[3H]GBR 12935 binding to dopamine uptake sites: subcellular localizatio and reduction in Parkinson's disease and progressive supranuclear palsy

Maloteaux, Jean‐Marie; Vanisberg, Marie-Agnès; Laterre, C.; Javoy‐Agid, F.; Agid, Yves; Laduron, P M

doi:10.1016/0014-2999(88)90278-6

Cited by 86 publications

(34 citation statements)

References 29 publications

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“…The saturation experiments showed that the [3H]GBR-12935 binding to rat striatum was saturable and of high affinity within the nanomolar range, in agreement with other studies of rat striatum [6,8,13] …”

Section: Discussionsupporting

confidence: 75%

“…In addition, [3H]GBR-12935 binding was found to be reduced by intracerebroventricular administration of the neurotoxin 6-hydroxydopamine, a finding supporting the close association between dopamine neurites and [3H]GBR-12935 binding. Also, a close parallelism has been observed between the subcellular localization pro files in rat striatum for [3H]dopamine uptake and [3H]GBR-12935 specific binding [8].…”

mentioning

confidence: 88%

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[<sup>3</sup>H]GBR-12935 Binding to Dopamine Uptake Sites in Rat Striatum

et al. 1990

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The binding of the selective dopamine uptake inhibitor [³H]GBR-12935 to rat striatum was studied. Competition by mazindol and dopamine against [³H]GBR-12935 binding revealed monophasic binding curves. The addition of 100 μM dopamine to the mazindol competition inhibited only 80% of the binding, indicating more than one [³H]GBR-12935 binding site in rat striatum. When a binding fraction that could be discriminated by 1 μM mazindol or 1 mM dopamine was defined as specific binding, a single site binding model was obtained. The [³H]GBR-12935 binding was of protein nature, since it was abolished after protease treatment. Drug inhibition studies with the addition of low concentrations of mazindol and dopamine resulted in alterations in apparent K_d values only, suggesting competitive inhibition by these compounds against [³H]GBR-12935 binding. It is concluded that the [³H]GBR-12935 binding to rat striatum discriminated by 1 μM mazindol reflects binding to the substrate recognition site for the dopamine uptake.

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Section: Discussionsupporting

confidence: 75%

mentioning

confidence: 88%

[<sup>3</sup>H]GBR-12935 Binding to Dopamine Uptake Sites in Rat Striatum

et al. 1990

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“…[ These results are consistent with previous reports showing an important loss of striatal dopamine uptake binding sites following degeneration of nigrostriatal dopamine neurons in humans or in rats (14,15). The binding of [ 3 H]-neurotensin, a modulator of dopamine release, was also found to be nearly abolished in the neostriatum after this treatment, indicating a specific localization in dopaminergic terminals (16).…”

supporting

confidence: 91%

Selective destruction of nigrostriatal dopaminergic neurons does not alter [3H]-ryanodine binding in rat striatum

Noël

Geurts

Maloteaux

2000

Braz J Med Biol Res

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Dopamine nigrostriatal neurons are important for motor control and may contain a particularly dense population of ryanodine receptors involved in the control of dopamine release. To test this hypothesis, we used a classical model of unilateral selective lesion of these neurons in rats based on 6-hydroxydopamine (6-OHDA) injection into the substantia nigra. Binding of [ 3 H]-GBR 12935, used as a presynaptic marker since it labels specifically the dopamine uptake complex, was dramatically decreased by 83-100% in striatum homogenates after 6-OHDA lesion. On the contrary, no reduction of [ 3 H]-ryanodine binding was observed. The present data indicate that [ 3 H]-ryanodine binding sites present in rat striatum are not preferentially localized in dopaminergic terminals.

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“…It could be pointed out that one of the most consistent findings in Parkinson's disease, is the reduced number of striatal DA uptake sites [5,[21][22][23], changes that could be explained by the dopaminergic degeneration that is the main neurobiological lesion in PD. In this disorder, dementia is a frequently occurring symptom [24].…”

Section: Discussionmentioning

confidence: 99%

Reduced Number of Caudate Nucleus Dopamine Uptake Sites in Vascular Dementia

Allard¹,

Englund²,

Marcusson³

1999

Dement Geriatr Cogn Disord

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The dopamine (DA) uptake sites in the caudate nucleus were studied in patients with vascular dementia (VAD) and in a control group using the presynaptic DA uptake site marker [³H][2β-carbomethoxy-3β-(4-fluorophenyl) tropane] as radioligand. There was a significant decrease in the number of DA uptake sites in the VAD group, while the binding affinity was unchanged. The present results indicate that in the patients investigated, the cerebrovascular disease process involves dopaminergic neuron terminals in the caudate nucleus. Our findings are discussed in relation to the reductions in number of DA uptake sites that have previously been revealed in Alzheimer’s and Parkinson’s diseases.

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[3H]GBR 12935 binding to dopamine uptake sites: subcellular localizatio and reduction in Parkinson's disease and progressive supranuclear palsy

Cited by 86 publications

References 29 publications

[<sup>3</sup>H]GBR-12935 Binding to Dopamine Uptake Sites in Rat Striatum

[<sup>3</sup>H]GBR-12935 Binding to Dopamine Uptake Sites in Rat Striatum

Selective destruction of nigrostriatal dopaminergic neurons does not alter [3H]-ryanodine binding in rat striatum

Reduced Number of Caudate Nucleus Dopamine Uptake Sites in Vascular Dementia

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