Desensitization of the μ‐opioid activation of phospholipase C in SH‐SY5Y cells: the role of protein kinases C and A and Ca2+‐activated K+ currents

Smart, Darren; Lambert, David G.

doi:10.1111/j.1476-5381.1995.tb17222.x

Cited by 24 publications

(22 citation statements)

References 36 publications

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“…The time-course of BRE (10 -6 M)-induced increases in the formation of IPs in the iris-ciliary body demonstrated a response similar to that observed in other documented studies involving opioid agonists and their effects on IP production [14,22,23]. In the presence of 10 -6 M BRE, IP levels peaked at F1 min and returned to basal by 5 min.…”

Section: Discussionsupporting

confidence: 52%

Effect of Bremazocine, a Kappa-Opioid Receptor Agonist, on Inositol Phosphate Formation in Isolated Iris-Ciliary Bodies

Dortch-Carnes

Potter²

2002

Pharmacology

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The goal of the current study was to examine the effect of the kappa-opioid agonist, bremazocine (BRE), on inositol phosphate (IP) formation in the rabbit iris-ciliary body (ICB). Concentrations of BRE (10^–7 to 10^–5M) augmented levels of IP. Incubation of ICBs with BRE (10^–6M) produced a time-dependent increase in IP levels that peaked at 60 s and declined to basal levels by 5 min. The increase in IP levels produced by BRE (10^–6M) was inhibited by the kappa-opioid receptor antagonist, nor-binaltorphimine (nor-BNI, 10^–7 to 10^–5M) and by activation of PKC with PDBu (10^–7M). These results demonstrate that kappa-opioid receptor activation by BRE in the rabbit ICB is linked to IP production. Thus, opioid agonist-induced increases in IP activity could play a role in BRE-induced increases in atrial natriuretic peptide release and alterations in aqueous humor dynamics.

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Section: Discussionsupporting

confidence: 52%

Effect of Bremazocine, a Kappa-Opioid Receptor Agonist, on Inositol Phosphate Formation in Isolated Iris-Ciliary Bodies

Dortch-Carnes

Potter²

2002

Pharmacology

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“…Opioid receptors, in fact, have been demonstrated to act mainly by opening L-type channels and activating PLC [34]. That naloxone at high concentrations can possess a partial agonist activity and produce effects similar to those observed with morphine has been reported in many in vivo and in vitro test systems [35, 36].…”

Section: Discussionmentioning

confidence: 99%

Naloxone Inhibits A6 Cell Na+/H+ Exchange by Activating Protein Kinase C via the Mobilization of Intracellular Calcium

Sole

Guerra²,

Bagorda³

et al. 2001

Nephron Exp Nephrol

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The opioid receptor antagonist, naloxone, has been shown to have beneficial effects in the kidney and to be implicated in renal salt and water balance. In the present study the signal transduction pathways utilized by naloxone were studied in an epithelial cell line model of the cortical collecting duct, A6 cells. We found that naloxone has a dual effect depending on the concentration used: at a low concentration (10^–6M) it antagonized the β-endorphin-dependent increase in cytoplasmic calcium [Ca²⁺]_i, while at higher concentrations (>10^–5M) it increased [Ca²⁺]_i and intracellular inositol phosphate levels. While naloxone-induced increases in [Ca²⁺]_i occurred in the absence of external calcium, it was significantly stimulated by increasing the external calcium concentration, suggesting that naloxone increases [Ca²⁺]_i via both calcium release and calcium influx. In polarized A6 cell monolayers naloxone inhibited the activity of the Na⁺/H⁺ exchanger (NHE) only when added to the basolateral cell surface. This inhibition of the NHE was prevented by pretreatment of the cells with either the intracellular calcium chelator, BAPTA or with the protein kinase C inhibitor, calphostin C. These findings demonstrate that naloxone induces a rapid increase in intracellular calcium which inhibits the NHE via the calcium-dependent protein kinase C regulatory pathway.

