Gintonin, a novel ginseng-derived lysophosphatidic acid receptor ligand, stimulates neurotransmitter release

Hwang, Sung‐Hee; Lee, Byung-Hwan; Choi, Sun-Hye; Kim, Hyeonjoong; Jung, Sung-Jin; Kim, Hyun‐Sook; Shin, Ho‐Chul; Park, Hyun Jin; Park, Keun Hong; Lee, Myung Koo; Nah, Seung‐Yeol

doi:10.1016/j.neulet.2014.11.007

Cited by 32 publications

(31 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Gintonin also enhances NMDA receptor channel currents [14]. In addition, we demonstrated that gintonin-mediated [Ca 2+ ] i transients in PC12 cells are coupled to dopamine release [15]. However, the relationship between gintonin and astrocytes, and whether gintonin can regulate gliotransmitter release in astrocytes, was previously unknown, even though primary astrocytes abundantly express LPA receptor subtypes [4,5].…”

Section: Discussionmentioning

confidence: 90%

Gintonin stimulates gliotransmitter release in cortical primary astrocytes

Kim

Lee

Choi

et al. 2015

Neuroscience Letters

Self Cite

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 90%

Gintonin stimulates gliotransmitter release in cortical primary astrocytes

Kim

Lee

Choi

et al. 2015

Neuroscience Letters

Self Cite

View full text Add to dashboard Cite

“…More recently, it has been shown that gintonin-mediated intracellular Ca 2+ transients and dopamine release via LPA receptor activation in PC12 cells could be one mechanism of gintonin-mediated inter-neuronal modulation in the nervous system [33]. Furthermore, LPA is also known to facilitate dopamine release from PC12 cells, indicating that LPA stimulates dopamine release via specific LPA receptors presumably by activating the IP 3 mediated Ca 2+ release [45].…”

Section: Discussionmentioning

confidence: 99%

“…TMB-8 is reported to inhibit the Ca 2+ release from intracellular stores or increased the up-take of Ca 2+ into sarcoplasmic reticulum and the inhibition of Ca 2+ -influx from extracellular site may be an indirect mechanism [70]. Recently, it has also been shown that gintonin-mediated [Ca 2+ ] i transients are coupled to the stimulation of dopamine release in PC12 cells [33]. Thus, in light of these findings, our result shows that gintonin can trigger Ca 2+ release from the intracellular Ca 2+ store of the rat adrenomedullary chromaffin cells that participates in the CA secretion.…”

Section: Discussionmentioning

confidence: 99%

“…Meanwhile, some studies have shown that ginseng contains a novel G protein-coupled lysophosphatidic acid (LPA) receptor ligand, known as gintonin [303132]. Recently, it has been reported that treatment of gintonin to PC12 cells increased intracellular calcium ([Ca 2+ ] i ) as well as the release of dopamine in a concentration-dependent manner [33]. It was concluded that this gintonin-mediated [Ca 2+ ] i elevation is coupled to dopamine release via LPA receptor activation.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Gintonin facilitates catecholamine secretion from the perfused adrenal medulla

Kim

Choi

et al. 2016

Korean J Physiol Pharmacol

View full text Add to dashboard Cite

The present study was designed to investigate the characteristics of gintonin, one of components isolated from Korean Ginseng on secretion of catecholamines (CA) from the isolated perfused model of rat adrenal gland and to clarify its mechanism of action. Gintonin (1 to 30 µg/ml), perfused into an adrenal vein, markedly increased the CA secretion from the perfused rat adrenal medulla in a dose-dependent fashion. The gintonin-evoked CA secretion was greatly inhibited in the presence of chlorisondamine (1 µM, an autonomic ganglionic bloker), pirenzepine (2 µM, a muscarinic M1 receptor antagonist), Ki14625 (10 µM, an LPA1/3 receptor antagonist), amiloride (1 mM, an inhibitor of Na+/Ca2+ exchanger), a nicardipine (1 µM, a voltage-dependent Ca2+ channel blocker), TMB-8 (1 µM, an intracellular Ca2+ antagonist), and perfusion of Ca2+-free Krebs solution with 5mM EGTA (a Ca2+chelater), while was not affected by sodium nitroprusside (100 µM, a nitrosovasodialtor). Interestingly, LPA (0.3~3 µM, an LPA receptor agonist) also dose-dependently enhanced the CA secretion from the adrenal medulla, but this facilitatory effect of LPA was greatly inhibited in the presence of Ki 14625 (10 µM). Moreover, acetylcholine (AC)-evoked CA secretion was greatly potentiated during the perfusion of gintonin (3 µg/ml). Taken together, these results demonstrate the first evidence that gintonin increases the CA secretion from the perfused rat adrenal medulla in a dose-dependent fashion. This facilitatory effect of gintonin seems to be associated with activation of LPA- and cholinergic-receptors, which are relevant to the cytoplasmic Ca2+ increase by stimulation of the Ca2+ influx as well as by the inhibition of Ca2+ uptake into the cytoplasmic Ca2+ stores, without the increased nitric oxide (NO). Based on these results, it is thought that gintonin, one of ginseng components, can elevate the CA secretion from adrenal medulla by regulating the Ca2+ mobilization for exocytosis, suggesting facilitation of cardiovascular system. Also, these findings show that gintonin might be at least one of ginseng-induced hypertensive components.

show abstract

“…A study has demonstrated that a ginseng derived-compound attenuated amyloid deposition in the brain parenchyma of mice models, although the molecular mechanisms of exerted effects are not completely elucidated [Hwang et al 2012]. Apigenin (4′,5,7-trihydroxyflavone) is a pharmacologically active compound currently at the experimental stage.…”

Section: Tau-related Immunotherapymentioning

confidence: 99%

Anti-dementia medications: current prescriptions in clinical practice and new agents in progress

Stella

Radanovic

Canineu

et al. 2015

Therapeutic Advances in Drug Safety

View full text Add to dashboard Cite

Almost three decades after the publication of the first clinical studies with tacrine, the pharmacological treatment of Alzheimer's disease (AD) remains a challenge. Randomized clinical trials have yielded evidence of significant - although modest and transient - benefit from cholinergic replacement therapy for people diagnosed with AD, and disease modification with antidementia compounds is still an urgent, unmet need. The natural history of AD is very long, and its pharmacological treatment must acknowledge different needs according to the stage of the disease process. Cognitive and functional deterioration evolves gradually since the onset of clinical symptoms, which may be preceded by several years or perhaps decades of silent, presymptomatic neurodegeneration. Therefore, the pharmacological treatment of AD must ideally comprise both a symptomatic effect to preserve or improve cognition and a disease-modifying effect to tackle the progression of the pathological process. Primary prevention is the ultimate goal, should these strategies be delivered to patients with preclinical AD. In this article, we briefly address the pharmaceutical compounds that are currently used for the symptomatic treatment of AD and discuss the ongoing strategies designed to modify its natural course.

show abstract

Gintonin, a novel ginseng-derived lysophosphatidic acid receptor ligand, stimulates neurotransmitter release

Cited by 32 publications

References 18 publications

Gintonin stimulates gliotransmitter release in cortical primary astrocytes

Gintonin stimulates gliotransmitter release in cortical primary astrocytes

Gintonin facilitates catecholamine secretion from the perfused adrenal medulla

Anti-dementia medications: current prescriptions in clinical practice and new agents in progress

Contact Info

Product

Resources

About