf-citationHan, W.-Y., Du, P., Fu, S.-Y., Wang, F., Song, M.-H., Wu, C.-F., & Yang, J.-Y. (2014) · Pharmacology, Biochemistry and Behavior · doi:10.1016/j.pbb.2013.11.014 · Cited by 61 · see citing works
Methamphetamine Dysregulation of the Central Nervous System and Peripheral Immunity
Miller, D. R., Bu, M., Gopinath, A., Martinez, L. R., & Khoshbouei, H. (2021) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.121.000767 · Cited by 68 · see citing works
“…levels in the brain (Mantle et al., 1976; Wall et al., 1995; Jones et al., 1999; Khoshbouei et al., 2003; Binda et al., 2005; Kahlig et al., 2005; Sulzer et al., 2005; Fog et al., 2006; Goodwin et al., 2009; Saha et al., 2014; Lin et al., 2016; Sambo et al., 2017; Miller et al., 2021).”
BackgroundSelf-citationPhosphorylation of Dopamine Transporter Serine 7 Modulates Cocaine Analog Binding*
Moritz, A. E., Foster, J., Gorentla, B. K., Mazei-Robison, M., Yang, J.-W., Sitte, H., Blakely, R., & Vaughan, R. (2012) · Journal of Biological Chemistry · doi:10.1074/jbc.m112.407874 · Cited by 55 · see citing works
“Several properties of DAT including forward and reverse transport, endocytosis, and phosphorylation are affected by PKC and AMPH/METH exposure [reviewed in (18-20)], and AMPH/METH-stimulated DA efflux has also been linked to Ca and CaMKII (7, 21, 22).”
BackgroundDopamine transporter activity is modulated by α-synuclein.
Butler, B., Goodwin, S. J., Saha, K., Becker, J., Sambo, D. O., Davari, P., & Khoshbouei, H. (2015) · Journal of Biological Chemistry · doi:10.1074/jbc.a115.639880 · Cited by 54
Self-citationMorrow, B. A., Roth, R. H., Redmond, D. E., & Elsworth, J. D. (2011) · Neuroscience · doi:10.1016/j.neuroscience.2011.05.046 · Cited by 53 · see citing works
“Amphetamine itself has detrimental impact on DA neurons, but this is generally thought to be less severe than that exerted by methamphetamine (Goodwin et al., 2009; NIDA, 2005).”
BackgroundRoth, J., Li, Z., Sridhar, S., & Khoshbouei, H. (2013) · Neurotoxicology · doi:10.1016/j.neuro.2013.01.002 · Cited by 51
“Our previous findings (Goodwin et al., 2009; Kahlig et al., 2005; Khoshbouei et al., 2004; Khoshbouei et al., 2003) suggest that 5–8 min after the patch assumed whole-cell configuration, the intracellular ionic environment and pipette solution reached equilibrium.”
BackgroundMethodInfluentialSelf-citationStructural plasticity of the brain to psychostimulant use
Nyberg, F. (2014) · Neuropharmacology · doi:10.1016/j.neuropharm.2014.07.004 · Cited by 49 · see citing works
Neural and Cardiac Toxicities Associated With 3,4-Methylenedioxymethamphetamine (MDMA)
Baumann, M. H., & Rothman, R. B. (2009) · International review of neurobiology · doi:10.1016/s0074-7742(09)88010-0 · Cited by 47 · see citing works
“…the DA transporter (DAT) have shown that inward transport of a substrate like amphetamine is accompanied by an inward sodium current, which increases the concentration of intracellular sodium at the transporter, thereby facilitating reverse transport of DA (Goodwin et al., 2008; Pifl et al., 2009).”
BackgroundMechanism of Manganese Dysregulation of Dopamine Neuronal Activity
Lin, M., Colon-Perez, L., Sambo, D. O., Miller, D. R., Lebowitz, J., Jimenez-Rondan, F. R., Cousins, R., Horenstein, N., Aydemir, T., Febo, M., et al. (2019) · Journal of Neuroscience · doi:10.1101/792143 · Cited by 45
“The cells were cultured as described previously (Goodwin et al., 2009; Saha et al., 2014; Wang et al., 2009).”
