Muscarinic (Mi) receptor‐mediated inhibition of K+‐evoked [3H]‐noradrenaline release from human neuroblastoma (SH‐SY5Y) cells via inhibition of L‐ and N‐type Ca2+ channels

McDonald, Ruth; Vaughan, Peter F. T.; Peers, Chris

doi:10.1111/j.1476-5381.1994.tb17035.x

Cited by 21 publications

(9 citation statements)

References 34 publications

(36 reference statements)

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“…Thus, the data presented in Fig. 1 Release of [3HINA from SH-SY5Y cells in response to either 100 mM K~or DMPP involves depolarization and Ca2~influx through both L-and N-type voltage-gated Ca2~channels (Murphy et al, 1991a;Vaughan et al, 1993;McDonald et al, 1994;Reeve et al, 1994). This was confirmed in the present study, which demonstrated that DMPP-evoked release ( Fig.…”

Section: Dmpp-evoked [supporting

confidence: 84%

“…Previous studies from our laboratory have used static bath assays to monitor I I 3H] NA release from SH-SY5Y evoked by various agents, including raised [K~] and nAChR agonists (Murphy et al, 1991a;Vaughan et al, 1993;McDonald et al, 1994). In this study, we have established a perfusion assay system in which cells can be repeatedly challenged with a stimulus.…”

Section: Resultsmentioning

confidence: 99%

“…Vesicles can be loaded with [3HINA to monitor exocytosis, and several groups including our own have used these cells to investigate the mechanisms underlying regulation of NA release by various transmitters and stimuli (Murphy et al, 1991a-c;Forsythe et al, 1992;McDonald et al, 1994McDonald et al, , 1995McDonald et al, , 1997Turner et al, 1996;Goodall et al, 1997). Of particular relevance to the present study are our observations that SH-SYSY cells possess both L-and N-type Ca 2~channels, which are coupled to release of NA in response to depolarizing stimuli (McDonald et a!., 1994;Reeve et al, 1994). We have also shown that activation of nicotinic acetylcholine receptors (nAChRs) also triggers cell depolarization and consequent Ca2~influx (Vaughan et al, 1993).…”

mentioning

confidence: 99%

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Hypoxia Enhances [³H]Noradrenaline Release Evoked by Nicotinic Receptor Activation from the Human Neuroblastoma SH‐SY5Y

Wade

Vaughan

Peers

1998

Journal of Neurochemistry

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We have used the human sympathetic neuronal line SH-SY5Y to investigate the effects of hypoxia on noradrenaline (NA) release evoked by either raised [K~}O (100 mM) or the nicotinic acetylcholine receptor (nAChR) agonist dimethyiphenylpiperazinium iodide (DMPP). NA release was monitored by loading cells with [3H}NAand collecting effluent fractions from perfused cells kept in a sealed perifusion chamber. Cells were challenged twice with either stimulus and release was expressed as that evoked by the second challenge as a fraction of that evoked by the first. K~-evokedrelease was unaffected by hypoxia (P0 2 30-38 mm Hg), but release evoked by DMPP was significantly increased. For both stimuli, replacement of Ca 2~0with 1 mM EGTA abolished NA release. K~-evokedrelease was also dramatically reduced in the presence of 200 ,uM Cd

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Section: Dmpp-evoked [supporting

confidence: 84%

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

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Hypoxia Enhances [³H]Noradrenaline Release Evoked by Nicotinic Receptor Activation from the Human Neuroblastoma SH‐SY5Y

Wade

Vaughan

Peers

1998

Journal of Neurochemistry

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“…This mixture included (final concentration in the extracellular solution): 20 mM tetraethylammonium (TEA) ions to block potassium channels (Forsythe et al 1992; Mathie et al 1998; Tosetti et al 1998; Guyon et al 2005), 1 μM tetrodotoxin to block sodium channels (Forsythe et al 1992; Toselli et al 1996; Guyon et al 2005), 2 μM nifedipine to block L-type calcium channels, and 2 μM ω -conotoxin to block N-type calcium channels (McDonald et al 1994, 1995; Reeve et al 1994, 1995; Furukawa et al 2003; Billups et al 2006). Figure 6a shows that A β -induced ion flux persisted in the presence of these blockers.…”

Section: Resultsmentioning

confidence: 99%

Amyloid-β-Induced Ion Flux in Artificial Lipid Bilayers and Neuronal Cells: Resolving a Controversy

et al. 2009

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Understanding the pathogenicity of amyloid-beta (Ab) peptides constitutes a major goal in research on Alzheimer's disease (AD). One hypothesis entails that Ab peptides induce uncontrolled, neurotoxic ion flux through cellular membranes. The exact biophysical mechanism of this ion flux is, however, a subject of an ongoing controversy which has attenuated progress toward understanding the importance of Ab-induced ion flux in AD. The work presented here addresses two prevalent controversies regarding the nature of transmembrane ion flux induced by Ab peptides. First, the results clarify that Ab can induce stepwise ion flux across planar lipid bilayers as opposed to a gradual increase in transmembrane current; they show that the previously reported gradual thinning of membranes with concomitant increase in transmembrane current arises from residues of the solvent hexafluoroisopropanol, which is commonly used for the preparation of amyloid samples. Second, the results provide additional evidence suggesting that Ab peptides can induce ion channel-like ion flux in cellular membranes that is independent from the postulated ability of Ab to modulate intrinsic cellular ion channels or transporter proteins.

