Enhancement of noradrenaline release by 12-O-tetradecanoyl phorbol-13-acetate, an activator of protein kinase C

Allgaier, Clemens; Kügelgen, Oda V.; Hertting, G.

doi:10.1016/0014-2999(86)90454-1

Cited by 60 publications

(19 citation statements)

References 10 publications

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“…Increases in PKC levels have also been suggested to lead to activation of transmitter release in various systems [57][58][59]. In the present studies, our observations suggest a role for PKC in the dopamine-mediated inhibition of NPY-ir release.…”

Section: Discussionsupporting

confidence: 74%

Mechanism of dopamine mediated inhibition of neuropeptide Y release from pheochromocytoma cells (PC12 cells)

Gui-Hua¹,

Gardner²,

Westfall³

2007

Biochemical Pharmacology

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In rat pheochromocytoma (PC-12) cells the dopamine D 2 receptor agonists apomorphine (APO) and n-propylnorapomorphine (NPA) produced a concentration dependent inhibition of K + -evoked neuropeptide Y release (NPY-ir). The effect of APO was blocked by the dopamine D 2 -receptor antagonist, eticlopride, but not the D 1 /D 3 or the D 4 /D 2 antagonists, SCH23390 or clozapine, respectively. The D 1 /D 5 receptor agonist, SKF38393 or the D 3 agonists PD128907 and 7-OH DPAT had no effect. Selective N and L-type voltage gated Ca 2+ channel blockers, ω-Conotoxin GVIa (CtxGVIa) and nifedipine, respectively, produced a concentration dependent inhibition of NPY-ir release but were not additive with APO. The Ca 2+ /calmodulin-dependent protein kinase (CaM kinase) II inhibitor KN-62 produced a concentration-dependent inhibition of NPY-ir release but the combination of KN-62 and APO produced no further inhibition. PMA-mediated protein kinase C stimulation significantly increased both basal and K + -evoked release of NPY-ir, and in the presence of PMA APO had no inhibitory effect. The PKC antagonist, chelerythrine, inhibited K + -evoked NPYir release but was not additive with APO. Neither forskolin-mediated adenylate cyclase activation and the active cAMP analog Sp-cAMPS, nor the adenylate cyclase inhibitor SQ 22536, and the competitive inhibitor of cAMP-dependent protein kinases Rp-cAMPS, had any significant effect on K + -evoked NPY-ir release. This suggests the inhibitory effect of APO on K + -evoked release of NPYir from PC 12 cells is most likely mediated through activation of dopamine D 2 receptors leading to direct inhibition of N and L-type voltage gated Ca 2+ channels, or indirect inhibition of PKC, both of which would reduce [Ca 2+ ] i and inactivate CaM kinase.

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Section: Discussionsupporting

confidence: 74%

Mechanism of dopamine mediated inhibition of neuropeptide Y release from pheochromocytoma cells (PC12 cells)

Gui-Hua¹,

Gardner²,

Westfall³

2007

Biochemical Pharmacology

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“…The involvement of protein kinase C in signal transduction may be supported by the observation that phorbol esters that fail to activate protein kinase C (Castagna et al, 1982) do not induce neurotransmitter release (Allgaier et al, 1986;Murphy & Smith, 1987). The observation that PMA enhanced NA release, together with the lack of enhancement of release by the inactive phorbol ester 4a-PDD, suggested that PMA enhanced release by activation of protein kinase C. Similarly, the inactive phorbol ester 4a-PDD has previously been reported to have no significant effect on acetylcholine release in cholinergic synaptosomes (Guitart et al, 1990) and guinea-pig caudate slices (Tanaka et al, 1986).…”

Section: Discussionmentioning

confidence: 68%

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

Murphy

McCormack

Ball

et al. 1992

Biochemical Journal

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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.