MethodSelf-citationIntracellular Methamphetamine Prevents the Dopamine-induced Enhancement of Neuronal Firing*
Saha, K., Sambo, D. O., Richardson, B. D., Lin, L. M., Butler, B., Villarroel, L., & Khoshbouei, H. (2014) · Journal of Biological Chemistry · doi:10.1074/jbc.m114.563056 · Cited by 45 · see citing works
“Recently, we demonstrated at equipotent concentrations, methamphetamine evokes a greater dopamine efflux via DAT than amphetamine and at a lower membrane potential (29).”
BackgroundInfluentialSelf-citationGENETICS OF NOVELTY SEEKING, AMPHETAMINE SELF-ADMINISTRATION AND REINSTATEMENT USING INBRED RATS
Meyer, A. C., Rahman, S., Charnigo, R., Dwoskin, L., Crabbe, J. C., & Bardo, M. (2010) · Genes, Brain and Behavior · doi:10.1111/j.1601-183x.2010.00616.x · Cited by 45 · see citing works
“Finally, while the neural mechanisms involved in the straindependent behavioral effects observed here are unknown, AMPH is known to reverse the dopamine transporter (DAT; Goodwin et al. 2009).”
BackgroundMethamphetamine acts on subpopulations of neurons regulating sexual behavior in male rats
Frohmader, K. S., Wiskerke, J., Wise, R. A., Lehman, M. N., & Coolen, L. (2010) · Neuroscience · doi:10.1016/j.neuroscience.2009.12.070 · Cited by 43 · see citing works
Pei, Y., Asif-Malik, A., Hoener, M. C., & Canales, J. J. (2016) · Addiction Biology · doi:10.1111/adb.12410 · Cited by 46 · see citing works
“METH also interacts with the vesicular monoamine transporter-2 resulting in depleted vesicular storage of monoamines and increased cytoplasmic DA that is available for reverse transport by the DAT (Fleckenstein, Volz, & Hanson 2009; Sulzer et al. 2005).”
BackgroundInfluentialHofford, R. S., Darna, M., Wilmouth, C. E., Dwoskin, L. P., & Bardo, M. T. (2014) · Behavioural Brain Research · doi:10.1016/j.bbr.2014.05.007 · Cited by 42 · see citing works
Abar, B. W., LaGasse, L. L., Derauf, C., Newman, E., Shah, R., Smith, L. M., Arria, A. M., Huestis, M. A., Grotta, S. A. D., Dansereau, L. M., et al. (2012) · Psychology of Addictive Behaviors · doi:10.1037/a0030157 · Cited by 45 · see citing works
“It is important to note that amphetamine and methamphetamine are very similar substances chemically, with the primary differences experienced by users being that methamphetamine is stronger and acts more quickly in the body than amphetamine (Goodwin et al., 2009).”
Marusich, J. A., Darna, M., Charnigo, R. J., Dwoskin, L. P., & Bardo, M. T. (2011) · Experimental and Clinical Psychopharmacology · doi:10.1037/a0023897 · Cited by 40 · see citing works
“Since AMP is known to reverse the dopamine transporter (DAT; Goodwin et al., 2009; Kahlig et al., 2005; Sulzer et al., 2005), rats were examined for [3H]DA uptake in medial prefrontal cortex (mPFC) and orbitofrontal cortex (OFC) using in vitro procedures.”
MethodMethamphetamine-induced locomotor changes are dependent on age, dose and genotype
Good, R. L., & Radcliffe, R. A. (2010) · Pharmacology Biochemistry and Behavior · doi:10.1016/j.pbb.2010.12.004 · Cited by 38 · see citing works
“METH and AMPH have been shown to influence DAT function differently (Goodwin et al., 2009).”
