Differential expression of protein kinase C isoforms in glial and neuronal cells. Translocation and down-regulation of PKC isoforms in C6 glioma and ng 108-15 hybrid cells: Effects of extracellular Ca2+-depletion

Chen, Ching-Chow; Chang, Jason; Lin, Wan-Wan

doi:10.1016/0197-0186(94)00157-p

Cited by 14 publications

(9 citation statements)

References 33 publications

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“…The result that the 5-HT-induced membrane depolarization in P and N1 neurons persisted without a [Ca 2ϩ ] i increase (Fig. 5) points to a Ca 2ϩ -independent form of PKC (see Chen et al, 1995;Way et al, 2000), which is in line with previous results (Catarsi and Drapeau, 1997;Drapeau et al, 1989;Garcia-Gil et al, 1991;Sanchez-Armass et al, 1991).…”

Section: ؉ -Independentsupporting

confidence: 86%

Ca²⁺ influx into identified leech neurons induced by 5‐hydroxytryptamine

Dierkes

Schlue

2004

J. Neurobiol.

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The role of 5-hydroxytryptamine (5-HT, serotonin) in the control of leech behavior is well established and has been analyzed extensively on the cellular level; however, hitherto little is known about the effect of 5-HT on the cytosolic free calcium concentration ([Ca(2+)](i)) in leech neurons. As [Ca(2+)](i) plays a pivotal role in numerous cellular processes, we investigated the effect of 5-HT on [Ca(2+)](i) (measured by Fura-2) in identified leech neurons under different experimental conditions, such as changed extracellular ion composition and blockade of excitatory synaptic transmission. In pressure (P), lateral nociceptive (N1), and Leydig neurons, 5-HT induced a [Ca(2+)](i) increase which was predominantly due to Ca(2+) influx since it was abolished in Ca(2+)-free solution. The 5-HT-induced Ca(2+) influx occurred only if the cells depolarized sufficiently, indicating that it was mediated by voltage-dependent Ca(2+) channels. In P and N1 neurons, the membrane depolarization was due to Na(+) influx through cation channels coupled to 5-HT receptors, whereby the dose-dependency suggests an involvement in excitatory synaptic transmission. In Leydig neurons, 5-HT receptor-coupled cation channels seem to be absent. In these cells, the membrane depolarization activating the voltage-dependent Ca(2+) channels was evoked by 5-HT-triggered excitatory glutamatergic input. In Retzius, anterior pagoda (AP), annulus erector (AE), and median nociceptive (N2) neurons, 5-HT had no effect on [Ca(2+)](i).

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Section: ؉ -Independentsupporting

confidence: 86%

Ca²⁺ influx into identified leech neurons induced by 5‐hydroxytryptamine

Dierkes

Schlue

2004

J. Neurobiol.

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“…In some systems, phorbol esters and Ca 2 ionophores work synergistically to produce a full second messenger response (Kaibuchi et al, 1983;Yamanishi et al, 1983;Casado et al, 1993). Up to six different PKC isoforms, both Ca2~dependent and Ca2 independent, have been identified in C6 glioma (Chen et a!., 1995;Kronfeld et al, 1995). In our system, A23187 did not increase basal levels of L-[3H1GIu transport nor did it enhance the stimulation of L-[3H] -Glu transport caused by PMA.…”

Section: Effect Of Amiloride On Phorbol Ester Stimulation Of L-[3hi Gcontrasting

confidence: 45%

Rapid Stimulation of EAAC1‐Mediated Na⁺‐Dependent l‐Glutamate Transport Activity in C6 Glioma Cells by Phorbol Ester

Dowd

Robinson

1996

Journal of Neurochemistry

126

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06 glioma cells were used as a model system to study the regulation of EAAC1 -mediated Na~-dependent L-[ 3H]glutamate transport. Although a 30-mm preincubation with forskolin had no effect on transport activity, preincubation with phorbol 12-myristate 13-acetate (PMA) increased transport activity two-to threefold. PMA caused a time-dependent and concentration-dependent increase in EAAC1-mediated L-[3H]glutamate transport activity. A 2-mm preincubation with PMA was sufficient to cause more than a twofold increase in transport activity and the protein synthesis inhibitor cycloheximide had no effect on the increase. These data suggest that this increase is independent of protein synthesis. The E0 50 value of PMA for stimulation of transport activity was 80 nM. Kinetic analyses demonstrated that the increase in transport activity was due to a 2.5-fold increase in Vmax with no change in Km. PMA also increased the transport of the nonmetabolizable analogue, D-[ 3H]aspartate to the same extent. In parallel assays, PMA did not, however, increase Nat-dependent glycine transport activity in 06 glioma. The inactive phorbol ester 4a-phorbol 12,13-didecanoate, did not stimulate L-[3H]glutamate transport activity, and the protein kinase C inhibitor chelerythrine blocked the stimulation caused by PMA. Okadaic acid and cyclosporin A, which are phosphatase inhibitors, had no effect on the stimulation of transport activity caused by PMA. The Ca2~ionophore A23187 did not act synergistically to increase PMA stimulation. In previous studies, PMA caused a rapid increase in amiloride-sensitive Na~/Htransport activity in 06 glioma. In the present study, pre-and coincubation with amiloride had no effect on the stimulation of transport activity caused by PMA. These studies suggest that activation of protein kinase C causes a rapid increase in EAAC1-mediated transport activity. This rapid increase in Nat-dependent L-[3H]glutamate transport activity may provide a novel mechanism for protection against acute insults to the CNS. Key Words: Glutamate-Transport-Uptake-EAAC 1-06 glioma-Phorbol ester.

