Lithium‐induced decrease in spontaneous Ca<sup>2+</sup> oscillations in single GH<sub>3</sub> rat pituitary cells

Varney, Mark A.; Galione, Antony; Watson, Steve P.

doi:10.1111/j.1476-5381.1994.tb13084.x

Cited by 6 publications

(3 citation statements)

References 24 publications

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“…Consistent with the results of studies conducted in hippocampal neurons, cerebellar granule cells, ganglion neurons, and GH3 rat pituitary cells (Ogura et al, 1987;Nohmi et al, 1991;Lawrie et al, 1993;Varney et al, 1994), spontaneous oscillation of [Ca2+]i were observed in cultured cortical neurons. In this study, oscillations of [Ca2+]i were greatly reduced by voltage-dependent Ca 2+ channel antagonists and NMDA antagonists.…”

Section: Discussionsupporting

confidence: 90%

Effect of dantrolene on KCl- or NMDA-induced intracellular Ca2+ changes and spontaneous Ca2+ oscillation in cultured rat frontal cortical neurons

Hayashi

Kagaya

Takebayashi

et al. 1997

J. Neural Transmission

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Dantrolene has been known to affect intracellular Ca2+ concentration ([Ca2+]i) by inhibiting Ca2+ release from intracellular stores in cultured neurons. We were interested in examining this property of dantrolene in influencing the [Ca2+]i affected by the NMDA receptor ligands, KCl, L-type Ca2+ channel blocker nifedipine, and two other intracellular Ca2(+)-mobilizing agents caffeine and bradykinin. Effect of dantrolene on the spontaneous oscillation of [Ca2+]i was also examined. Dantrolene in microM concentrations dose-dependently inhibited the increase in [Ca2+]i elicited by NMDA and KCl. AP-5, MK-801 (NMDA antagonists), and nifedipine respectively reduced the NMDA and KCl-induced increase in [Ca2+]i. Dantrolene, added to the buffer solution together with the antagonists or nifedipine, caused a further reduction in [Ca2+]i to a degree similar to that seen with dantrolene alone inhibiting the increase in [Ca2+]i caused by NMDA or KCl. At 30 microM, dantrolene partially inhibited caffeine-induced increase in [Ca2+]i whereas it has no effect on the bradykinin-induced change in [Ca2+]i. The spontaneous oscillation of [Ca2+]i in frontal cortical neurons was reduced both in amplitude and in base line concentration in the presence of 10 microM dantrolene. Our results indicate that dantrolene's mobilizing effects on intracellular Ca2+ stores operate independently from the influxed Ca2+ and that a component of the apparent increase in [Ca2+]i elicited by NMDA or KCl represents a dantrolene-sensitive Ca2+ release from intracellular stores. Results also suggest that dantrolene does not affect the IP3-gated release of intracellular Ca2+ and that the spontaneous Ca2+ oscillation is, at least partially, under the control of Ca2+ mobilization from internal stores.

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Section: Discussionsupporting

confidence: 90%

Effect of dantrolene on KCl- or NMDA-induced intracellular Ca2+ changes and spontaneous Ca2+ oscillation in cultured rat frontal cortical neurons

Hayashi

Kagaya

Takebayashi

et al. 1997

J. Neural Transmission

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“…Further support for a more selective localized effect of lithium on PI signaling was obtained in experiments with cultured cells in vitro [8–13]. While earlier work with brain slices (for review see [5]) and later investigations of neural cell cultures in vitro [14–17] had identified inhibitory effects of lithium on the agonist‐stimulated release of inositolphosphates or Ca 2+ ions, measurements of IP 3 in vivo [18–20] did not provide evidence for an inhibition by lithium of PI signaling. Furthermore, work by Hokin and his colleagues made clear that brain slices from species like rat and mice are particularly vulnerable to artificial depletion of inositol during the assay procedures and showed that in slices from primate brain and in neuronal cells of human origin, lithium increases PI signaling [21,22].…”

Section: The Inositol‐depletion Hypothesismentioning

confidence: 99%

The high affinity inositol transport system – implications for the pathophysiology and treatment of bipolar disorder

Calker¹,

Belmaker²

2000

Bipolar Disorders

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The 'inositol-depletion hypothesis' postulates that the therapeutic effects of lithium are due to inhibition of inositol monophosphatase, which leads to depletion of brain cells of myo-inositol and consequently to dampening of phosphoinositide (PI) signaling. This article examines the potential relevance of an alternative mechanism for inositol depletion: inhibition of myo-inositol uptake that proceeds via the sodium/myo-inositol cotransport (SMIT). We discuss recent in vitro experiments that show a pronounced downregulation of SMIT after chronic treatment with lithium, carbamazepine, and valproate at therapeutically relevant concentrations. It is concluded that downregulation of SMIT could represent a common mechanism of action of mood stabilizers.