BackgroundThe complex role of inflammation and gliotransmitters in Parkinson's disease
Gopinath, A., Mackie, P. M., Phan, L. T., Tansey, M. G., & Khoshbouei, H. (2022) · Neurobiology of Disease · doi:10.1016/j.nbd.2022.105940 · Cited by 45 · see citing works
Self-citationGlutamate homeostasis and dopamine signaling: Implications for psychostimulant addiction behavior
Fischer, K. D., Knackstedt, L. A., & Rosenberg, P. A. (2020) · Neurochemistry International · doi:10.1016/j.neuint.2020.104896 · Cited by 40 · see citing works
“Additionally, using in vitro electrophysiology in DA neurons, Goodwin and colleagues demonstrated greater DAT-mediated whole-cell currents for METH stimulation than for AMP stimulation and also that METH produced five times greater extracellular levels of DA compared to AMP (Goodwin et al., 2009).”
BackgroundAmphetamine activates calcium channels through dopamine transporter-mediated depolarization
Cameron, K. N., Solis, E., Ruchala, I., de Felice, L. D., & Eltit, J. (2015) · Cell Calcium · doi:10.1016/j.ceca.2015.06.013 · Cited by 39
Rothman, R., Partilla, J., Baumann, M., Lightfoot-Siordia, C., & Blough, B. (2012) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.111.188946 · Cited by 39
“The increased concentration of internal cellular sodium at the transporter also facilitates reverse transport of dopamine (Goodwin et al., 2009; Pifl et al., 2009).”
BackgroundNagai, T., Kitahara, Y., Shiraki, A., Hikita, T., Taya, S., Kaibuchi, K., & Yamada, K. (2010) · Neuroscience Letters · doi:10.1016/j.neulet.2009.12.071 · Cited by 38 · see citing works
Microglia in neuroimmunopharmacology and drug addiction
Li, H., Watkins, L. R., & Wang, X. (2024) · Molecular Psychiatry · doi:10.1038/s41380-024-02443-6 · Cited by 41 · see citing works
“METH and AMPH increase the excessive release of neurotransmitters such as DA and glutamate [139 – 141].”
Miyamoto, Y., Ishikawa, Y., Iegaki, N., Sumi, K., Fu, K., Sato, K., Furukawa‐Hibi, Y., Muramatsu, S., Nabeshima, T., Uno, K., et al. (2014) · The International Journal of Neuropsychopharmacology · doi:10.1017/s146114571400011x · Cited by 37 · see citing works
“The efficacy of METH depends primarily on its ability to increase extracellular DA levels in the brain (Clarke et al., 1988; Kuczenski et al., 1995; Goodwin et al., 2009).”
BackgroundMolecular Mechanisms of Amphetamines.
Reith, M., & Gnegy, M. (2019) · Handbook of Experimental Pharmacology · doi:10.1007/164_2019_251 · Cited by 32 · see citing works
Salvatore, M. F. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25021131 · Cited by 36 · see citing works
“Conversely, under conditions that increase DA release, such as induced by amphetamine or methamphetamine [125–127], there is increased locomotor activity [128–130].”
BackgroundKohno, M., Dennis, L. E., McCready, H. D., & Hoffman, W. F. (2021) · Molecular Psychiatry · doi:10.1038/s41380-021-01180-4 · Cited by 42 · see citing works
Jedynak, J., Cameron, C. M., & Robinson, T. (2012) · PLoS ONE · doi:10.1371/journal.pone.0034227 · Cited by 31 · see citing works
“Methamphetamine was recently demonstrated to be more effective at releasing DA and increasing internal calcium concentrations relative to d-amphetamine [32], which may be relevant to the drug-induced changes in Fos expression reported here.”
BackgroundRothman, R., Dersch, C., Ananthan, S., & Partilla, J. (2009) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.108.149088 · Cited by 31
“strate such as amphetamine induces an inward current of sodium, which increases the concentration of internal cellular sodium at the transporter, thereby facilitating reverse transport of the dopamine (Goodwin et al., 2009; Pifl et al., 2009).”