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“…Differential expression of new PKC isoforms in guai and neuronal cells has been observed in this laboratory (Chen et al,l995a). Glial cells, including C6 glioma cells and cultured astrocytes, express an abundance of PKC6 (Chen et al, 1995a,b), whereas neuronal cells, including NG 108-15 hybrid, Neuro 2A, SK-N-SH, and NCB-20 cells (Chen et al, 1995a;present study), express an abundance of PKCe. PKCÖ in C6 glioma cells was found to be involved in the stimulation of the Na~-H~exchanger (Chen and Wu, 1995); PKCa and 6 in astrocytes are involved in the tonic inhibition of BK-and ATP-stimulated Pi breakdown (Chen et al, 1995b;.…”

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confidence: 99%

P2Y Receptor Linked to Phospholipase C: Stimulation of Neuro 2A Cells by UTP and ATP and Possible Regulation by Protein Kinase C Subtype ε

Chen

1997

Journal of Neurochemistry

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Incubation of Neuro 2A mouse neuroblastoma cells with UTP and UDP results in a concentration-dependent increase in the accumulation of inositol phosphates with equal potency and maximal effect; ATP, ADP, and 2-methylthioadenosine 5 '-triphosphate were much less potent, indicating the expression of P2Y receptor in these cells. The effects of UTP and ATP were not affected by pretreatment of cells with pertussis toxin, indicating that the P2Y receptor in Neuro 2A cells is coupled to pertussis toxin-insensitive Gq protein. Short-term (10 mm) treatment of cells with 1 p~M12-O-tetradecanoylphorbol 13-acetate (TPA) resulted in the inhibition of the UTP and ATP effects; this inhibitory effect was gradually attenuated with increased length of TPA treatment (1.5-6 h) and was not seen after long-term (24 h) treatment. Western blot analysis showed the expression of protein kinase

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Differential expression of protein kinase C isoforms in glial and neuronal cells. Translocation and down-regulation of PKC isoforms in C6 glioma and ng 108-15 hybrid cells: Effects of extracellular Ca2+-depletion

Cited by 14 publications

References 33 publications

Ca²⁺ influx into identified leech neurons induced by 5‐hydroxytryptamine

Ca²⁺ influx into identified leech neurons induced by 5‐hydroxytryptamine

Rapid Stimulation of EAAC1‐Mediated Na⁺‐Dependent l‐Glutamate Transport Activity in C6 Glioma Cells by Phorbol Ester

P2Y Receptor Linked to Phospholipase C: Stimulation of Neuro 2A Cells by UTP and ATP and Possible Regulation by Protein Kinase C Subtype ε

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Differential expression of protein kinase C isoforms in glial and neuronal cells. Translocation and down-regulation of PKC isoforms in C6 glioma and ng 108-15 hybrid cells: Effects of extracellular Ca2+-depletion

Cited by 14 publications

References 33 publications

Ca2+ influx into identified leech neurons induced by 5‐hydroxytryptamine

Ca2+ influx into identified leech neurons induced by 5‐hydroxytryptamine

Rapid Stimulation of EAAC1‐Mediated Na+‐Dependent l‐Glutamate Transport Activity in C6 Glioma Cells by Phorbol Ester

P2Y Receptor Linked to Phospholipase C: Stimulation of Neuro 2A Cells by UTP and ATP and Possible Regulation by Protein Kinase C Subtype ε

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Ca²⁺ influx into identified leech neurons induced by 5‐hydroxytryptamine

Ca²⁺ influx into identified leech neurons induced by 5‐hydroxytryptamine

Rapid Stimulation of EAAC1‐Mediated Na⁺‐Dependent l‐Glutamate Transport Activity in C6 Glioma Cells by Phorbol Ester