Serotonin induces inward potassium and calcium currents in rat cortical astrocytes

Jalonen, Tuula O.; Margraf, Russell R.; Wielt, D.B.; Charniga, Carol; Linne, Marja-Leena; Kimelberg, Harold K.

doi:10.1016/s0006-8993(97)00163-7

Cited by 43 publications

(25 citation statements)

References 56 publications

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“…One acute effect could be the activation of Ca 2+ -activated K + channels in the pituicyte membrane. Such an activation has already been reported with glutamate [9] and serotonin [21] in cultured rat astrocytes, and with histamine in C6 glial cells [47]. Moreover, in cultured non-proliferating microglial cells, ATP has been shown to open K + channels, via the P 2Y receptor [20].…”

Section: Discussionmentioning

confidence: 71%

ATP acting on P 2Y receptors triggers calcium mobilization in primary cultures of rat neurohypophysial astrocytes (pituicytes)

Troadec¹,

Thirion²,

Petturiti³

et al. 1999

Pfl�gers Archiv European Journal of Physiology

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The effect of adenosine triphosphate (ATP) on the intracellular Ca2+ concentration ([Ca2+]i) of cultured neurohypophysial astrocytes (pituicytes) was studied by fluorescence videomicroscopy. ATP evoked a [Ca2+]i increase, which was dose dependent in the 2.5-50 microM range (EC50=4.3 microM). The ATP-evoked [Ca2+]i rise was not modified during the first minute following the removal of external Ca2+. Application of 500 nM thapsigargin inhibited the ATP-dependent [Ca2+]i increase. Caffeine (10 mM) and ryanodine (1 microM) did not affect the ATP-induced [Ca2+]i rise. The pituicytes responded to various P2 purinoceptor agonists with the following order of potency: ATP=ATP[gamma-S]=2-MeSATP>/=ADP, where ATP[gamma-S] is adenosine 5'-O-(3-thiotriphosphate) and 2-MeSATP is 2-methylthio-adenosine-5'-triphosphate. Adenosine, AMP, alpha, beta-methylene adenosine-5'-triphosphate (alpha,beta-MeATP), beta, gamma methylene adenosine-5'-triphosphate (beta,gamma-MeATP) and uridine 5'-triphosphate (UTP) were ineffective. The P2 purinoceptor antagonists blocked the ATP-evoked [Ca2+]i increase with the following selectivity: RB-2>suramin>PPADS, where RB-2 is Reactive Blue 2 and PPADS is pyridoxal-phosphate-6-azophenyl-2', 4'-disulphonic acid. The ATP-evoked [Ca2+]i increase was substantially blocked by pertussis toxin treatment, suggesting that it might be mediated by a pertussis-toxin-sensitive G protein. The phospholipase C (PLC) inhibitor U-73122 (0.5 microM) abolished the ATP-evoked [Ca2+]i rise, whereas its inactive stereoisomer U-73343 (0.5 microM) remained ineffective. Our results indicate that, in rat cultured pituicytes, ATP stimulation induces an increase in [Ca2+]i due to PLC-mediated release from intracellular stores through activation of a pertussis-toxin-sensitive, G-protein-linked P2Y receptor.

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Section: Discussionmentioning

confidence: 71%

ATP acting on P 2Y receptors triggers calcium mobilization in primary cultures of rat neurohypophysial astrocytes (pituicytes)

Troadec¹,

Thirion²,

Petturiti³

et al. 1999

Pfl�gers Archiv European Journal of Physiology

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“…Astrocytes, as well as other glial cells, use both spontaneous and stimulated variations of the Ca concentration for intra- and intercellular signaling [25], [26]. Previous electrophysiological and Ca imaging studies have shown how already micromolar concentration of 5-HT cause transient release of Ca from intracellular stores followed by prolonged transmembrane inward Ca flow [17], [27]. We here have used rat cortical astrocytes, similarly to our earlier studies on A25–35 and A1–40 [16], to study the special effects of A25–35 to Ca signals when added together with transmitters.…”

Section: Introductionmentioning

confidence: 99%

Effects of Transmitters and Amyloid-Beta Peptide on Calcium Signals in Rat Cortical Astrocytes: Fura-2AM Measurements and Stochastic Model Simulations