BackgroundHavlickova, T., Charalambous, C., Lapka, M., Puskina, N., Jeřábek, P., & Sustkova-Fiserova, M. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19102925 · Cited by 30 · see citing works
“However, several studies showed more potent effects of methamphetamine in neurochemical and behavioral studies [27,28].”
BackgroundHaddar, M., Uno, K., Azuma, K., Muramatsu, S., & Nitta, A. (2019) · Addiction Biology · doi:10.1111/adb.12749 · Cited by 29 · see citing works
“Effectively, reward is mainly controlled by the NAc, while psychomotor activity is controlled by the STR.26 Additionally, DA terminals in the NAc shell and dorsolateral STR originate mainly from the VTA and substantia nigra, pars compacta, respectively.27 This theory is also supported by nicotine addiction experiments.”
BackgroundRen, K., Guo, B., Dai, C., Yao, H., Sun, T., Liu, X., Bai, Z.-T., Wang, W.-T., & Wu, S.-X. (2017) · Front. Neural Circuits · doi:10.3389/fncir.2017.00057 · Cited by 29 · see citing works
“Previous reports suggested that D-AMPH could induce manic like behavior and increase DA releasing in the striatum (Frey et al., 2006; Goodwin et al., 2009).”
ResultRau, T. F., Ziemniak, J., & Poulsen, D. (2016) · Progress in Neuro-psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2015.02.013 · Cited by 28
Colon-Perez, L., Pino, J., Saha, K., Pompilus, M., Kaplitz, S., Choudhury, N., Jagnarine, D. A., Geste, J. R., Levin, B., Wilks, I., et al. (2018) · Neuropharmacology · doi:10.1016/j.neuropharm.2018.04.031 · Cited by 26 · see citing works
“Such potent and prolonged molecular actions of MDPV on DAT could result in downregulation, as observed with other amphetamines (Cervinski et al., 2005; Goodwin et al., 2009; Richards and Zahniser, 2009).”
Self-citationAndres, M. A., Cooke, I. M., Bellinger, F., Berry, M., Zaporteza, M. M., Rueli, R. H., Barayuga, S. M., & Chang, L. (2015) · Journal of Neurochemistry · doi:10.1111/jnc.13104 · Cited by 26 · see citing works
“In non-neuronal cells (kidney cells expressing human dopamine transporters), METH elevates intracellular Ca2+ concentration, but this increase is attributed to Ca2+ released from intracellular Ca2+ stores (Goodwin et al. 2009).”
Keller, C. M., Salvatore, M. F., Pruett, B. S., Guerin, G. F., & Goeders, N. E. (2011) · Psychopharmacology · doi:10.1007/s00213-011-2301-9 · Cited by 25 · see citing works
“To replenish DA stores normally maintained through DA reuptake but lost due to MA-induced reverse DA transport (Goodwin et al. 2009), Courtney M.”
BackgroundBanks, M., & Blough, B. (2015) · Neuropsychopharmacology · doi:10.1038/npp.2015.63 · Cited by 25 · see citing works
“In vitro and ex vivo studies suggest methamphetamine was more potent than amphetamine to induce dopamine (DA) release (Goodwin et al, 2009).”
BackgroundProgrammed neuronal cell death induced by HIV‐1 tat and methamphetamine
Li, Q., Lu, G., Kwong, W.-H., Choi, H.-L., Zeng, X.-F., Li, Z., Wai, Y. D., & Poon, W.-S. (2011) · Microscopy research and technique (Print) · doi:10.1002/jemt.21006 · Cited by 24
“Evidence shows that Meth has dopaminergic activation properties, either through inhibiting the reuptake of dopamine (DA) or by disrupting the vesicular storage of DA (Goodwin et al., 2009; Guillot et al., 2008; Westphalen and Stadlin, yL.”
