Bradykinin-evoked release of [3H]noradrenaline from the human neuroblastoma sh-sy5y

McDonald, Ruth; Kaye, David F.; Reeve, Helen L.; Ball, Stephen G.; Peers, Chris; Vaughan, Peter F. T.

doi:10.1016/0006-2952(94)90219-4

Cited by 17 publications

(11 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…was reduced by -85% if 3 pM tetrodotoxin was present in the HBS containing Ba2+. Nifedipine at 5 pM, a concentration previously shown to completely inhibit L-type Ca2+ channels in SH-SY5Y (Reeve et al, 1994). inhibited BaC12-evoked [3H]noradrenalin release by 95% (Fig.…”

Section: Electrophysiological Studiesmentioning

confidence: 88%

The Effect of Barium on [³H]Noradrenalin Release from the Human Neuroblastoma SH‐SY5Y

Vaughan

Kaye

Ball

et al. 1995

Eur J of Neuroscience

Self Cite

View full text Add to dashboard Cite

Replacement of Ca2+ with Ba2+ in HEPES-buffered saline stimulated [3H]noradrenalin release in the human neuroblastoma clone SH-SY5Y by up to 20% of the cell content in the absence of other secretory stimuli. The Ba(2+)-evoked release was inhibited by 85% by 3 microM tetrodotoxin and 95% by 5 microM nifedipine. Ba2+ also increased the potency of K(+)-evoked release of [3H]noradrenalin, as maximal release was observed with 60 mM K+ compared with the 100 mM K+ necessary to achieve maximal release in the presence of Ca2+. In contrast, replacing Ca2+ with Ba2+ had little effect on carbachol- and bradykinin-evoked release of [3H]noradrenalin. No evidence was obtained from studies on changes in [Ca2+]i (in response to 100 microM carbachol) using fura-2 that Ba2+ could enter intracellular stores in SH-SY5Y cells. Whole-cell patch-clamp studies showed that Ba2+ depolarizes SH-SY5Y cells as well as enhancing inward Ca2+ channel currents and shifting their voltage dependence to more negative values. These results are discussed in terms of the hypothesis that Ba2+ blocks K+ channels, leading to depolarization followed by opening of voltage-sensitive Na+ channels. This in turn opens voltage-sensitive L-type Ca2+ channels, which are coupled to the release of [3H]noradrenalin in SH-SY5Y cells.

show abstract

Section: Electrophysiological Studiesmentioning

confidence: 88%

The Effect of Barium on [³H]Noradrenalin Release from the Human Neuroblastoma SH‐SY5Y

Vaughan

Kaye

Ball

et al. 1995

Eur J of Neuroscience

Self Cite

View full text Add to dashboard Cite

show abstract

“…By determining the centroid locations of the fluorescence signals we could map Ca 2+ puffs with sub-micron precision[14], allowing us to compare the locations of IP 3 R clusters activated in the same cell by sequential stimulation by GPCR agonists, followed by global photolysis of caged IP 3 . SH-SY5Y cells endogenously express BK2 [15] and mACh3 [16]receptors, which we activated by extracellular application of bradykinin (BK) and carbachol (CCH).…”

