Influence of lithium on second messenger accumulation in NG 108-15 cells

Brami, Brigitte; Leli, Ubaldo; Hauser, George

doi:10.1016/0006-291x(91)91460-t

Cited by 33 publications

(22 citation statements)

References 31 publications

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“…Lithium has been reported to increase the levels of diacylglycerol, an endogenous activator of PKC in rat cortical slices (Godfrey et al . 1989) and various other cell types (Downes & Stone 1986; Brami et al . 1991).…”

Section: Discussionmentioning

confidence: 99%

“…1989) and in various other cell types (Drummond & Raeburn 1984; Bocckino et al . 1985; Downes & Stone 1986; Brami et al . 1991).…”

Section: Introductionmentioning

confidence: 99%

“…Lithium has been shown to effectively inhibit inositol monophosphatase, thus breaking up the cyclic event with the accumulation of inositol monophosphates and inositol depletion (Allison et al, 1976;Sherman et al, 1981Sherman et al, , 1985. In addition to the inhibitory effects on the inositol phosphate degradation, lithium has been reported to increase the levels of diacylglycerol, an endogenous activator of protein kinase C (PKC), in rat cortical slices (Godfrey et al, 1989) and in various other cell types (Drummond & Raeburn, 1984;Bocckino et al, 1985;Downes & Stone, 1986;Brami et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

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Action potential broadening induced by lithium may cause a presynaptic enhancement of excitatory synaptic transmission in neonatal rat hippocampus

Colino¹,

García-Seoane²,

Valentı́n³

1998

Eur J of Neuroscience

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Lithium enhances excitatory synaptic transmission in CA1 pyramidal cells, but the mechanisms remain unclear. The present study demonstrates that lithium enhances the N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-isoxazole propionic acid (AMPA) receptor-mediated components of the excitatory postsynaptic current (EPSC). Lithium decreased the magnitude of paired-pulse facilitation and presented an inverse correlation between the lithium-induced enhancement of synaptic transmission and initial paired-pulse facilitation, which is consistent with a presynaptic mode of action. The enhancement of synaptic strength is likely to act, at least in part, by increasing the amplitude of the presynaptic Ca2+ transient. One mechanism which could account for this change of the presynaptic Ca2+ transient is an increase in the duration of the action potential. We investigated action potential in hippocampal pyramidal neurons and found that lithium (0.5-6 mM) increased the half-amplitude duration and reduced the rate of repolarization, whereas the rate of depolarization remained similar. To find out whether the lithium synaptic effects might be explained by spike broadening, we investigated the field recording of the excitatory postsynaptic potential (EPSP) in hippocampal slices and found three lines of evidence. First, the prolongation of the presynaptic action potential with 4-aminopyridine and tetraethylammonium blocked or reduced the synaptic effects of lithium. Second, the lithium-induced synaptic enhancement was modulated when presynaptic Ca2+ influx was varied by changing the external Ca2+ concentration. Finally, both effects, the synaptic transmission increment and the action potential broadening, were independent of inositol depletion. These results suggest that lithium enhances synaptic transmission in the hippocampus via a presynaptic site of action: the mechanism underlying the potentiating effect may be attributable to an increased Ca2+ influx consequent to the broadening effect of lithium on the action potential.

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Section: Discussionmentioning

confidence: 99%

“…1989) and in various other cell types (Drummond & Raeburn 1984; Bocckino et al . 1985; Downes & Stone 1986; Brami et al . 1991).…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Action potential broadening induced by lithium may cause a presynaptic enhancement of excitatory synaptic transmission in neonatal rat hippocampus

Colino¹,

García-Seoane²,

Valentı́n³

1998

Eur J of Neuroscience

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“…7). Conversely, the bradykinin-induced oscillations in cells not expressing the ras on cogene but pretreated with lithium could be secondary to enhanced cellular 1,4,5-InsPj and 1,3,4.5-InsP.j, as shown in other tissues [15,30], However, the effect of lithium is not confined to inositol phosphate metabolism but in addition leads to increases in cellular diacylgiycerol [30],…”

Section: Resultsmentioning

confidence: 99%

Further Studies on the Nature of Cell Membrane Potential Oscillations in NIH 3T3 Fibroblasts Expressing the Ras Oncogene