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“…Human neuroblastoma SH-SY5Y is a dopaminergic neuronal cell line which has been used as an in vitro model for Parkinson's disease. They exhibit calcium-dependent release of norepinephrine in response to membrane depolarization with 100 mM K ϩ (23). However, it is still unknown whether ASICs are expressed in SH-SY5Y cells, as well as the response of SH-SY5Y cells to extracellular acidification.…”

mentioning

confidence: 99%

Acid-sensing ion channels contribute to the increase in vesicular release from SH-SY5Y cells stimulated by extracellular protons

Xiong

et al. 2012

American Journal of Physiology-Cell Physiology

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Acid-sensing ion channels (ASICs) have been reported to play a role in the neuronal dopamine pathway, but the exact role in neurotransmitter release remains elusive. Human neuroblastoma SH-SY5Y is a dopaminergic neuronal cell line, which can release monoamine neurotransmitters. In this study, the expression of ASICs was identified in SH-SY5Y cells to further explore the role of ASICs in vesicular release stimulated by acid. We gathered evidence that ASICs could be detected in SH-SY5Y cells. In whole cell patch-clamp recording, a rapid decrease in extracellular pH evoked inward currents, which were reversibly inhibited by 100 μM amiloride. The currents were pH dependent, with a pH of half-maximal activation (pH(0.5)) of 6.01 ± 0.04. Furthermore, in calcium imaging and FM 1-43 dye labeling, it was shown that extracellular protons increased intracellular calcium levels and vesicular release in SH-SY5Y cells, which was attenuated by PcTx1 and amiloride. Interestingly, N-type calcium channel blockers inhibited the vesicular release induced by acidification. In conclusion, ASICs are functionally expressed in SH-SY5Y cells and involved in vesicular release stimulated by acidification. N-type calcium channels may be involved in the increase in vesicular release induced by acid. Our results provide a preliminary study on ASICs in SH-SY5Y cells and neurotransmitter release, which helps to further investigate the relationship between ASICs and dopaminergic neurons.

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Muscarinic (Mi) receptor‐mediated inhibition of K⁺‐evoked [³H]‐noradrenaline release from human neuroblastoma (SH‐SY5Y) cells via inhibition of L‐ and N‐type Ca²⁺ channels

Cited by 21 publications

References 34 publications

Hypoxia Enhances [³H]Noradrenaline Release Evoked by Nicotinic Receptor Activation from the Human Neuroblastoma SH‐SY5Y

Hypoxia Enhances [³H]Noradrenaline Release Evoked by Nicotinic Receptor Activation from the Human Neuroblastoma SH‐SY5Y

Amyloid-β-Induced Ion Flux in Artificial Lipid Bilayers and Neuronal Cells: Resolving a Controversy

Acid-sensing ion channels contribute to the increase in vesicular release from SH-SY5Y cells stimulated by extracellular protons

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Muscarinic (Mi) receptor‐mediated inhibition of K+‐evoked [3H]‐noradrenaline release from human neuroblastoma (SH‐SY5Y) cells via inhibition of L‐ and N‐type Ca2+ channels

Cited by 21 publications

References 34 publications

Hypoxia Enhances [3H]Noradrenaline Release Evoked by Nicotinic Receptor Activation from the Human Neuroblastoma SH‐SY5Y

Hypoxia Enhances [3H]Noradrenaline Release Evoked by Nicotinic Receptor Activation from the Human Neuroblastoma SH‐SY5Y

Amyloid-β-Induced Ion Flux in Artificial Lipid Bilayers and Neuronal Cells: Resolving a Controversy

Acid-sensing ion channels contribute to the increase in vesicular release from SH-SY5Y cells stimulated by extracellular protons

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Product

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Muscarinic (Mi) receptor‐mediated inhibition of K⁺‐evoked [³H]‐noradrenaline release from human neuroblastoma (SH‐SY5Y) cells via inhibition of L‐ and N‐type Ca²⁺ channels

Hypoxia Enhances [³H]Noradrenaline Release Evoked by Nicotinic Receptor Activation from the Human Neuroblastoma SH‐SY5Y

Hypoxia Enhances [³H]Noradrenaline Release Evoked by Nicotinic Receptor Activation from the Human Neuroblastoma SH‐SY5Y