Toivari

Manninen

Nahata³

et al. 2011

PLoS ONE

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BackgroundTo better understand the complex molecular level interactions seen in the pathogenesis of Alzheimer's disease, the results of the wet-lab and clinical studies can be complemented by mathematical models. Astrocytes are known to become reactive in Alzheimer's disease and their ionic equilibrium can be disturbed by interaction of the released and accumulated transmitters, such as serotonin, and peptides, including amyloid- peptides (A). We have here studied the effects of small amounts of A25–35 fragments on the transmitter-induced calcium signals in astrocytes by Fura-2AM fluorescence measurements and running simulations of the detected calcium signals.Methodology/Principal FindingsIntracellular calcium signals were measured in cultured rat cortical astrocytes following additions of serotonin and glutamate, or either of these transmitters together with A25–35. A25–35 increased the number of astrocytes responding to glutamate and exceedingly increased the magnitude of the serotonin-induced calcium signals. In addition to A25–35-induced effects, the contribution of intracellular calcium stores to calcium signaling was tested. When using higher stimulus frequency, the subsequent calcium peaks after the initial peak were of lower amplitude. This may indicate inadequate filling of the intracellular calcium stores between the stimuli. In order to reproduce the experimental findings, a stochastic computational model was introduced. The model takes into account the major mechanisms known to be involved in calcium signaling in astrocytes. Model simulations confirm the principal experimental findings and show the variability typical for experimental measurements.Conclusions/SignificanceNanomolar A25–35 alone does not cause persistent change in the basal level of calcium in astrocytes. However, even small amounts of A25–35, together with transmitters, can have substantial synergistic effects on intracellular calcium signals. Computational modeling further helps in understanding the mechanisms associated with intracellular calcium oscillations. Modeling the mechanisms is important, as astrocytes have an essential role in regulating the neuronal microenvironment of the central nervous system.

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“…SK2, SK3, and SK1 channels, expressed in Xenopus oocytes (Köhler et al 1996) and in mammalian cells (Strobaek et al 2000), respectively, were blocked by apamin. In glial cells, electrophysiological and molecular studies have demonstrated the expression of SK channels (Burnard et al 1990;Manor et al 1994;Khanna et al 2001;Seagar et al 1987;Jalonen et al 1997). However, there is little data concerning the localization of SK channels in glial cells in vivo.…”

Section: Introductionmentioning

confidence: 99%

Expression of the small conductance Ca 2+ -activated K + channel, SK3, in the olfactory ensheathing glial cells of rat brain

Fujita

Takeuchi

Hanai

et al. 2003

Cell and Tissue Research

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Olfactory sensory neurons are wrapped by ensheathing glial cells in the olfactory nerve layer (ONL). Neither functional roles nor electrical properties of ensheathing glial cells have been, as yet, fully clarified. Four subunits (SK1-4) of small conductance Ca2+-activated K+ (SK) channels have been cloned. In the present study, immunohistochemical analyses showed that SK3 channels are expressed in ensheathing glial cells in the rat olfactory bulb, in addition to neuronal cells in other regions. Western blotting analysis demonstrated that SK3 was predominantly expressed in the olfactory bulb, thalamus, moderately in the hippocampus and cerebellum and modestly in the cerebral cortex of the rat brain. SK3 immunoreactivity was detected in the ONL of the olfactory bulb, neural cell body and fibers of the substantia nigra and hypothalamus. SK3 immunoreactivity was quite intense in the outer (superficial) part of the ONL. SK3-immunoreactive structures were overlapped with glial fibrillary acidic protein (GFAP), but not with vimentin, markers for glial cells and olfactory sensory axons, respectively. Immunoelectron microscopy showed that SK3 immunoreactivity was localized in thin processes that enfolded fascicles of immunonegative olfactory nerve axons. These results indicate that SK3 is expressed specifically in the olfactory ensheathing glial cells in olfactory regions.

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Serotonin induces inward potassium and calcium currents in rat cortical astrocytes

Cited by 43 publications

References 56 publications

ATP acting on P 2Y receptors triggers calcium mobilization in primary cultures of rat neurohypophysial astrocytes (pituicytes)

ATP acting on P 2Y receptors triggers calcium mobilization in primary cultures of rat neurohypophysial astrocytes (pituicytes)

Effects of Transmitters and Amyloid-Beta Peptide on Calcium Signals in Rat Cortical Astrocytes: Fura-2AM Measurements and Stochastic Model Simulations

Expression of the small conductance Ca 2+ -activated K + channel, SK3, in the olfactory ensheathing glial cells of rat brain

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