Endogenous dopamine release induced by repetitive transcranial magnetic stimulation over the primary motor cortex: an [11C]raclopride positron emission tomography study in anesthetized macaque monkeys

Ohnishi, Takashi; Hayashi, Takuya; Okabe, Shingo; Nonaka, Ikuo; Matsuda, Hiroshi; Iida, Hidehiro; Imabayashi, Etsuko; Watabe, Hiroshi; Miyake, Yoshihiro; Ogawa, Mikako; Teramoto, Noboru; Ohta, Y.; Ejima, Norimasa; Sawada, Tohru; Ugawa, Yoshikazu

doi:10.1016/j.biopsych.2003.09.016

Cited by 92 publications

(51 citation statements)

References 49 publications

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“…The novel aspect of this work is to associate a measure of striatal dopamine release to the structure of the frontal cortex in humans. This association is of particular interest because alterations in both striatal dopamine and thickness of the frontal cortex have been observed in disease states, including addiction (Volkow et al, 1997;Martinez et al, 2005Martinez et al, , 2007Makris et al, 2008a,b;Durazzo et al, 2011a,b), Parkinson's disease (Brooks, 2003Lyoo et al, 2010;Sioka et al, 2010;Jubault et al, 2011;Pereira et al, 2012), and schizophrenia (Laruelle et al, 1996(Laruelle et al, , 1999AbiDargham et al, 1998;Bertolino et al, 2000;Kuperberg et al, 2003;Nesvåg et al, 2008;Goldman et al, 2009;Kegeles et al, 2010;Rimol et al, 2012). Evidence from these disease states suggests that the relationship between cortex and striatal dopamine function is complex.…”

Section: Discussionmentioning

confidence: 99%

“…They are coactivated in fMRI studies (Postuma and Dagher, 2006;Choi et al, 2012;Robinson et al, 2012), and frontostriatal connections are apparent with diffusion tensor imaging (Leh et al, 2007;Kamali et al, 2010;Robinson et al, 2012). Transcranial magnetic stimulation of parts of the frontal cortex alters striatal dopamine release (Strafella et al, 2001(Strafella et al, , 2003(Strafella et al, , 2005Ohnishi et al, 2004;Ko et al, 2008), and increased metabolic activity in prefrontal regions is associated with smaller amphetamine-induced striatal dopamine release in healthy subjects (Volkow et al, 2007). In laboratory animals, ablation of prefrontal dopamine terminals results in increased striatal dopamine function (Pycock et al, 1980).…”

Section: Introductionmentioning

confidence: 99%

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Individual Differences in Frontal Cortical Thickness Correlate with the d-Amphetamine-Induced Striatal Dopamine Response in Humans

Casey¹,

Cherkasova

Larcher³

et al. 2013

J. Neurosci.

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The meso-striatal dopamine system influences responses to rewards and the motivation to seek them out. Marked individual differences in these responses are seen in laboratory animals, related in part to input from the prefrontal cortex. Here we measured the relation between cortical morphology and drug-induced striatal dopamine release in healthy young people. Participants were 24 (17 male, 7 female; age 23.0 Ϯ 6.2 years) stimulant drug-naive subjects who underwent PET [ 11 C]raclopride scans with 0.3 mg/kg d-amphetamine orally and placebo, and an anatomical MRI scan for measuring cortical thickness. As expected, d-amphetamine produced significant reductions in [ 11 C]raclopride binding potential in the striatum as a percentage of the value in the placebo condition. There was substantial individual variability in this response, which was correlated with cortical thickness in the frontal lobe as a whole. The association was strongest in the anterior part of the right lateral prefrontal cortex and bilateral supplementary motor area. A thicker cortex was correlated with a smaller dopamine response. Together, this work demonstrates in humans an association between cortical thickness and the striatal dopamine response to drugs of abuse. Although prefrontal regulation of striatal function has been well studied, it was unclear whether the thickness of the prefrontal cortex was an acceptable proxy to the function of that region. These results suggest it is.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Individual Differences in Frontal Cortical Thickness Correlate with the d-Amphetamine-Induced Striatal Dopamine Response in Humans