BackgroundHeysieattalab, S., Naghdi, N., Zarrindast, M., Haghparast, A., Mehr, S. E., & Khoshbouei, H. (2015) · Pharmacology Biochemistry and Behavior · doi:10.1016/j.pbb.2015.12.008 · Cited by 23 · see citing works
Self-citationDopamine Transporter Is a Master Regulator of Dopaminergic Neural Network Connectivity
Miller, D. R., Guenther, D., Maurer, A. P., Hansen, C. A., Zalesky, A., & Khoshbouei, H. (2021) · Journal of Neuroscience · doi:10.1101/2021.01.22.427804 · Cited by 22
“The literature suggests that 10 mM methamphetamine evokes its maximum responses (Goodwin et al., 2009; Lin et al., 2016), which is blocked by 10mM nomifensine (Sambo et al.”
BackgroundMethodSelf-citationHensleigh, E., & Pritchard, L. M. (2014) · Behavioural Brain Research · doi:10.1016/j.bbr.2014.03.045 · Cited by 22 · see citing works
“Methamphetamine acutely decreases clearance of dopamine in the synaptic cleft by inhibiting reuptake through the dopamine transporter (Goodwin et al., 2009; Zahniser & Sorkin, 2004).”
InfluentialBhimani, R., Vik, M., Wakabayashi, K. T., Szalkowski, C., Bass, C., & Park, J. (2021) · Journal of Neurochemistry · doi:10.1111/jnc.15470 · Cited by 21 · see citing works
“…the increase in extracellular baseline DA signal may be a consequence of both enhanced phasic and tonic DA concentrations (Figures 3, 4, 6 & 7) as well as METH eliciting some non- exocytotic DA efflux (Goodwin et al., 2009), similar to a previous FSCV study with amphetamine (Daberkow et al., 2013).”
BackgroundResultTargeting dopamine transporter to ameliorate cognitive deficits in Alzheimer's disease
Shaikh, A., Ahmad, F., Teoh, S., Kumar, J., & Yahaya, M. F. (2023) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2023.1292858 · Cited by 20 · see citing works
Neurobehavioral effects of environmental enrichment and drug abuse vulnerability: An updated review
Malone, S. G., Shaykin, J. D., Stairs, D. J., & Bardo, M. T. (2022) · Pharmacology Biochemistry and Behavior · doi:10.1016/j.pbb.2022.173471 · Cited by 21 · see citing works
Uno, K., Miyazaki, T., Sodeyama, K., Miyamoto, Y., & Nitta, A. (2017) · PLoS ONE · doi:10.1371/journal.pone.0174196 · Cited by 20 · see citing works
Prolactin protects against the methamphetamine-induced cerebral vascular toxicity.
Rosas-Hernández, H., Cuevas, E., Lantz-MPeak, S. M., Ali, S. F., & Gonzalez, C. (2013) · Current Neurovascular Research · doi:10.2174/15672026113109990031 · Cited by 20
Winkler, M. C., Greager, E. M., Stafford, J., & Bachtell, R. (2016) · Addiction Biology · doi:10.1111/adb.12476 · Cited by 19 · see citing works
“The observed MA-induced decrease in alcohol intake was surprising because MA is frequently co-administered with alcohol in humans, and dexamphetamine use, an active metabolite of MA, has been shown to facilitate heavy drinking (Green & Moore 2009; Bujarski et al. 2014).”
BackgroundFerragud, A., Velazquez-Sanchez, C., & Canales, J. J. (2014) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2014.03.015 · Cited by 19 · see citing works
“METH, as do other amphetamine derivatives, exerts part of its effects by activating norepinephrine pathways but it is recognized that its stimulant actions and rewarding properties result mainly from interactions with the DA system, especially the DAT (Fleckenstein et al., 2007; Sofuoglu and Sewell, 2009; Goodwin et a…”
BackgroundLee, K.-N., Pellom, S., Oliver, E., & Chirwa, S. (2014) · Synapse · doi:10.1002/syn.21731 · Cited by 19 · see citing works
“…of extracellular dopamine, serotonin, and norepinephrine by redistributing these neurotransmitters from synaptic vesicles to the cytosol, in addition to inducing reverse transport and competing for transmitter uptake at their cognate transporters (Goodwin et al., 2009; Sulzer et al., 2005).”
