Effect of vigabatrin on striatal dopamine receptors: evidence in humans for interactions of GABA and dopamine systems.

Ring, Howard; Trimble, M R; Costa, Durval C.; George, Mark S.; Verhoeff, Paul; Ell, Peter J.

doi:10.1136/jnnp.55.9.758

Cited by 34 publications

(10 citation statements)

References 20 publications

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“…These five cases had a disease history and presentation similar to postictal psychosis. The lower striatal D2 binding may reflect an increased activity of the nigrostriatal dopamine pathway 22,23 . Baumgartner et al also demonstrated frontal hyperperfusion, especially in the mesial frontal areas in postictal psychosis 24 .…”

Section: Discussionmentioning

confidence: 98%

“…The lower striatal D2 binding may reflect an increased activity of the nigrostriatal dopamine pathway. 22,23 Baumgartner et al also demonstrated frontal hyperperfusion, especially in the mesial frontal areas in postictal psychosis. 24 This finding implied that the frontalsubcortical structures are involved in the development of postictal psychosis.…”

Section: Discussionmentioning

confidence: 98%

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Characteristics of postictal psychosis in a psychiatric center

Liu¹,

Chen

Yeh

et al. 2001

Psychiatry Clin Neurosci

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The clinical characteristics of 12 cases of postictal psychosis treated at Taipei City Psychiatric Center, Taipei, Taiwan, were retrospectively reviewed. Increased seizure frequency, especially with generalized tonic-clonic seizures, was the major risk factor predisposing to postictal psychosis. The psychotic symptoms were variable with delusions and/or hallucinations. These patients showed a much longer history of epilepsy (21.9 ± 10.7 years) prior to the development of postictal psychosis than has been previously reported. The possible mechanisms in the pathophysiology of psychosis in epileptics were discussed.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 98%

Characteristics of postictal psychosis in a psychiatric center

Liu¹,

Chen

Yeh

et al. 2001

Psychiatry Clin Neurosci

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“…First, in schizophrenic patients, both increased EBR (Karson, 1990; Mackert, Flectner, Woyth & Frick, 1991) and greater left than right dopaminergic activity in the striatum have been reported (Farde et al,1990; Nozaki et al, 2009). Second, children with left, but not right, focal epileptic activity displayed significantly lower EBR than those with a right focus (Caplan et al, 1998), and epilectic patients show lower DA D2 receptor binding in the left basal ganglia (Ring et al, 1992). These findings provide indirect support for the idea that greater activity in left striatal structures may drive both higher EBR and a rightward attentional bias (Tomer, 2008).…”

Section: Discussionmentioning

confidence: 99%

Eye-blink rate predicts individual differences in pseudoneglect

Slagter¹,

Davidson²,

Tomer³

2010

Neuropsychologia

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Most healthy individuals display a subtle spatial attentional bias, exhibiting relative inattention for stimuli on one side of the visual field, a phenomenon known as pseudoneglect. Prior work in animals and patients has implicated dopamine in spatial attention asymmetries. The current study therefore examined - in healthy individuals - the relationship between the attentional bias and spontaneous eye-blink rate (EBR), a putative measure of central dopaminergic function. We found that those individuals, who blinked more often under resting conditions, displayed greater preference for the right side of the visual display in a subsequent attention task. This finding may support the idea that the observed attentional bias in healthy individuals reflects asymmetries in dopaminergic circuits, and corroborates previous findings implicating dopamine in spatial attention.

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“…GABA interacts with the dopaminergic system [2] and there are several studies supporting the hypothesis of a GABAergic involvement in schizophrenia. Decreased benzodiazepine binding is correlated with poorer cognitive functioning among patients with schizophrenia [3], and there are significant correlations between the severity of schizophrenic symptoms and benzodiazepine binding [4].…”

Section: Introductionmentioning

confidence: 99%

Increased [<sup>3</sup>H]Tiagabine Binding to GAT-1 in the Cingulate Cortex in Schizophrenia

et al. 2002

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Postmortem samples from individuals with schizophrenia (n = 13) and control subjects (n = 10) were investigated for binding of [³H]tiagabine to GABA transporter-1 GAT-1. The binding was analyzed in the cingulate cortex and the caudate nucleus. There were no differences in binding affinity between the groups in any of the investigated areas. The maximum number of binding sites (B_max) was elevated in the schizophrenic cingulate cortex compared to controls (1,264 ± 96 vs. 860 ± 123 fmol/mg of protein). The B_max in the caudate nucleus for schizophrenics (426 ± 40 fmol/mg of protein) was the same as for controls (495 ± 69 fmol/mg of protein). The increase in GAT-1 in schizophrenia could be explained by a modulatory upregulation in the cingulate cortex.

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Effect of vigabatrin on striatal dopamine receptors: evidence in humans for interactions of GABA and dopamine systems.

Cited by 34 publications

References 20 publications

Characteristics of postictal psychosis in a psychiatric center

Characteristics of postictal psychosis in a psychiatric center

Eye-blink rate predicts individual differences in pseudoneglect

Increased [<sup>3</sup>H]Tiagabine Binding to GAT-1 in the Cingulate Cortex in Schizophrenia

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