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“…Lithium exerts significant effects on inositol lipid metabolism in cultured GH3 pituitary cells when these are exposed to lithium concentrations seen in treated patients (8). Treatment of GH3 cells with 1 mM lithium for 7 days reduces basal and TRH-stimulated levels of inositol 1,4,5trisphosphate, and this is associated with a reduction in the number of cells showing basal calcium oscillations (9).…”

Section: Introductionmentioning

confidence: 99%

The Effects of Lithium Therapy on Thyroid and Thyrotropin-Releasing Hormone

Lazarus¹

1998

Thyroid

171

102

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Lithium is used in the prophylaxis of bipolar depressive disorder in augmentation treatment of depression and in the therapy of some cases of unipolar depression. Lithium affects cell function via its inhibitory action on adenosine triphosphatase (ATPase) activity, cyclic adenosine monophosphate (cAMP), and intracellular enzymes. The inhibitory effect of lithium on inositol phospholipid metabolism affects signal transduction and may account for part of the action of the cation in manic depression. Lithium also alters the in vitro response of cultured cells to thyrotropin-releasing hormone (TRH) and can stimulate DNA synthesis. Lithium is concentrated by the thyroid and inhibits thyroidal iodine uptake. It also inhibits iodotyrosine coupling, alters thyroglobulin structure, and inhibits thyroid hormone secretion. The latter effect is critical to the development of hypothyroidism and goiter. Effects on brain deiodinase enzymes and alterations in thyroid hormone receptor concentration in the hypothalamus are under investigation in relation to the therapeutic effect of lithium. The ion affects many aspects of cellular and humoral immunity in vitro and in vivo. This accounts for a rise in antithyroid antibody titer in patients having these antibodies before lithium administration whereas there is no induction of thyroid antibody synthesis de novo. Goiter, due to increased thyrotropin (TSH) after inhibition of thyroid hormone release, occurs at various reported incidence rates from 0%-60% and is smooth and nontender. Subclinical and clinical hypothyroidism due to lithium is usually associated with circulating anti-thyroid peroxidase (TPO) antibodies but may occur in their absence. Iodine exposure, dietary goitrogens, and immunogenetic background may all contribute to the occurrence of goiter and hypothyroidism during long-term lithium therapy. It is currently unclear whether the reported association of lithium therapy and hyperthyroidism are causal, although there is suggestive epidemiological evidence. Finally, lithium therapy is associated with exaggerated response of both TSH and prolactin to TRH in 50%-100% of patients, although basal levels are not usually high. It is probable that the hypothalamic pituitary axis adjusts to a new setting in patients receiving lithium.

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Lithium‐induced decrease in spontaneous Ca²⁺ oscillations in single GH₃ rat pituitary cells

Cited by 6 publications

References 24 publications

Effect of dantrolene on KCl- or NMDA-induced intracellular Ca2+ changes and spontaneous Ca2+ oscillation in cultured rat frontal cortical neurons

Effect of dantrolene on KCl- or NMDA-induced intracellular Ca2+ changes and spontaneous Ca2+ oscillation in cultured rat frontal cortical neurons

The high affinity inositol transport system – implications for the pathophysiology and treatment of bipolar disorder

The Effects of Lithium Therapy on Thyroid and Thyrotropin-Releasing Hormone

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Lithium‐induced decrease in spontaneous Ca2+ oscillations in single GH3 rat pituitary cells

Cited by 6 publications

References 24 publications

Effect of dantrolene on KCl- or NMDA-induced intracellular Ca2+ changes and spontaneous Ca2+ oscillation in cultured rat frontal cortical neurons

Effect of dantrolene on KCl- or NMDA-induced intracellular Ca2+ changes and spontaneous Ca2+ oscillation in cultured rat frontal cortical neurons

The high affinity inositol transport system – implications for the pathophysiology and treatment of bipolar disorder

The Effects of Lithium Therapy on Thyroid and Thyrotropin-Releasing Hormone

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Product

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Lithium‐induced decrease in spontaneous Ca²⁺ oscillations in single GH₃ rat pituitary cells