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“…Up to now all investigations with phorbol esters as activators of PKC point to the possibility of an involvement of PKC in controlling neurotransmitter release both in the central (Baraban et al, 1985b;Allgaier & Hertting, 1986;Allgaier et al, 1986b;Malenka et al, 1986;Tanaka et al, 1986;Feuerstein et al, 1987) and in the peripheral (Wakade et al, 1985;Baraban et al, 1985a) nervous system. In the present paper, the conclusion that phorbol esters enhance noradrenaline release as a result of their effect on PKC is mainly supported by three observations discussed below; the facilitatory effects of two potent PKC activators, TPA and 4P-PDB (Castagna et al, 1982), the lack ofeffects of phorbol compounds which do not activate PKC, and the inhibitory effect of the PKC inhibitor polymyxin B.…”

Section: Discussionmentioning

confidence: 99%

“…In this regard the action of TPA resembles that of islet-activating protein or N-ethylmaleimide. Recently, we demonstrated that phorbol esters similar to islet-activating protein or N-ethylmaleimide enhanced noradrenaline release from noradrenergic nerve terminals of the rabbit hippocampus (Allgaier & Hertting, 1986;Allgaier et al, 1986b). Hence, the question arises as to whether activation of PKC may lead to an inactivation of the a2-autoinhibitory feedback system of noradrenergic nerve terminals.…”

Section: Introductionmentioning

confidence: 99%

Protein kinase C activation and α₂‐autoreceptor‐modulated release of noradrenaline

Allgaier

Hertting

Huang

et al. 1987

British J Pharmacology

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1Effects of phorbol esters on the evoked noradrenaline release were studied in slices of the rabbit hippocampus, labelled with [3HJ-noradrenaline, superfused continuously with a medium containing the reuptake inhibitor cocaine and stimulated electrically for 2 min (stimulation parameters: 2 ms, 24mA, 5Vcm-', 3 or 0.3Hz).2 The electrically-evoked overflow of [3H]-noradrenaline in the slices was increased in a concentration-dependent manner by the protein kinase C (PKC) activators 12-0-tetradecanoylphorbol 13-acetate (TPA) and 4f-phorbol 12,13-dibutyrate (4p-PDB). Phorbol esters, which do not activate PKC, 4-0-methyl-TPA and 4a-PDB, showed no effect on neurotransmitter release. The effect of4P-PDB was abolished in the presence of tetrodotoxin and in the absence of calcium. The PKC inhibitor polymyxin B inhibited the evoked noradrenaline release.3 In the presence of 4P-PDB the inhibitory effects of the o2-adrenoceptor agonist clonidine or the facilitatory effects ofthe z2-adrenoceptor antagonist yohimbine seemed to be modified only by changes in the concentration of noradrenaline in the synaptic region. At a stimulation frequency of 3 Hz the inhibitory action of clonidine was reduced whereas the facilitatory effect of the yohimbine was even slightly enhanced by the phorbol ester. At 0.3 Hz and in the presence of 4P-PDB the effect of clonidine remained and that of yohimbine was strongly enhanced. 4 Pretreatment of the slices with islet-activating protein or N-ethylmaleimide significantly reduced the enhancement of noradrenaline release caused by 4P-PDB. It is possible that a regulatory N-protein is involved in steps following PKC activation. 5 These results suggest that PKC participates in the mechanism of action-potential-induced noradrenaline release from noradrenergic nerve terminals of the rabbit hippocampus and that effects on the autoinhibitory feedback system were not responsible for the 4P-PDB-induced increase of neurotransmitter release.

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Enhancement of noradrenaline release by 12-O-tetradecanoyl phorbol-13-acetate, an activator of protein kinase C

Cited by 60 publications

References 10 publications

Mechanism of dopamine mediated inhibition of neuropeptide Y release from pheochromocytoma cells (PC12 cells)

Mechanism of dopamine mediated inhibition of neuropeptide Y release from pheochromocytoma cells (PC12 cells)

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

Protein kinase C activation and α₂‐autoreceptor‐modulated release of noradrenaline

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Enhancement of noradrenaline release by 12-O-tetradecanoyl phorbol-13-acetate, an activator of protein kinase C

Cited by 60 publications

References 10 publications

Mechanism of dopamine mediated inhibition of neuropeptide Y release from pheochromocytoma cells (PC12 cells)

Mechanism of dopamine mediated inhibition of neuropeptide Y release from pheochromocytoma cells (PC12 cells)

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

Protein kinase C activation and α2‐autoreceptor‐modulated release of noradrenaline

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Protein kinase C activation and α₂‐autoreceptor‐modulated release of noradrenaline