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“…Mu-opioid activation of SH-SY5Y cells has also been reported to stimulate Ca 2+ influx via L-type Ca 2+ channels [14]. Furthermore, opioids have been shown to mobilize Ca 2+ from intracellular stores in SH-SY5Y cells but require ongoing muscarinic receptor activation [2].…”

Section: Mobilization Of Intracellular Camentioning

confidence: 99%

Met-enkephalin-induced mobilization of intracellular Ca2+ in rat intracardiac ganglion neurones

Smith

Adams

1999

Neuroscience Letters

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The effects of Met-enkephalin on Ca 2+-dependent K + channel activity were investigated using the cell-attached patch recording technique on isolated parasympathetic neurones of rat intracardiac ganglia. Large-conductance, Ca 2+ -dependent K + channels (BK Ca ) were examined as an assay of agonist-induced changes in the intracellular free calcium ion concentration ([Ca 2+ ] i ). These BK Ca channels had a conductance of ˜200 pS and were charybdotoxin-and voltage-sensitive. Caffeine (5 mM), used as a control, evoked a large increase in BK Ca channel activity, which was inhibited by 10 μM ryanodine. Met-enkephalin (10 μM) evoked a similar increase in BK Ca channel activity, which was dependent on the presence of extracellular Ca 2+ and inhibited by either ryanodine (10 μM) or naloxone (1 μM). In Fura-2-loaded intracardiac neurones, Met-enkephalin evoked a transient increase in [Ca 2+ ] i . Metenkephalin-induced mobilization of intracellular Ca 2+ may play a role in neuronal excitability and firing behaviour in mammalian intracardiac ganglia.Keywords: Parasympathetic ganglia; Intracellular Ca 2+ ; Caffeine; Ryanodine; Opioid receptor; CaIndex Terms: heart innervation Endogenous opioid peptides have been found in the extrinsic and intrinsic innervation of the rat heart [7] and vagal transmission to the heart has been shown to be inhibited by exogenous opioid substances [11,18] channels via a Pertussis toxin-sensitive G-protein [1]. However, the action potential after-hyperpolarization due to a Ca 2+ -dependent K + conductance(s) in these neurones was unaltered in the presence of Met-enkephalin. In the present study, the actions of Met-enkephalin and caffeine, a known intracellular Ca 2+ mobilizing agent, on intracellular Ca 2+ mobilization and activation of the large conductance Ca 2+ -dependent K + channels (BK Ca ) were investigated.Parasympathetic neurones from neonatal rat intracardiac ganglia were isolated as previously described [19]. The dissociated neurones were plated onto glass coverslips coated with laminin, incubated at 37°C in 95% O 2 -5% CO 2 atmosphere and used for experiments within 36-72 h. At the time of experiments, the neuroneplated glass coverslips were transferred to a recording chamber (0.5 ml volume) and mounted on the stage of an inverted phase contrast microscope. Unitary current recordings were obtained using the cell-attached patch recording configuration of the patch clamp technique [6]. In the cell-attached configuration, K + currents in the membrane patch follow the relationship i K =γ(V m −V h −E K ). When the cells were bathed in a depolarizing external solution (V m ˜0 mV) and V h was held at 0 mV, the membrane potential in the patch was close to 0 mV. Unitary currents were recorded using an Axopatch 200B patch clamp amplifier (Axon Instruments, Foster City, CA), filtered at 5 kHz, and stored on digital tape using a DAT digital recorder (DTR-1204, Biologic Science Instruments, Claix, France). Records were transferred to a Pentium computer using an analogue-to-digit...

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Desensitization of the μ‐opioid activation of phospholipase C in SH‐SY5Y cells: the role of protein kinases C and A and Ca²⁺‐activated K⁺ currents

Cited by 24 publications

References 36 publications

Effect of Bremazocine, a Kappa-Opioid Receptor Agonist, on Inositol Phosphate Formation in Isolated Iris-Ciliary Bodies

Effect of Bremazocine, a Kappa-Opioid Receptor Agonist, on Inositol Phosphate Formation in Isolated Iris-Ciliary Bodies

Naloxone Inhibits A6 Cell Na<sup>+</sup>/H<sup>+</sup> Exchange by Activating Protein Kinase C via the Mobilization of Intracellular Calcium

Met-enkephalin-induced mobilization of intracellular Ca2+ in rat intracardiac ganglion neurones

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