Amphetamine-Induced Dopamine Release and Post-Synaptic Specific Binding in Patients with Mild Tardive Dyskinesia

Adler, Caleb M.; Malhotra, Anil K.; Elman, Igor; Pickar, David; Breier, Alan

doi:10.1016/s0893-133x(01)00309-8

Cited by 11 publications

(9 citation statements)

References 35 publications

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“…Direct evidence for this hypothesis in humans is not as strong. Whereas chronic antipsychotic use has been shown to increase striatal D2‐receptor binding on PET imaging with a possible association with TD,33 larger studies have not shown this change to be correlated with severity of dyskinesia 34–36. Also, postmortem studies have not shown significant differences in D2‐receptor numbers between patients with and without tardive movement disorders,37 implying that D2‐receptor hypersensitivity may result from chronic antipsychotic use, but that TD does not always result.…”

Section: Pathophysiologymentioning

confidence: 99%

Tardive dyskinesia is caused by maladaptive synaptic plasticity: A hypothesis

2012

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It has been 50 years since the first patients with tardive dyskinesia (TD) were described, but the pathophysiology is only partially understood and effective treatments have remained elusive. Newer atypical antipsychotics with less nonspecific activity at dopamine receptors have not heralded the end of tardive dyskinesia and merely highlight the incomplete understanding of the disorder. We present an overview of the existing pathophysiology of the disorder and incorporate recent developments in genetics and the study of human synaptic plasticity in other hyperkinetic movement disorders. We propose a hypothesis that dopamine-receptor sensitization and altered function of the N-methyl-D-aspartate receptor produces maladaptive synaptic plasticity, which allows the encoding of abnormal motor programs, and propose studies that would falsify or support this hypothesis. In conclusion, a maladaptive synaptic plasticity" hypothesis goes some way toward filling in the gaps of existing theories of TD with the pathophysiology of other hyperkinetic movement disorders. © 2012 Movement Disorder Society.

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Section: Pathophysiologymentioning

confidence: 99%

Tardive dyskinesia is caused by maladaptive synaptic plasticity: A hypothesis

2012

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“…In vitro theory on competition between endogenous ligand, i.e., acetylcholine in the present study, and radioligand indicates that the binding of the latter should be affected by the concentration of the former. This competition has been demonstrated in vivo using positron emission tomography (PET) for the dopaminergic system and the D2 antagonist [ 11 C]raclopride (Adler et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Acute effects of physostigmine and galantamine on the binding of [¹⁸F]fluoro-A-85380: A PET study in monkeys

Valette

Bottlaender

Dollé

et al. 2005

Synapse

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2-[18F]fluoro-3-[2S-2-azetidinylmethoxy]pyridine ([18F]fluoro-A-85380) is an alpha4beta2 subtype selective nicotinic cholinergic agonist with potential suitability for studying changes in endogenous acetylcholine synaptic concentration. Physostigmine, a potent AChE inhibitor, and galantamine, an allosteric modulator of nAChRs, are widely used for the treatment of Alzheimer's disease. Before studying patients with this neurodegenerative disease, positron emission tomography (PET) studies in monkeys were performed to assess the impact of these two compounds on the radiotracer distribution volumes. Physostigmine was administered i.v. at two dosages: 150 microg/kg/h and 37.5 microg/kg/h for 160 min. Galantamine was administered i.v. at two dosages: 2 or 4 mg over 20 min. For PET data analysis, a model with one tissue (radioactivity of the parent compound in plasma and radioactivity in brain tissue) compartment was chosen because reliable parameter estimates could not be obtained with a more complex model. The higher dose of physostigmine produced a 40%, 23%, and 30% reduction of distribution volumes in the putamen, the temporal, and frontal cortices, respectively. The lower dose of physostigmine produced a reduction of 33%, 31%, and 24% in the same structures, respectively. Galantamine (4 mg or 2 mg) produced no significant change of distribution volumes in the basal ganglia, the temporal and frontal cortex. The effects of physostigmine, a more potent AChE inhibitor than galantamine, could be interpreted as a desensitization of nAChRs, due to a prolonged exposure to high synaptic concentration of acetylcholine or as a competition with acetylcholine.

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“…Moreover, it should be noted that D 2 supersensitivity does not always follow long-term administration of antipsychotic drugs. [7][8][9][10][11]20 The effects of previous antipsychotic drug treatment in subjects with schizophrenia may be a confounding factor and limitation to the study. Although all drugs were withdrawn at least 1 week prior to the study, this may have not been enough time to exclude persisting effects of antipsychotics on the brain.…”

Section: Discussionmentioning

confidence: 99%

“…6 However, this is not consistently reported, and some investigators have found no significant association between the D 2 system and TD. [7][8][9][10][11] Methodological issues have contributed to these reported differences. First, medication effects relating to the evaluation of TD are a primary consideration.…”

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confidence: 99%

Tardive Dyskinesia Predicts Prolactin Response to Buspirone Challenge in People With Schizophrenia

Shim

Kim²,

Kelly³

et al. 2005

JNP

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Prolactin response to buspirone was evaluated in patients with schizophrenia, with and without tardive dyskinesia (TD). Prolactin response in patients with schizophrenia without TD was significantly decreased, compared to healthy comparison subjects (F = 6.36, df = 5, p < 0.0001). Furthermore, prolactin levels after administration of buspirone were not significantly increased from baseline. In contrast, there was no prolactin response difference between patients with schizophrenia and TD and healthy subjects. This finding suggests that decreased dopamine (D(2)) receptor sensitivity may result in lower risk of developing TD and may lead to a fuller understanding of the variable expression of D(2)-receptor mediated side effects.

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Amphetamine-Induced Dopamine Release and Post-Synaptic Specific Binding in Patients with Mild Tardive Dyskinesia

Abstract: Several lines of evidence suggest that changes in dopamine release and/or post-synaptic sensitivity may be involved in the pathogenesis of tardive dyskinesia (TD

Cited by 11 publications

References 35 publications

Tardive dyskinesia is caused by maladaptive synaptic plasticity: A hypothesis

Tardive dyskinesia is caused by maladaptive synaptic plasticity: A hypothesis

Acute effects of physostigmine and galantamine on the binding of [¹⁸F]fluoro-A-85380: A PET study in monkeys

Tardive Dyskinesia Predicts Prolactin Response to Buspirone Challenge in People With Schizophrenia

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Amphetamine-Induced Dopamine Release and Post-Synaptic Specific Binding in Patients with Mild Tardive Dyskinesia

Abstract: Several lines of evidence suggest that changes in dopamine release and/or post-synaptic sensitivity may be involved in the pathogenesis of tardive dyskinesia (TD

Cited by 11 publications

References 35 publications

Tardive dyskinesia is caused by maladaptive synaptic plasticity: A hypothesis

Tardive dyskinesia is caused by maladaptive synaptic plasticity: A hypothesis

Acute effects of physostigmine and galantamine on the binding of [18F]fluoro-A-85380: A PET study in monkeys

Tardive Dyskinesia Predicts Prolactin Response to Buspirone Challenge in People With Schizophrenia

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Acute effects of physostigmine and galantamine on the binding of [¹⁸F]fluoro-A-85380: A PET study in monkeys