Solubilisation of high-affinity dopamine receptors

Gorissen, H.; Laduron, Pierre M.

doi:10.1038/279072a0

Cited by 73 publications

(12 citation statements)

References 22 publications

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“…almost three times higher than the corresponding value for membrane-bound receptors which was 1.25 ± 0.10nM. Similar effect was observed by several authors working on receptor solubilization (Gorissen et al, 1979;Madras et al, 1982;Davis et al, 1982;Witkin & Harden, 1982;Kuno et al, 1983) and it very probably results from the change in chemical environment of the receptor molecule.…”

Section: Discussionsupporting

confidence: 79%

“…Dopamine receptors were isolated from several sources and solubilization was achieved with different detergents (Laduron & Ilien, 1982;Hall et al, 1983;Kuno et al, 1983). Using plant glycoside digitonin, Gorissen & Laduron (1979) reported the solubilization of binding sites from dog striatum which retained the characteristics of membranebound dopamine receptors. Gorissen et al (1980) showed that digitonin-solubilized dopamine receptors from rat striatum are masked by a high number of non-stereospecific spirodecanone sites, the number of which was much higher in the frontal cortex than in the striatum.…”

Section: Introductionmentioning

confidence: 99%

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Solubilization of dopamine‐D₂receptors from synaptosomal membranes of the bovine caudate nucleus

Kidrič

Petrović²,

Šoškić

et al. 1984

British J Pharmacology

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Section: Discussionsupporting

confidence: 79%

Section: Introductionmentioning

confidence: 99%

Solubilization of dopamine‐D₂receptors from synaptosomal membranes of the bovine caudate nucleus

Kidrič

Petrović²,

Šoškić

et al. 1984

British J Pharmacology

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“…5d). The role of dopaminergic D1-like receptors in exercise was also confirmed in vivo by using butaclamol, a well-characterized D1-receptor antagonist (Denef et al, 1980; Gorissen and Laduron, 1979). Administration of butaclamol before the exercise prevented the potential of exercise to attenuate serum TNF levels in endotoxemia (Fig.…”

Section: Resultsmentioning

confidence: 88%

“…Given that dopamine signals through either D1-like (D1R, D5R) or D2-like (D2R, D3R, D4R) dopaminergic receptors, we analyzed specific dopaminergic agonists including fenoldopam (a highly selective agonist for D1-like receptors) and pergolide (a selective agonist for D2-like receptors) (Gingrich and Caron, 1993; Grenader and Healy, 1991; Weber et al, 1998). Fenoldopam and pergolide are well-characterized stable and specific dopaminergic agonist with about 100-fold greater affinity for D1-like or D2-like receptors, respectively (Denef et al, 1980; Gorissen and Laduron, 1979; Grenader and Healy, 1991; Tiberi and Caron, 1994; Torres-Rosas et al, 2014; Weber et al, 1998). Fenoldopam was more effective than dopamine and pergolide at inhibiting LPS-induced TNF production in primary culture of splenocytes (Fig.…”

Section: Resultsmentioning

confidence: 99%

Exercise activates vagal induction of dopamine and attenuates systemic inflammation

Shimojo

Joseph

Shah

et al. 2019

Brain, Behavior, and Immunity

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Physical exercise is one of the most important factors improving quality of life, but it is not feasible for patients with morbidity or limited mobility. Most previous studies focused on high-intensity or long-term exercise that causes metabolic stress or physiological adaption, respectively. Here, we studied how moderate-intensity swimming affects systemic inflammation in 6–8 week old C57BL/6J male mice during endotoxemia. One-hour swimming prevented hypokalemia, hypocalcemia, attenuated serum levels of inflammatory cytokines, increased anti-inflammatory cytokines but affected neither IL6 nor glycemia before or after the endotoxic challenge. Exercise attenuated serum TNF levels by inhibiting its production in the spleen through a mechanism mediated by the subdiaphragmatic vagus nerve but independent of the splenic nerve. Exercise increased serum levels of dopamine, and adrenalectomy prevented the potential of exercise to induce dopamine and to attenuate serum TNF levels. Dopaminergic agonist type-1, fenoldopam, inhibited TNF production in splenocytes. Conversely, dopaminergic antagonist type-1, butaclamol, attenuated exercise control of serum TNF levels. These results suggest that vagal induction of dopamine may contribute to the anti-inflammatory potential of physical exercise.

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“…Fenoldopam was more efficient than dopamine and pergolide at inhibiting LPS-induced TNF production both ex vivo and in vivo (Fig.4a,b). The role of D1-receptors was confirmed by using butaclamol, a standard D1-receptor antagonist 32,33 that inhibited the anti-inflammatory effects of electroacupuncture (Fig.4c,d; Supplementary Fig.3c). One dose of fenoldopam right after the induction of sepsis prevented mortality in polymicrobial peritonitis (Supplementary Fig.3d), and inhibited serum HMGB1 levels (Fig.4e).…”

mentioning

confidence: 79%

Dopamine mediates vagal modulation of the immune system by electroacupuncture

Torres‐Rosas

Yehia

Peña

et al. 2014

Nat Med

484

498

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Previous anti-inflammatory strategies against sepsis, a leading cause of death in hospitals, had limited efficacy in clinical trials, in part because they targeted single cytokines and the experimental models failed to mimic clinical settings1-3. Neuronal networks represent physiological mechanisms selected by evolution to control inflammation that can be exploited for the treatment of inflammatory and infectious disorders3. Here, we report that sciatic nerve activation with electroacupuncture controls systemic inflammation and rescues mice from polymicrobial peritonitis. Electroacupuncture at the sciatic nerve controls systemic inflammation by inducing a vagal activation of DOPA decarboxylase leading to the production of dopamine in the adrenal medulla. Experimental models with adrenolectomized animals mimic clinical adrenal insufficiency4, increase the susceptibility to sepsis, and prevent the anti-inflammatory potential of electroacupuncture. Dopamine inhibits cytokine production via dopaminergic type-1 receptors. Dopaminergic D1-agonists suppress systemic inflammation and rescue mice from polymicrobial peritonitis in animals with adrenal insufficiency. Our results suggest a novel anti-inflammatory mechanism mediated by the sciatic and the vagus nerves modulating the production of catecholamines in the adrenal glands. From a pharmacological perspective, selective dopaminergic agonists mimic the anti-inflammatory potential of electroacupuncture and can provide therapeutic advantages to control inflammation in infectious and inflammatory disorders.

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Solubilisation of high-affinity dopamine receptors

Cited by 73 publications

References 22 publications

Solubilization of dopamine‐D₂receptors from synaptosomal membranes of the bovine caudate nucleus

Solubilization of dopamine‐D₂receptors from synaptosomal membranes of the bovine caudate nucleus

Exercise activates vagal induction of dopamine and attenuates systemic inflammation

Dopamine mediates vagal modulation of the immune system by electroacupuncture

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Solubilisation of high-affinity dopamine receptors

Cited by 73 publications

References 22 publications

Solubilization of dopamine‐D2receptors from synaptosomal membranes of the bovine caudate nucleus

Solubilization of dopamine‐D2receptors from synaptosomal membranes of the bovine caudate nucleus

Exercise activates vagal induction of dopamine and attenuates systemic inflammation

Dopamine mediates vagal modulation of the immune system by electroacupuncture

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Solubilization of dopamine‐D₂receptors from synaptosomal membranes of the bovine caudate nucleus

Solubilization of dopamine‐D₂receptors from synaptosomal membranes of the bovine caudate nucleus