Brain SPECT Imaging of Amphetamine-Induced Dopamine Release in Euthymic Bipolar Disorder Patients

Anand, Amit; Verhoeff, Paul; Seneca, Nicholas; Zoghbi, Sami S.; Seibyl, John; Charney, Dennis S.; Innis, Robert B.

doi:10.1176/appi.ajp.157.7.1108

Cited by 206 publications

(108 citation statements)

References 17 publications

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“…There is also evidence that the presence of psychosis may moderate patterns of DA receptor binding. Specifically, striatal D 2 receptor signaling seems to be greater in psychotic patients with bipolar disorder [286,287], whereas no differences in D 2 availability were found between non-psychotic patients with bipolar disorder and controls [288,289]. …”

Section: Reviewmentioning

confidence: 99%

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Dichter

Damiano

Allen

2012

J Neurodevelop Disord

254

207

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This review summarizes evidence of dysregulated reward circuitry function in a range of neurodevelopmental and psychiatric disorders and genetic syndromes. First, the contribution of identifying a core mechanistic process across disparate disorders to disease classification is discussed, followed by a review of the neurobiology of reward circuitry. We next consider preclinical animal models and clinical evidence of reward-pathway dysfunction in a range of disorders, including psychiatric disorders (i.e., substance-use disorders, affective disorders, eating disorders, and obsessive compulsive disorders), neurodevelopmental disorders (i.e., schizophrenia, attention-deficit/hyperactivity disorder, autism spectrum disorders, Tourette’s syndrome, conduct disorder/oppositional defiant disorder), and genetic syndromes (i.e., Fragile X syndrome, Prader–Willi syndrome, Williams syndrome, Angelman syndrome, and Rett syndrome). We also provide brief overviews of effective psychopharmacologic agents that have an effect on the dopamine system in these disorders. This review concludes with methodological considerations for future research designed to more clearly probe reward-circuitry dysfunction, with the ultimate goal of improved intervention strategies.

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Section: Reviewmentioning

confidence: 99%

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Dichter

Damiano

Allen

2012

J Neurodevelop Disord

254

207

View full text Add to dashboard Cite

show abstract

“…Clinical evidence suggests that excessive or abnormal dopaminergic signaling contributes to this neurotransmission imbalance [13,28,31]. Thus, drugs that inhibit dopaminergic transmission (e.g., haloperidol) have an antimanic action in bipolar disorder [20], whereas drugs that stimulate dopamine synthesis (levodopa), bind to dopamine receptors (bromocriptine), or reduce dopamine reuptake (amphetamine), often precipitate mania [1,40].…”

Section: Introductionmentioning

confidence: 99%

“…The signaling process can be imaged in unanesthetized rats by injecting intravenously [1][2][3][4][5][6][7][8][9][10][11][12][13][14] C]AA and measuring tracer AA uptake into brain using quantitative autoradiography. Regional brain AA incorporation coefficients k* (brain radioactivity/integrated plasma radioactivity) are calculated and, if multiplied by unlabeled unesterified plasma AA concentrations, are converted to regional incorporation rates J in that represent regional brain AA consumption.…”

Section: Introductionmentioning

confidence: 99%

Chronic Carbamazepine Administration Attenuates Dopamine D2-like Receptor-Initiated Signaling via Arachidonic Acid in Rat Brain

