7-OH-DPAT-Induced Inhibition of Norepinephrine Release in PC12 Cells

Chu, Eugenia; Chu, Jane; Socci, Robin R.; Chu, Teh-Ching

doi:10.1159/000074976

Cited by 11 publications

(13 citation statements)

References 42 publications

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“…Consistent with other reports, we showed that the activation of LPA5 (in response to peptone, LPA, and FPP) induced the expression of c-Fos (an early marker of neuronal activity) both in a nerve cell line and primary nerve cells. The expression of c-Fos is often used as an indicator for neuronal activities and differentiation in PC12 cells (18). In addition to the expression of c-Fos, activated LPA5 also induced the transactivation of CRE reporter activities in PC12 cells, which can be induced by increases in [ (17).…”

Section: Discussionmentioning

confidence: 99%

Feeding-dependent activation of enteric cells and sensory neurons by lymphatic fluid: evidence for a neurolymphocrine system

Poole

Lee

Tso

et al. 2014

American Journal of Physiology-Gastrointestinal and Liver Physi

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GW. Feeding-dependent activation of enteric cells and sensory neurons by lymphatic fluid: evidence for a neurolymphocrine system. Am J Physiol Gastrointest Liver Physiol 306: G686 -G698, 2014. First published February 27, 2014 doi:10.1152/ajpgi.00433.2013.-Lymphatic fluid is a plasma filtrate that can be viewed as having biological activity through the passive accumulation of molecules from the interstitial fluid. The possibility that lymphatic fluid is part of an active self-contained signaling process that parallels the endocrine system, through the activation of G-protein coupled receptors (GPCR), has remained unexplored. We show that the GPCR lysophosphatidic acid 5 (LPA5) is found in sensory nerve fibers expressing calcitonin gene-related peptide (CGRP) that innervate the lumen of lymphatic lacteals and enteric nerves. Using LPA5 as a model for nutrient-responsive GPCRs present on sensory nerves, we demonstrate that dietary protein hydrolysate (peptone) can induce c-Fos expression in enterocytes and nerves that express LPA5. Mesenteric lymphatic fluid (MLF) mobilizes intracellular calcium in cell models expressing LPA5 upon feeding in a time-and dose-dependent manner. Primary cultured neurons of the dorsal root ganglia expressing CGRP are activated by MLF, which is enhanced upon LPA5 overexpression. Activation is independent of the known LPA5 agonists, lysophosphatidic acid and farnesyl pyrophosphate. These data bring forth a pathway for the direct stimulation of sensory nerves by luminal contents and interstitial fluid. Thus, by activating LPA5 on sensory nerves, MLF provides a means for known and yet to be identified constituents of the interstitial fluid to act as signals to comprise a "neurolymphocrine" system. G protein-coupled receptor; intestine; lacteal; lysophosphatidic acid 5; nutrient sensing NUTRIENT SENSING IS INCREASINGLY being recognized as affecting the etiology of diseases resulting from obesity, inflammation, dysregulation of intracellular metabolism, and modification of behavior such as food intake.

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Section: Discussionmentioning

confidence: 99%

Feeding-dependent activation of enteric cells and sensory neurons by lymphatic fluid: evidence for a neurolymphocrine system

Poole

Lee

Tso

et al. 2014

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…These cells are catecholaminergic rat pheochromocytoma cells and can display a DA phenotype after differentiation with nerve growth factor (NGF) (Greene and Tischler, 1976;Tischler et al, 1983). They express D 2 , D 3 and D 4 receptors (Jorgensen and Richter-Landsberg, 1983;Damon et al, 1990;Pothos et al, 1998;Kobayashi et al, 1999;Chu et al, 2004) and DAT (Kadota et al, 1996). We report that DA agonists, Br and Qp, amplify specifically the effect of MPP + on cellular death and this event is prevented in the presence of DA antagonists.…”

Section: Fp Graham Publishing Comentioning

confidence: 96%

“…Differential PCR amplification of each targeted mRNA and ribosomal 18S subunit (internal control) were amplified using 4 µl of the cDNA reaction mixture, 10 µl of HotMasterMix and 0.2 µM each forward and reverse primers in a total volume of 25 µl. Primers for D 2 (5'-GCA GTC GAG CTT TCA GAG CC-3' and 5'-TCT GCG GCT CAT CGT CTT AAG-3') (Bunzow et al, 1988) and D 3 (5'-TCC TGT CTG AGG CTG CAT CC-3' and 5'-TCG AAG TGG TAC TCC CCG AG-3') (Chu et al, 2004) were synthesized at Sigma Genosys. Expected numbers of base pairs are 404 bp and 201 bp for D 2 and D 3 , respectively.…”

