Inhibitory effect of reserpine on dopamine transporter function

Metzger, Ryan R.; Brown, Jeffrey M.; Sandoval, Verónica; Rau, Kristi S.; Elwan, Mohamed A.; Miller, Gary W.; Hanson, Glen R.; Fleckenstein, Annette E.

doi:10.1016/s0014-2999(02)02647-x

Cited by 50 publications

(41 citation statements)

References 13 publications

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“…Our findings are consistent with an upregulation of noradrenaline reuptake in the LC area, which is well compatible with enhanced noradrenaline release [19,20].…”

Section: Increased Fp-cit Binding In the Lc Areasupporting

confidence: 89%

Anticipatory postural adjustments stabilise the whole upper-limb prior to a gentle index finger tap

Caronni

Cavallari

2008

Exp Brain Res

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“…Our findings are consistent with an upregulation of noradrenaline reuptake in the LC area, which is well compatible with enhanced noradrenaline release [19,20].…”

Section: Increased Fp-cit Binding In the Lc Areasupporting

confidence: 89%

Anticipatory postural adjustments stabilise the whole upper-limb prior to a gentle index finger tap

Caronni

Cavallari

2008

Exp Brain Res

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“…Given that DCs express machinery to synthesize and store DA, we hypothesized that intracellular stores of DA may stimulate D5R in an autocrine manner and promote IL-12 stimulation upon maturation. To test this possibility, we performed LPS-induced maturation experiments in which WT DCs were previously depleted of intracellular stores of DA by treatment with reserpine (42). Depletion of DA caused a significant decrease in IL-12 secretion in mDCs without affecting IL-10 or IL-6 production (Supplemental Fig.…”

Section: D5r Selectively Modulates Cytokine Secretion By Lps-stimulatmentioning

confidence: 99%

Stimulation of Dopamine Receptor D5 Expressed on Dendritic Cells Potentiates Th17-Mediated Immunity

Prado

Contreras

González

et al. 2012

The Journal of Immunology

115

132

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Dendritic cells (DCs) are responsible for priming T cells and for promoting their differentiation from naive T cells into appropriate effector cells. Emerging evidence suggests that neurotransmitters can modulate T cell-mediated immunity. However, the involvement of specific neurotransmitters or receptors remains poorly understood. In this study, we analyzed the role of dopamine in the regulation of DC function. We found that DCs express dopamine receptors as well as the machinery necessary to synthesize, store, and degrade dopamine. Notably, the expression of D5R decreased upon LPS-induced DC maturation. Deficiency of D5R on the surface of DCs impaired LPS-induced IL-23 and IL-12 production and consequently attenuated the activation and proliferation of Ag-specific CD4+ T cells. To determine the relevance of D5R expressed on DCs in vivo, we studied the role of this receptor in the modulation of a CD4+ T cell-driven autoimmunity model. Importantly, D5R-deficient DCs prophylactically transferred into wild-type recipients were able to reduce the severity of experimental autoimmune encephalomyelitis. Furthermore, mice transferred with D5R-deficient DCs displayed a significant reduction in the percentage of Th17 cells infiltrating the CNS without differences in the percentage of Th1 cells compared with animals transferred with wild-type DCs. Our findings demonstrate that by contributing to CD4+ T cell activation and differentiation to Th17 phenotype, D5R expressed on DCs is able to modulate the development of an autoimmune response in vivo.

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“…It is a naturally occurring potent alkaloid, derived from roots of several members of genus (Doyle et al, 1955). Reserpine depletes biogenic amines such as noradrenalin, dopamine and serotonin and is a potent oxidant (Osubor and Nwanze, 1994;Metzger et al, 2002). It has deteriorating effects on rat liver structure and function Inhibition property of green tea extract in relation to reserpine-induced ribosomal strips of rough endoplasmic reticulum (rER) of the rat kidney proximal tubule cells (Al-Bloushi et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Inhibition property of green tea extract in relation to reserpine-induced ribosomal strips of rough endoplasmic reticulum (rER) of the rat kidney proximal tubule cells

et al. 2009

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-The aim of this study was to evaluate the effect of green tea in inhibiting and reversing the nephrotoxicity of reserpine -a potent oxidative stress inducer -which induced cellular kidney damage. Serum biochemical parameters, antioxidant enzyme levels, thiobarbituric acid reactive substances (TBARS) and serum transaminases (glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT)) values and histopathology were systematically evaluated. Reserpine exposure led -ters and ultrastructural evaluation. Sprague-Dawely (S.D.) rats were intraperitonealy administered reserpine to induce oxidative kidney damage. Experimental rats were given green tea extract according to the protocol given below. Sixty rats were randomly divided into six groups, with 10 rats in each group. Reserpine was found to cause kidney proximal tubule damage, such as stripping and clustering of ribosomes from the rough endoplasmic reticulum (rER) and demolishing of mitochondrial christae with elevated level of oxidative stress markers, such as TBARS. While the ultrastructural study showed a revival of kidney proximal tubule cells as a result of the administration of green tea extract to rats. We suggest that green tea might elevate antioxidant defense system, clean up free radicals, lessen oxidative damages and protect kidney against reserpine -induced toxicity and thus had a potential protective effect.

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Inhibitory effect of reserpine on dopamine transporter function

Cited by 50 publications

References 13 publications

Anticipatory postural adjustments stabilise the whole upper-limb prior to a gentle index finger tap

Anticipatory postural adjustments stabilise the whole upper-limb prior to a gentle index finger tap

Stimulation of Dopamine Receptor D5 Expressed on Dendritic Cells Potentiates Th17-Mediated Immunity

Inhibition property of green tea extract in relation to reserpine-induced ribosomal strips of rough endoplasmic reticulum (rER) of the rat kidney proximal tubule cells

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