Dopaminergic dysfunction in attention deficit hyperactivity disorder (ADHD), differences between pharmacologically treated and never treated young adults: A 3,4-dihdroxy-6-[18F]fluorophenyl-l-alanine PET study

Ludolph, Andrea G.; Kassubek, Jan; Schmeck, Klaus; Glaser, Cornelia; Wunderlich, Arthur; Buck, Andreas K.; Reske, Sven N.; Fegert, Jöerg M.; Mottaghy, Felix M.

doi:10.1016/j.neuroimage.2008.02.025

Cited by 75 publications

(43 citation statements)

References 45 publications

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“…1). Ludolph et al (2008) reported a decreased FDOPA influx rate. In both studies, the wash out phase was only 1 week prior to the scanning session, while in our study ADHD subjects were free of medication at least 1 year.…”

Section: Discussionmentioning

confidence: 97%

“…One year of treatment had no effect on the key area of hypofunction, the anterior cingulate cortex, in an attentional reorientation task, but decreased activity in the insula and striatum (Konrad et al 2007). Evidence for an influence of early treatment with MPH on the dopamine metabolism has been shown by Ludolph et al (2008). They found a lower FDOPA influx rate in the insula and putamen in MPHtreated subjects.…”

Section: Introductionmentioning

confidence: 98%

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Reward processing in male adults with childhood ADHD—a comparison between drug-naïve and methylphenidate-treated subjects

et al. 2011

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Basal ganglia reward processing seemed to be unrelated to MPH pretreatment, but was related to remission. On the other hand, the revealed differences between treated and drug-naïve subjects with childhood ADHD, i.e., in the insula, give evidence for more pronounced abnormal activation in reward-associated brain regions in untreated subjects with childhood ADHD and underpin the need of prospective studies on long-term effects of psychostimulant treatment.

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 98%

Reward processing in male adults with childhood ADHD—a comparison between drug-naïve and methylphenidate-treated subjects

et al. 2011

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“…5 Broadly speaking, the physiological function of the DA molecules themselves is to bind to post-and presynaptic receptors to modulate the activity of the postsynaptic targets 6 and to self-regulate DAergic activity, 7 respectively. Consequently, numerous drugs act by modulating extracellular DA concentrations (e.g., L-DOPA, MAO inhibitors, and inhibitors of the dopamine transporter (DAT) 8−11 ) or by modulating or mimicking the binding of DA to its receptors (DA agonists and antagonists).…”

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confidence: 99%

Restricted Diffusion of Dopamine in the Rat Dorsal Striatum

Taylor

Ilitchev

Michael

2013

ACS Chem. Neurosci.

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Recent evidence has shown that the dorsal striatum of the rat is arranged as a patchwork of domains that exhibit distinct dopamine kinetics and concentrations. This raises the pressing question of how these distinct domains are maintained, especially if dopamine is able to diffuse through the extracellular space. Diffusion between the domains would eliminate the concentration differences and, thereby, the domains themselves. The present study is a closer examination of dopamine's ability to diffuse in the extracellular space. We used voltammetry to record dopamine overflow in dorsal striatum while stimulating the medial forebrain bundle over a range of stimulus currents and frequencies. We also examined the effects of drugs that modulated the dopamine release (raclopride and quinpirole) and uptake (nomifensine). Examining the details of the temporal features of the evoked profiles reveals no clear evidence for long-distance diffusion of dopamine between fast and slow domains, even though uptake inhibition by nomifensine clearly prolongs the time that dopamine resides in the extracellular space. Our observations support the conclusion that striatal tissue has the capacity to retain dopamine molecules, thereby limiting its tendency to diffuse through the extracellular space. KEYWORDS: Dopamine, dopamine transporter, diffusion, evoked release, voltammetry, dorsal striatum C entral dopamine (DA) systems participate in numerous aspects of brain function, 1,2 and their dysfunction contributes to a broad array of disorders and diseases including Parkinson's disease, 3 schizophrenia, 4 and attention deficit hyperactivity disorder. 5 Broadly speaking, the physiological function of the DA molecules themselves is to bind to post-and presynaptic receptors to modulate the activity of the postsynaptic targets 6 and to self-regulate DAergic activity, 7 respectively. Consequently, numerous drugs act by modulating extracellular DA concentrations (e.g., L-DOPA, MAO inhibitors, and inhibitors of the dopamine transporter (DAT) 8−11 ) or by modulating or mimicking the binding of DA to its receptors (DA agonists and antagonists). 12,13 Some of the drugs that target DA systems have important therapeutic applications 14,15 while others have high potential for illicit abuse: 16−18 some therapeutic drugs are also abused. 19 Thus, it is significant to know the extracellular DA concentration per se, to know the kinetics of DA release and clearance that determine the concentration, and to know the actions of drugs that target DA systems.Recently, we have demonstrated that the DA terminal field in the rat dorsal striatum contains a patchwork of kinetic spatial domains. The fast and slow domains were brought to light by recordings of extracellular DA with fast-scan cyclic voltammetry (FSCV) at carbon fiber microelectrodes during electrical stimulation of the medial forebrain bundle (MFB). The extracellular concentration of DA, the kinetics of DA release and clearance, the short-term plasticity of DA release, and the actions of DA-ta...

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“…Therefore, proper dopaminergic neurotransmission can mediate many physiologic processes including addiction, movement, and lactation (Kahlig and Galli 2003;Oades 2000). Thus, the metabolic disorder of DA (Ernst et al 1997;Ludolph et al 2008;Solanto 2002) may cause poor motor impulse control, trigger hypoactivity of the dopamine systems in the brain, and be involved in the pathophysiology of ADHD (Coccaro et al 2007;Krain and Castellanos 2006;Russell 2003;Sagvolden and Sergeant 1998). As a main metabolite of DA, HVA is released back into the blood after the metabolism of DA in the central neural system, and its concentration in plasma has been widely used to study the function of central DA in psychiatric disorders (Baeza et al 2009;Dhir and Kulkarni 2007;Lv et al 2009;Soderstrom et al 2001a, b, Soderstrom et al 2003.…”

Section: Discussionmentioning

confidence: 99%

“…Attention deficit/hyperactivity disorder (ADHD) is characterized by excessive inattention, hyperactivity, and impulsivity, either alone or in combination (Krain and Castellanos 2006;Ludolph et al 2008). It is the most common psychiatric and neurobehavioural disorder in childhood: 3% to 10% of school-age children suffer from ADHD worldwide (Akhondzadeh et al 2003;Farias et al 2010;Goldman et al 1998;Puumala and Sirvio 1998;Salehi et al 2010).…”

Section: Introductionmentioning

confidence: 99%

Ningdong granule: a complementary and alternative therapy in the treatment of attention deficit/hyperactivity disorder

Wang

et al. 2011

Psychopharmacology

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Dopaminergic dysfunction in attention deficit hyperactivity disorder (ADHD), differences between pharmacologically treated and never treated young adults: A 3,4-dihdroxy-6-[18F]fluorophenyl-l-alanine PET study

Cited by 75 publications

References 45 publications

Reward processing in male adults with childhood ADHD—a comparison between drug-naïve and methylphenidate-treated subjects

Reward processing in male adults with childhood ADHD—a comparison between drug-naïve and methylphenidate-treated subjects

Restricted Diffusion of Dopamine in the Rat Dorsal Striatum

Ningdong granule: a complementary and alternative therapy in the treatment of attention deficit/hyperactivity disorder

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