Section: Reverse Transcriptase Pcr (Rt-pcr)mentioning

confidence: 99%

Dopamine D2 agonists, bromocriptine and quinpirole, increase MPP+-induced toxicity in PC12 cells

et al. 2006

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Dopaminergic cell loss in the mesencephalic substantia nigra is the hallmark of Parkinson's disease and may be associated with abnormal oxidative metabolic activity. However, the delicate balance underlying dopamine decline and oxidative stress is still a matter of debate. The aim of this study was to analyze the possible modulation of D2 agonists and antagonists on MPP+ (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridinium ion) -induced cellular death in differentiated and undifferentiated PC12 cells. Using colorimetric assays, western blots and reverse transcriptase-PCR, we demonstrated that two D2 agonists, bromocriptine and quinpirole, consistently increased MPP+ -induced cytotoxicity in both differentiated and undifferentiated PC12 cells, whereas D2 antagonists do not modulate cell death. However, this increase in cellular death was reversed when bromocriptine or quinpirole were used in presence of D2 antagonists. On the other hand, 1-{2-[bis-(4-fluorophenyl)methoxy]ethyl}-4-(3-phenylpropyl)piperazine (GBR 12909), a potent inhibitor of the dopamine transporter, partially reversed MPP+ -induced cellular death and completely abolished the increase of cellular death induced by bromocriptine. Dopamine agonists and antagonists also modulate the expression of the dopamine transporter in PC12 cells; in particular, bromocriptine may alter MPP+ uptake by increasing DAT expression We also show that, in our cellular paradigm, D2 receptor mRNA levels are more abundant that D3 mRNA levels and MPP+ and /or bromocriptine could not modulate D2 gene expression while D3 gene expression clearly decrease after MPP+ and /or bromocriptine treatment.

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“…Upon exposure to nerve growth factor (NGF), PC12 cells undergo neuronal differentiation [4]. NGF-treated PC12 cells release several neurotransmitters including dopamine [5], noradrenaline [6] and acetylcholine [7]. …”

Section: Introductionmentioning

confidence: 99%

Comparison of neurons derived from mouse P19, rat PC12 and human SH-SY5Y cells in the assessment of chemical- and toxin-induced neurotoxicity

Popova

Karlsson

Jacobsson

2017

BMC Pharmacol Toxicol

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BackgroundExposure to chemicals might be toxic to the developing brain. There is a need for simple and robust in vitro cellular models for evaluation of chemical-induced neurotoxicity as a complement to traditional studies on animals. In this study, neuronally differentiated mouse embryonal carcinoma P19 cells (P19 neurons) were compared with human neuroblastoma SH-SY5Y cells and rat adrenal pheochromocytoma PC12 cells for their ability to detect toxicity of methylmercury (MeHg), okadaic acid and acrylamide.MethodsRetinoic acid-treated P19 and SH-SY5Y cells and nerve growth factor-stimulated PC12 cells, allowed to differentiate for 6 days, were exposed to MeHg, okadaic acid and acrylamide for 48 h. Cell survival and neurite outgrowth were assessed with the calcein-AM assay and fluorescence detection of antibodies against the cytoskeletal neuron-specific protein βIII-tubulin, respectively. The effects of glutathione (GSH) and the potent inhibitor of GSH synthesis buthionine sulfoximine (BSO) on the MeHg induced-toxicity were assessed using the PrestoBlue™ cell viability assay and the TMRE mitochondrial membrane potential assay.ResultsDifferentiated P19 cells developed the most extensive neuronal network among the three cell models and were the most sensitive neuronal model to detect neurotoxic effects of the test compounds. MeHg produced a concentration-dependent toxicity in differentiated P19 cells and SH-SY5Y cells, with statistically significant effects at concentrations from 0.1 μM in the P19 neurons and 1 μM in the SH-SY5Y cells. MeHg induced a decrease in the cellular metabolic activity and mitochondrial membrane potential (ΔΨm) in the differentiated P19 cells and SH-SY5Y cells, that were attenuated by GSH. Okadaic acid and acrylamide also showed statistically significant toxicity in the P19 neurons, but not in the SH-SY5Y cells or the P12 cells.ConclusionsP19 neurons are more sensitive to detect cytotoxicity of MeHg, okadaic acid and acrylamide than retinoic acid-differentiated SH-SY5Y cells and nerve growth factor-treated PC12 cells. P19 neurons are at least as sensitive as differentiated SH-SY5Y cells to detect the loss of mitochondrial membrane potential produced by MeHg and the protective effects of extracellular GSH on MeHg toxicity. P19 neurons may be a useful model to study neurotoxic effects of chemicals.

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7-OH-DPAT-Induced Inhibition of Norepinephrine Release in PC12 Cells

Cited by 11 publications

References 42 publications

Feeding-dependent activation of enteric cells and sensory neurons by lymphatic fluid: evidence for a neurolymphocrine system

Feeding-dependent activation of enteric cells and sensory neurons by lymphatic fluid: evidence for a neurolymphocrine system

Dopamine D2 agonists, bromocriptine and quinpirole, increase MPP+-induced toxicity in PC12 cells

Comparison of neurons derived from mouse P19, rat PC12 and human SH-SY5Y cells in the assessment of chemical- and toxin-induced neurotoxicity

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