et al. 2008

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Observations that dopaminergic antagonists are beneficial in bipolar disorder and that dopaminergic agonists can produce mania suggest that bipolar disorder involves excessive dopaminergic transmission. Thus, mood stabilizers used to treat the disease might act in part by downregulating dopaminergic transmission. In agreement, we reported that dopamine D 2 -like receptor mediated signaling involving arachidonic acid (AA, 20:4n-6) was downregulated in rats chronically treated with lithium. To see whether chronic carbamazepine, another mood stabilizer, did this as well, we injected i.p. saline or the D 2 -like receptor agonist, quinpirole (1 mg/kg), into unanesthetized rats that had been pretreated for 30 days with i.p. carbamazepine (25 mg/kg/day) or vehicle, and used quantitative autoradiography to measure regional brain incorporation coefficients (k*) for AA, markers of signaling. We also measured brain prostaglandin E 2 (PGE 2 ), an AA metabolite. In vehicle-treated rats, quinpirole compared with saline significantly increased k* for AA in 35 of 82 brain regions examined, as well as brain PGE 2 concentration. Affected regions belong to dopaminergic circuits and have high D 2 -like receptor densities. Chronic carbamazepine pretreatment prevented the quinpirole-induced increments in k* and in PGE 2 . These findings are consistent with the hypothesis that effective mood stabilizers generally downregulate brain AA signaling via D 2 -like receptors, and that this signaling is upregulated in bipolar disorder.

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“…As inherent and quantifiable measures of brain function, endophenotypes can potentially be used to investigate the fundamental pathology of complex illnesses, the manifest symptoms of which often cannot be quantified (Gottesman and Gould, 2003). The use of dopaminergic stimulants has been associated with the onset of mania in bipolar patients and with manic-like symptoms in control subjects (Anand et al, 2000;Mamelak, 1978;Murphy et al, 1971;Peet and Peters, 1995). Some studies report that lithium can attenuate or prevent the behavioral and/or functional effects of dopaminergic drugs Huey et al, 1981;Silverstone et al, 1998;van Kammen et al, 1985;Van Kammen and Murphy, 1975;Willson et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Strain Differences in Lithium Attenuation of d-Amphetamine-Induced Hyperlocomotion: A Mouse Model for the Genetics of Clinical Response to Lithium

Gould

O’Donnell

Picchini

et al. 2006

Neuropsychopharmacol

109

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Lithium attenuation of stimulant-induced hyperlocomotion is a rodent model that may be useful both to understand the mechanism of the therapeutic action of lithium and to develop novel lithium-mimetic compounds. To lay the foundation for future investigations into the neurobiology and genetics of lithium as a therapeutic agent, we studied the effect of lithium on d-amphetamine-induced hyperlocomotion in 12 (3 outbred) mouse strains. In our initial screening, mice received either (1) no drugs, (2) LiCl only, (3) damphetamine only, or (4) d-amphetamine and LiCl. Whereas there was no significant effect of LiCl alone on locomotion in any strain, there was a large degree of strain variation in the effects of LiCl combined with d-amphetamine. LiCl attenuated d-amphetamine-induced hyperlocomotion in C57BL/6J, C57BL/6Tac, Black Swiss, and CBA/J mice, whereas CD-1, FVB/NJ, SWR/J, and NIH Swiss mice, which were responsive to d-amphetamine, showed no significant effect of LiCl. d-Amphetamine-induced hyperlocomotion in the C3H/HeJ strain was increased by pretreatment with lithium. A subset of strains were treated for 4 weeks with lithium carbonate before the damphetamine challenge, and in each of these strains, lithium produced effects identical to those seen following acute administration. Strain responsiveness to lithium was not dependent upon the dose of either d-amphetamine or LiCl. Further, the results are not explained by brain lithium levels, which suggests that these behavioral responses to lithium are under the control of inherent genetic or other biological mechanisms specific to the effects of lithium on brain function.

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Brain SPECT Imaging of Amphetamine-Induced Dopamine Release in Euthymic Bipolar Disorder Patients

Abstract: In a group of euthymic patients with bipolar disorder, this study did not find evidence for increased striatal dopamine release. Instead, these data are consistent with enhanced postsynaptic dopamine responsivity in patients with bipolar disorder.

Cited by 206 publications

References 17 publications

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Chronic Carbamazepine Administration Attenuates Dopamine D2-like Receptor-Initiated Signaling via Arachidonic Acid in Rat Brain

Strain Differences in Lithium Attenuation of d-Amphetamine-Induced Hyperlocomotion: A Mouse Model for the Genetics of Clinical Response to Lithium

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