Casey¹,

Cherkasova

Larcher³

et al. 2013

J. Neurosci.

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“…Strafella et al have shown recently in normal humans that rTMS of the PMC increases DA in the ipsilateral putamen 27,28 . Ohnishi et al showed that rTMS over PMC also increases DA release in macaques, here restricted to the mesolimbic ventral striatum 16 . These effects may be mediated via direct corticostriatal excitation of striatal DA terminals or via multisynaptic pathways 5 .…”

Section: Discussionmentioning

confidence: 99%

Motor cortex stimulation: mild transient benefit in a primate model of Parkinson disease

McCairn²,

Zada³

et al. 2007

JNS

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Objective-We sought to examine the therapeutic efficacy of motor cortex stimulation (MCS) in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated macaques, and to characterize therapeutic differences with varying modes, frequencies, and durations of stimulation.Methods-MCS was delivered at currents below motor threshold and at frequencies between 5Hz and 150Hz through epidural electrodes over primary motor cortex. The animals were studied on and off MCS using video analysis, activity logging, and food retrieval tasks. Animals were examined using two different stimulation protocols. The first protocol consisted of one hour of MCS therapy daily. The second protocol exposed the animal to continuous MCS for over 24 hours with at least 2 weeks between MCS therapy.Conclusions-Daily MCS revealed no consistent change in symptoms, but MCS at two-week intervals resulted in significant increases in activity. Effects of biweekly MCS disappeared, however, within 24 hours of the onset of continuous MCS. In this study, MCS only temporarily reduced the severity of MPTP-induced parkinsonism.

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“…In fact, positive results have been reported in clinical trials using stimulus intensity around the motor threshold (Elahi and Chen 2009 ). Human as well as monkey studies with the positron emission tomography also suggested dopamine secretion in the striatum by rTMS (Strafella et al 2003 ;Ohnishi et al 2004 ), but patient studies so far are not very promising. In early PD patients with unilateral symptoms, rTMS over the primary motor cortex (M1) contralateral to the symptomatic side did decrease […”

Section: Mechanisms Of Rtms For Pd Therapymentioning

confidence: 93%

Clinical Applications of rTMS in Parkinson’s Disease

Shirota

Hamada

Ugawa³

2015

Therapeutic rTMS in Neurology

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Parkinson's disease (PD) has wide-ranging clinical features, and repetitive transcranial magnetic stimulation (rTMS) therapy has been tried for many aspects of PD. Underlying mechanism of rTMS therapy in PD remains unclear, but several possibilities are proposed such as endogenous dopamine release or restoration of neural plasticity or network activity. Motor symptoms are a cardinal feature of PD, for which evidence suggested moderate effi cacy of rTMS. High-frequency (HF) rTMS over the M1 including less focal stimulation (e.g., leg and bilateral hand M1 rTMS) or over the DLPFC, and low-frequency (LF) rTMS over the SMA were most favorable. Long-term administration of levodopa, a major agent for medical therapy of PD, can induce a motor complication called levodopainduced dyskinesia (LID). Several types of rTMS were reported to be effective for the LID. rTMS has also been tried for non-pharmacological treatment of nonmotor symptoms of PD including depression. A "weak recommendation" in favor of HF rTMS of the left DLPFC can be given for the treatment of depressive symptoms associated with PD. These are examples of growing application of rTMS therapy to PD for symptoms other than the classical motor symptoms. As such, rTMS has a potential to become an important adjunctive treatment for PD. Well-designed large clinical trials are needed to establish its utility in the clinical settings.

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Endogenous dopamine release induced by repetitive transcranial magnetic stimulation over the primary motor cortex: an [11C]raclopride positron emission tomography study in anesthetized macaque monkeys

Cited by 92 publications

References 49 publications

Individual Differences in Frontal Cortical Thickness Correlate with the d-Amphetamine-Induced Striatal Dopamine Response in Humans

Individual Differences in Frontal Cortical Thickness Correlate with the d-Amphetamine-Induced Striatal Dopamine Response in Humans

Motor cortex stimulation: mild transient benefit in a primate model of Parkinson disease

Clinical Applications of rTMS in Parkinson’s Disease

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