BackgroundA review of methamphetamine use and stroke in the young
Hemphill, K. R., Tierney, S., Tirschwell, D., & Davis, A. P. (2024) · Frontiers in Neurology · doi:10.3389/fneur.2024.1397677 · Cited by 18 · see citing works
Banks, M. L. (2016) · Annals of the New York Academy of Sciences · doi:10.1111/nyas.13276 · Cited by 18 · see citing works
Evidence for Non-Competitive Modulation of Substrate-Induced Serotonin Release
Rothman, R. B., Baumann, M. H., Blough, B., Jacobson, A. E., Rice, K. C., & Partilla, J. (2010) · Synapse · doi:10.1002/syn.20804 · Cited by 18
“…have shown, for example, that the inward transport of a substrate like amphetamine induces an inward current of sodium, which increases the concentration of internal cellular sodium at the transporter, thereby facilitating reverse transport of dopamine (Goodwin et al., 2008; Pifl et al., 2009).”
BackgroundRole of Microglia in Psychostimulant Addiction
da Silva, M. C. M., Iglesias, L. P., Candelario‐Jalil, E., Khoshbouei, H., Moreira, F. A., & de Oliveira, A. C. P. (2022) · Current Neuropharmacology · doi:10.2174/1570159x21666221208142151 · Cited by 24 · see citing works
“Ad-ditionally, amphetamines can disrupt neurotransmitter storage by interacting with the vesicular monoamine transporters (VMAT2) [8] that underlie enhanced monoamine release via a reverse efflux transport mechanism [9-11].”
Self-citationTNFα increases tyrosine hydroxylase expression in human monocytes
Gopinath, A., Badov, M., Francis, M. L., Shaw, G., Collins, A., Miller, D. R., Hansen, C. A., Mackie, P. M., Tansey, M. G., Dagra, A., et al. (2021) · npj Parkinson s Disease · doi:10.1038/s41531-021-00201-x · Cited by 22 · see citing works
Self-citationChen, C., Hsu, F., Li, C., & Huang, M. (2019) · Psychiatry Research Neuroimaging · doi:10.1016/j.pscychresns.2019.06.002 · Cited by 20 · see citing works
Yu, S.-J., Wu, K.-J., Bae, E.-K., Hsu, M.-J., Richie, C. T., Harvey, B., & Wang, Y. (2014) · Addiction Biology · doi:10.1111/adb.12193 · Cited by 17
“2004), EM4 cells (Goodwin et al. 2009), neonatal rat cardiomyocytes and HEK-293T cells overexpressing L-type Ca++ channel (Sugimoto et al.”
BackgroundHuang, Y., Li, J., Wu, L., Qiu, J. F., Zhao, X., Li, J., & Zhu, G. (2012) · Journal of Molecular Neuroscience · doi:10.1007/s12031-012-9729-1 · Cited by 16 · see citing works
“…used to induce a reliable and valid animal model of the positive symptoms of schizophrenia (Peleg-Raibstein et al. 2008), activates dopamine receptors and downstream signaling pathways by increasing the reverse transport (efflux) of dopamine into the extracellular space (Goodwin et al. 2009).”
Cardenas, A., & Lotfipour, S. (2022) · Nicotine & Tobacco Research · doi:10.1093/ntr/ntab218 · Cited by 16 · see citing works
Salgueiro, W. G., Soares, M. V., Martins, C. F., Paula, F. R., Rios-Anjos, R. M., Carrazoni, T., Mori, M. A., Müller, R., Aschner, M., Belo, C. A. D., et al. (2023) · Chemico-Biological Interactions · doi:10.1016/j.cbi.2023.110610 · Cited by 18 · see citing works
Samikkannu, T., Rao, K. V. K., Salam, A., Atluri, V., Kaftanovskaya, E., Agudelo, M., Perez, S., Yoo, C., Raymond, A. D., Ding, H., et al. (2015) · Scientific Reports · doi:10.1038/srep11130 · Cited by 16 · see citing works
Heysieattalab, S., Naghdi, N., Hosseinmardi, N., Zarrindast, M., Haghparast, A., & Khoshbouei, H. (2016) · Synapse · doi:10.1002/syn.21905 · Cited by 17 · see citing works
“METH is a substrate for DAT.”