Waldegger¹,

Pinggera²,

Kloiber³

et al. 1993

Cell Physiol Biochem

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NIH 3T3 fibroblasts expressing the Ha-ras oncogene respond to bradykinin (100 nmol/l) with sustained oscillations of cell membrane potential. Otherwise identical cells not expressing the oncogene respond to bradykinin with a single, transient hyperpolarization of the cell membrane. The oscillations of cell membrane potential in ras oncogene-expressing cells are the result of intracellular calcium oscillations with subsequent activation of calcium-sensitive K⁺ channels. As shown here, oscillations of cell membrane potential are elicited by acute addition of 0.5% fetal calf serum. Acute addition of cAMP (1 mmol/l), on the other hand, did not elicit oscillations of cell membrane potential. The involvement of calmodulin was excluded by the use of trifluoperazine (10 µmol/l), pimozide (1 µmol/l) and compound 48/80 (3 µmol/l) and the involvement of cycloxygenase products by the use of indomethacin (1 µmol/l). Neither substance modified the oscillations significantly. Similarly, dantrolene (10 µmol/l), an inhibitor of calcium-induced calcium release remained without significant effect on the oscillations. On the other hand, thapsigargin (1 µmol/l), an inhibitor of endoplasmatic reticulum Ca²⁺⁺-ATPase, abolished the oscillations in 7 out of 10 cells. Furthermore, phorbolester TPA (10 µmol/l) acutely inhibited the oscillations. In cells not expressing the ras oncogene but pretreated for 24 h with lithium (10 mmol/l), oscillations of cell membrane potential similar to those in ras oncogene-expressing cells are observed following the addition of bradykinin. HPLC reveals markedly increased formation of 1,3,4,5-InsP₄ and 1,4,5-InsP₃ prior to the addition of bradykinin as well as an enhanced stimulatory effect of bradykinin on the inositol phosphates in ras oncogene-expressing cells. In conclusion, the calcium oscillations probably involve thapsigargin-sensitive intracellular calcium stores and may be secondary to enhanced formation of 1,3,4,5-InsP₄ and/or 1,4,5-InsP₃. Phorbolesters abolish the oscillations presumably by inhibiting phospholipase C, and lithium triggers the oscillations possibly by enhancing cellular 1,3,4,5-InsP₄ and/or 1,4,5-InsP₃.

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“…Cells were cultured in a humidified atmosphere of 95 % air and 5 % CO, at 37 "C. The medium was changed every other day. Differentiation of NGlO8-15 cells was obtained by culturing them for 4-5 days in the same medium supplemented with 2% fetal calf serum and 1 mM Bt,cAMP (Nh,2'-O-dibutyryl-adenosine 3',5'-phosphate) [22].…”

Section: Methodsmentioning

confidence: 99%

Changes in the Levels of Glycerophosphoinositols During Differentiation of Hepatic and Neuronal Cells

Falasca

Marino²,

Carvelli

et al. 1996

European Journal of Biochemistry

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Glycerophosphoinositols are metabolites formed by a phosholipase A, and a lysolipase specifically acting on membrane phosphoinositol lipids. High levels of these compounds characterize epithelial cells and fibroblasts transformed by ras and other cellular oncogenes. Here we have analyzed the glycerophosphoinositol levels in cells that are considered models of cell differentiation. Using rat hepatocytes at different stages of liver development we have shown that the glycerophosphoinositol basal levels of fetal cells were up to fourfold higher than in adult hepatocytes. No changes in glycerophosphoinositol were observed in regenerating rat liver, a model of differentiated cells proliferating in a synchronous manner, where only glycerophosphoinositol 4-phosphate increased by 80 %. Similarly to fetal hepatocytes, a modest but significant increase (30 %) in the levels of glycerophosphoinositols was observed in undifferentiated NG-108-15 cells as compared to the same cells induced to differentiate by CAMP. In a different neuronal cell line, PC12 cells, increased glycerophosphoinositol levels characterized the differentiated cells. Based on these observations we suggest that high glycerophosphoinositol levels characterize cellular phenomena associated with the activation of ruslmitogen-activated protein kinase pathways.

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Influence of lithium on second messenger accumulation in NG 108-15 cells

Cited by 33 publications

References 31 publications

Action potential broadening induced by lithium may cause a presynaptic enhancement of excitatory synaptic transmission in neonatal rat hippocampus

Action potential broadening induced by lithium may cause a presynaptic enhancement of excitatory synaptic transmission in neonatal rat hippocampus

Further Studies on the Nature of Cell Membrane Potential Oscillations in NIH 3T3 Fibroblasts Expressing the Ras Oncogene

Changes in the Levels of Glycerophosphoinositols During Differentiation of Hepatic and Neuronal Cells

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