Section: Introductionmentioning

confidence: 99%

Comparison of Ca2+ puffs evoked by extracellular agonists and photoreleased IP3

2017

View full text Add to dashboard Cite

The inositol trisphosphate (IP3) signaling pathway evokes local Ca2+ signals (Ca2+ puffs) that arise from the concerted openings of clustered IP3 receptor/channels in the ER membrane. Physiological activation is triggered by binding of agonists to G-protein-coupled receptors (GPCRs) on the cell surface, leading to cleavage of phosphatidyl inositol bisphosphate and release of IP3 into the cytosol. Photorelease of IP3 from a caged precursor provides a convenient and widely employed means to study the final stage of IP3-mediated Ca2+ liberation, bypassing upstream signaling events to enable more precise control of the timing and relative concentration of cytosolic IP3. Here, we address whether Ca2+ puffs evoked by photoreleased IP3 fully replicate those arising from physiological agonist stimulation. We imaged puffs in individual SH-SY5Y neuroblastoma cells that were sequentially stimulated by picospritzing extracellular agonist (carbachol, CCH or bradykinin, BK) followed by photorelease of a poorly-metabolized IP3 analog, i-IP3. The centroid localizations of fluorescence signals during puffs evoked in the same cells by agonists and photorelease substantially overlapped (within ~1 μm), suggesting that IP3 from both sources accesses the same, or closely co-localized clusters of IP3Rs. Moreover, the time course and spatial spread of puffs evoked by agonists and photorelease matched closely. Because photolysis generates IP3 uniformly throughout the cytoplasm, our results imply that IP3 generated in SH-SY5Y cells by activation of receptors to CCH and BK also exerts broadly distributed actions, rather than specifically activating a subpopulation of IP3Rs that are scaffolded in close proximity to cell surface receptors to form a signaling nanodomain.

show abstract

“…Like its parent line, SH-SY5Y cells express delta opioid receptors to a lesser extent than mu (Kazmi and Mishra, 1987; Yu and Sadee, 1988). SH-SY5Y cells also express ORL-1 receptors (Cheng et al, 1995), and signaling proteins like the Regulator of G protein signaling 4 (RGS4) (Lambert et al, 1989; McDonald et al, 1994; Wang et al, 2009; Levitt et al, 2011; Wang and Traynor, 2011). Given its repertoire of signaling proteins, SH-SY5Y cells have been widely used for the study of mu and delta opioid receptor activity, and receptor desensitization (Elliott et al, 1997; Nowoczyn et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

The delta opioid receptor tool box

2016

View full text Add to dashboard Cite

In recent years, the delta opioid receptor has attracted Increasing Interest as a target for the treatment of chronic pain and emotional disorders. Due to their therapeutic potential, numerous tools have been developed to study the delta opioid receptor from both a molecular and a functional perspective. This review summarizes the most commonly available tools, with an emphasis on their use and limitations. Here, we describe (1) the cell-based assays used to study the delta opioid receptor. (2) The features of several delta opioid receptor ligands, including peptide and non-peptide drugs. (3) The existing approaches to detect delta opioid receptors in fixed tissue, and debates that surround these techniques. (4) Behavioral assays used to study the in vivo effects of delta opioid receptor agonists; including locomotor stimulation and convulsions that are induced by some ligands, but not others. (5) The characterization of genetically modified mice used specifically to study the delta opioid receptor. Overall, this review aims to provide a guideline for the use of these tools with the final goal of increasing our understanding of delta opioid receptor physiology.

show abstract

Bradykinin-evoked release of [3H]noradrenaline from the human neuroblastoma sh-sy5y

Cited by 17 publications

References 25 publications

The Effect of Barium on [³H]Noradrenalin Release from the Human Neuroblastoma SH‐SY5Y

The Effect of Barium on [³H]Noradrenalin Release from the Human Neuroblastoma SH‐SY5Y

Comparison of Ca2+ puffs evoked by extracellular agonists and photoreleased IP3

The delta opioid receptor tool box

Contact Info

Product

Resources

About

Bradykinin-evoked release of [3H]noradrenaline from the human neuroblastoma sh-sy5y

Cited by 17 publications

References 25 publications

The Effect of Barium on [3H]Noradrenalin Release from the Human Neuroblastoma SH‐SY5Y

The Effect of Barium on [3H]Noradrenalin Release from the Human Neuroblastoma SH‐SY5Y

Comparison of Ca2+ puffs evoked by extracellular agonists and photoreleased IP3

The delta opioid receptor tool box

Contact Info

Product

Resources

About

The Effect of Barium on [³H]Noradrenalin Release from the Human Neuroblastoma SH‐SY5Y

The Effect of Barium on [³H]Noradrenalin Release from the Human Neuroblastoma SH‐SY5Y