BackgroundInfluentialSelf-citationSerial exposure to ethanol drinking and methamphetamine enhances glutamate excitotoxicity
Blaker, A. L., Moore, E. R., & Yamamoto, B. K. (2019) · Journal of Neurochemistry · doi:10.1111/jnc.14861 · Cited by 18 · see citing works
Clustered Kv2.1 decreases dopamine transporter activity and internalization
Lebowitz, J., Pino, J., Mackie, P., Lin, M., Hurst, C., Divita, K., Collins, A., Koutzoumis, D. N., Torres, G. E., & Khoshbouei, H. (2019) · Journal of Biological Chemistry · doi:10.1074/jbc.ra119.007441 · Cited by 14
“All traces shown are following subtraction of current in the presence of a DAT blocker (nomifensine, 10 M) as described previously (53).”
BackgroundMethodSelf-citationSon, J., Jeong, Y. C., & Kwon, Y. (2015) · Biological and Pharmaceutical Bulletin · doi:10.1248/bpb.b14-00539 · Cited by 14 · see citing works
Substance abuse and neurotransmission
Davis, S. E., & Zhu, J. (2022) · Advances in pharmacology · doi:10.1016/bs.apha.2021.10.007 · Cited by 12 · see citing works
- Authors
- Goodwin, J. S., Larson, G. A., Swant, J., Sen, N., Javitch, J. A., Zahniser, N. R., De Felice, L. J., & Khoshbouei, H.
- Affiliations
- Meharry Medical College (US)
- University of Colorado Denver (US)
- Columbia University (US)
- Corresponding author
- Khoshbouei, Habibeh
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2009-01
- Volume
- 284
- Issue
- 5
- Pages
- 2978-2989
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC2631950
- OpenAlex
- W2025188861
- Cited by
- 203
- References
- 82
- Citations by year
- 2026: 4 · 2025: 14 · 2024: 15 · 2023: 9 · 2022: 19 · 2021: 17 · 2020: 8 · 2019: 10 · 2018: 10 · 2017: 10 · 2016: 12 · 2015: 14 · 2014: 17 · 2013: 6 · 2012: 13
- FWCI
- 3.60
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Science Foundation (0642188)
- National Institutes of Health (DA012408, DA004216, DA022413)
- National Heart, Lung, and Blood Institute (T32HL076133, HL076133)
- National Institute on Drug Abuse (DA012408, P01DA012408, DA021471, DA015050, K05DA022413, DA-022413, DA-004216, K05DA015050, R01DA026947, DA06338, R24DA021471)
- National Cancer Institute (U54CA091408, U54CA91408)
- National Institute of Neurological Disorders and Stroke (U54NS041071, NS034075, R01NS034075)
- National Center for Research Resources (G12RR003032, U54RR019192, G12-RR03032)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Keywords
- amphetamine, methamphetamine, dopamine transporter, dopamine release, psychostimulants, intracellular calcium, N-terminal phosphorylation, calcium/calmodulin-dependent protein kinase II, protein kinase C, nucleus accumbens, dopamine clearance, drug addiction
- MeSH terms
- Amphetamine, Animals, Bacterial Proteins, Calcium, Cell Line, Dopamine, Humans, Luminescent Proteins, Male, Methamphetamine, Nucleus Accumbens, Rats, Sprague-Dawley, Patch-Clamp Techniques, Dopamine Plasma Membrane Transport Proteins, Rats, In Vitro Techniques
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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