The effect of protein kinase C activation on muscarinic-M3- and K+-evoked release of [3H]noradrenaline and increases in intracellular Ca2+ in human neuroblastoma SH-SY5Y cells

Abstract

Short-term pretreatment (9 min) with the phorbol ester 12-myristate 13-acetate (PMA) alone had no effect on the basal release of [3H]noradrenaline ([3H]NA), but enhanced K+ (100 mM)-, acetylcholine (0.1 mM)-, carbachol (1 mM)-, muscarine (I mM)-and arecoline (1 mM)-evoked release by 2.3-, 6.4-, 3.0-, 2.0-and 2.0-fold respectively in SH-SY5Y cells. the muscarinic-agonist-evoked initial peak (> 850%) and plateau phase in intracellular Ca2l. These results suggest that noradrenaline release evoked by muscarinic agonists was triggered not only by relatively small changes in Ca2+ but also by activation of protein kinase C.

Distinct mechanisms of neurotransmitter release from PC12 cells exposed to lead

“…For example, activation of protein kinase C increased the amount of [3H]NOR released by muscarinic agonists (Murphy et al, 1992) and bradykinin (Luo and Weinstein, 1993) in SH-SY5Y neuroblastoma cells. Activation of protein kinase C also increased the amount of [3H]dopamine released by ionomycin in PC 12 cells sensitivity is that cells maintain their viability and exhibit many more functions than cell-free preparations.…”

Activation of Protein Kinase C‐α and Translocation of the Myristoylated Alanine‐Rich C‐Kinase Substrate Correlate with Phorbol Ester‐Enhanced Noradrenaline Release from SH‐SY5Y Human Neuroblastoma Cells

“…Combining the results of our recent studies on the TPA enhancement of NA release in SH-SY5Y cells (Murphy et al, 1992;Turner et al, 1994Turner et al, , 1996 and the results of the present study, a model for the role of PKC-a and MARCKS in the TPA enhancement of NA release can be constructed. Short-term treatment of cells with 100 nM TPA causes activation of the a and e subtypes of PKC, with PKC-a translocating from the cytosol to the plasma membrane within 6…”

“…The release of neurotransmitters by exocytosis from brain preparations (reviewed by Dekker et al, 1991), isolated nerve terminals (Nichols et al, 1987), and cultured neuronal cells (Matthies et al, 1987;Murphy et al. 1992) can be potentiated by short-term pretreatment with phorbol esters, which are potent activators of the protein kinase C (PKC) family of serine/threonine kinases (Nishizuka, 1992).…”

“…1995). Activation of PKC by an 8-mm pretreatment of SH-SY5Y cells with the phorbol ester I 2-O-tetradecanoylphorbol 13-acetate (TPA; 100 nM) enhances noradrenaline (NA) release evoked by various stimuli (Murphy et al, 1992;McDonald et a!., 1994McDonald et a!., , 1995Turner et al, 1994Turner et al, , 1996. Short-term pretreatment with PKC inhibitors attenuates the TPA enhancement of NA release, as does selective down-regulation of the a subtype of PKC by long-term treatment with the phorhol ester phorbol 12,1 3-dibutyrate (PDBu) or biyostatin-1, suggesting that in SH-SY5Y cells the TPA enhancement of NA release is mainly due to activation of PKC-a (Turner et al, 1996).…”

Bradykinin-evoked Release of [3H]Noradrenaline from the Human Neuroblastoma SH-SY5Y

“…Previous work has shown that muscarinic M3-receptor subtypes in SHSYSY are coupled to phosholipase C and IP3 induced changes in intracellular calcium [4,5]. Furthermore we have reported that activation of protein kinase C with TPA enhances both depolarisation and M3-receptor-evoked release of NA [6].…”