Tetrabenazine, a monoamine-depleting drug used in the treatment of hyperkinetic movement disorders

Guay, David R.P.

doi:10.1016/j.amjopharm.2010.08.006

Cited by 124 publications

(66 citation statements)

References 93 publications

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“…Recent studies also characterized the effort-related effects of the vesicular monoamine transport (VMAT) inhibitor tetrabenazine (Nunes et al, 2013b;Randall et al, 2014). Tetrabenazine produces depressive symptoms in humans (Guay, 2010;Frank, 2009Frank, , 2010, and because of its selective inhibition of VMAT-2, it preferentially depletes striatal DA (Pettibone et al, 1984). Rats were tested on concurrent lever pressing/chow feeding choice tasks, and tetrabenazine shifted response choice from the high effort response (lever pressing) to the low effort alternative (approach and consumption of chow; Nunes et al, 2013b;Randall et al, 2014).…”

Section: Conceptual Background: Motivationmentioning

confidence: 99%

Neurobiological basis of motivational deficits in psychopathology

Salamone

Koychev

Correa

et al. 2015

European Neuropsychopharmacology

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Section: Conceptual Background: Motivationmentioning

confidence: 99%

Neurobiological basis of motivational deficits in psychopathology

Salamone

Koychev

Correa

et al. 2015

European Neuropsychopharmacology

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“…What is less clear is why there is loss of function in this projection system. The ability of D 2 receptor antagonists and an inhibitor of the type 2 vesicular monoamine transporter (tetrabenazine) -which decreases striatal dopamine (DA) release - to ameliorate chorea (16)(17)(18) suggests that the loss of function is a consequence of a deficit in the ability of cortical neurons to drive activity in iSPNs. D 2 DA receptors are important negative modulators of excitability and glutamatergic synaptic transmission in iSPNs (19) (see below for more discussion of the potential role of DA in HD).…”

mentioning

confidence: 99%

Brain networks in Huntington disease

Eidelberg¹,

Surmeier²

2011

J. Clin. Invest.

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Recent studies have focused on understanding the neural mechanisms underlying the emergence of clinical signs and symptoms in early stage Huntington disease (HD). Although cell-based assays have focused on cell autonomous effects of mutant huntingtin, animal HD models have revealed alterations in the function of neuronal networks, particularly those linking the cerebral cortex and striatum. These findings are complemented by metabolic imaging studies of disease progression in premanifest subjects. Quantifying metabolic progression at the systems level may identify network biomarkers to aid in the objective assessment of new disease-modifying therapies and identify new regions that merit mechanistic study in HD models. Neuropathology in Huntington diseaseHuntington disease (HD) is caused by expansion of a CAG repeat in the huntingtin (Htt) gene. Expansion of the repeat length beyond 35 CAGs significantly elevates disease risk (1). The Htt gene is ubiquitously expressed in the brain with relative enrichment in cortical pyramidal neurons projecting to the striatum but relatively low levels in striatal projection neurons (2, 3).Although there are clear effects in the cerebral cortex and hippocampus, the most pronounced neuropathology in HD is found in the striatum (4, 5). The striatum is a key component of the basal ganglia, an interconnected set of subcortical nuclei involved in the regulation of how to act (and not act) in particular contexts (6). The striatum is composed primarily of GABAergic projection neurons with dendrites that are heavily studded with spines. These spiny projection neurons (SPNs) can be subdivided into two major classes on the basis of their axonal projection, dendritic size, and physiology as well as their expression of dopamine receptors and releasable peptides (7,8). SPNs that project to the external segment of the globus pallidus (GPe) form what is called the indirect SPN (iSPN) pathway because they indirectly control the nuclei that interface between the basal ganglia and the rest of the brain. SPNs that project to the internal segment of the globus pallidus (GPi) and substantia nigra pars reticulata form the direct SPN (dSPN) pathway. iSPNs are smaller and more excitable than dSPNs (Figure 1 and ref. 9); this difference is very likely to reflect a tonic negative modulation of iSPNs by dopamine acting at D 2 receptors. In contrast, dSPNs are positively modulated by D 1 receptors that appear to only be activated by transient elevations in dopamine release produced by bursts of action potentials in dopaminergic neurons (10).iSPNs and dSPNs are generally thought to play complementary roles in movement control and action selection. Both SPN populations have a rich, highly convergent synaptic connectivity with glutamatergic neurons distributed throughout much of the cerebral cortex (11). Both populations also have rich connectivity with glutamatergic neurons in the thalamus (12). A broad array of experimental evidence supports the proposition that iSPNs help to suppress cortical selection of...

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“…As a synthetic benzoquinoline TBZ depletes monoamines by a mechanism similar to that of reserpine. It has several advantages over reserpine related to its rapid onset of action, CNS selectivity and lesser hypotensive effects [58].…”

Section: Tetrabenazinementioning

confidence: 99%

Identification and management of tardive dyskinesia: A case series and literature review

Khouzam

2015

Postgraduate Medicine

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Tardive dyskinesia (TD) is a serious, disabling and potentially permanent, neurological hyperkinetic movement disorder that occurs after months or years of taking dopamine receptor-blocking agents. The pathophysiology of TD is complex, multifactorial and still not fully understood. Although there is no identified effective and standard treatment for TD, several agents have been tried for the management of this motor disturbance. The aim of this case series is to review the literature in regard to the identification, diagnosis and the treatment of TD with anticholinergics, anticholinergic medication withdrawal, cholinergic agents, botulinum toxin intramuscular injections, tetrabenazine, levetiracetam, propranolol and zolpidem, and to describe one case of TD that responded favorably to clonazepam and two cases of TD that responded favorably to Ginkgo biloba.

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Tetrabenazine, a monoamine-depleting drug used in the treatment of hyperkinetic movement disorders

Cited by 124 publications

References 93 publications

Neurobiological basis of motivational deficits in psychopathology

Neurobiological basis of motivational deficits in psychopathology

Brain networks in Huntington disease

Identification and management of tardive dyskinesia: A case series and literature review

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