Mechanism of synchronized Ca2+ oscillations in cortical neurons

Wang, Xiao‐Shu; Gruenstein, Eric

doi:10.1016/s0006-8993(97)00585-4

Cited by 84 publications

(69 citation statements)

References 26 publications

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“…Because glutamate transmission generates action potentials leading to calcium influx through voltage-dependent calcium channels, we tested the effect of TTX and diltiazem on spontaneous calcium oscillations. Results presented in Figure S1, available at www.jneurosci.org as supplemental material, show that both inhibition of Na ϩ channels and L-type calcium channels completely inhibited calcium oscillations, confirming that L-type calcium channels play a key role in the generation of synchronous calcium oscillations observed in cultured cortical neurons (Wang and Gruenstein, 1997).…”

Section: Spontaneous Synchronous Calcium Oscillations Are Abolished Bsupporting

confidence: 60%

“…4 A). The effect of KCl-mediated depolarization on calcium oscillations has been previously described (Wang and Gruenstein, 1997), and is illustrated in figure S1D. In basal conditions, in the presence of 15 mM KCl, or after depolarization by 50 mM KCl, [Ca 2ϩ ] i was similar in ␤gal-or hAPP-expressing neurons (Fig.…”

Section: Increase Of L-type Calcium Currents By Happsupporting

confidence: 55%

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Expression of Human Amyloid Precursor Protein in Rat Cortical Neurons Inhibits Calcium Oscillations

Santos¹,

Pierrot²,

Morel³

et al. 2009

J. Neurosci.

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Synchronous calcium oscillations are observed in primary cultures of rat cortical neurons when mature networks are formed. This spontaneous neuronal activity needs an accurate control of calcium homeostasis. Alteration of intraneuronal calcium concentration is described in many neurodegenerative disorders, including Alzheimer disease (AD). Although processing of amyloid precursor protein (APP) that generates A␤ peptide has critical implications for AD pathogenesis, the neuronal function of APP remains unclear. Here, we report that expression of human APP (hAPP) in rat cortical neurons increases L-type calcium currents, which stimulate SK channels, calcium-dependent K ϩ channels responsible for medium afterhyperpolarization (mAHP). In a neuronal network, increased mAHP in some neurons expressing hAPP leads to inhibition of calcium oscillations in all the cells of the network. This inhibition is independent of production and secretion of A␤ and other APP metabolites. In a neuronal network, reduction of endogenous APP expression using shRNA increases the frequency and reduces the amplitude of calcium oscillations. Altogether, these data support a key role for APP in the control of neuronal excitability.

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Section: Spontaneous Synchronous Calcium Oscillations Are Abolished Bsupporting

confidence: 60%

Section: Increase Of L-type Calcium Currents By Happsupporting

confidence: 55%

Expression of Human Amyloid Precursor Protein in Rat Cortical Neurons Inhibits Calcium Oscillations

Santos¹,

Pierrot²,

Morel³

et al. 2009

J. Neurosci.

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“…Primary cultures of cortical neurons were prepared from embryonic day 17 Harlan Sprague-Dawley rats as described by Wang and Gruenstein (26). Cells were incubated at 37°C in 5% CO 2 for 7-10 days.…”

Section: Fluorescence Plate Reader Experiments On Neuronal Networkmentioning

confidence: 99%

Control of Electrical Activity in Central Neurons by Modulating the Gating of Small Conductance Ca2+-activated K+ Channels

Pedarzani

Mosbacher

Rivard

et al. 2001

Journal of Biological Chemistry

215

203

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In most central neurons, action potentials are followed by an afterhyperpolarization (AHP) that controls firing pattern and excitability. The medium and slow components of the AHP have been ascribed to the activation of small conductance Ca 2؉ -activated potassium (SK) channels. Cloned SK channels are heteromeric complexes of SK ␣-subunits and calmodulin. The channels are activated by Ca 2؉ binding to calmodulin that induces conformational changes resulting in channel opening, and channel deactivation is the reverse process brought about by dissociation of Ca 2؉ from calmodulin. Here we show that SK channel gating is effectively modulated by 1-ethyl-2-benzimidazolinone (EBIO). Application of EBIO to cloned SK channels shifts the Ca 2؉ concentration-response relation into the lower nanomolar range and slows channel deactivation by almost 10-fold. In hippocampal CA1 neurons, EBIO increased both the medium and slow AHP, strongly reducing electrical activity. Moreover, EBIO suppressed the hyperexcitability induced by low Mg 2؉ in cultured cortical neurons. These results underscore the importance of SK channels for shaping the electrical response patterns of central neurons and suggest that modulating SK channel gating is a potent mechanism for controlling excitability in the central nervous system.

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“…Synchronous spontaneous Ca 2+ oscillations are often observed among neuronal networks without external stimuli in vitro, resulting from periodic burst firing of action potentials through excitatory synaptic transmission [5][6][7]. These spontaneous and synchronous activities are believed to play a pivotal role during neuronal development including neuronal migration, differentiation and connection patterning [8][9][10][11][12].…”

Section: Spontaneous and Synchronous Camentioning

confidence: 99%

Ginsenoside Rg1 Modulates Spontaneous Synchronous Ca2+ Oscillations of Cultured Hippocampal Neurons

Wen-xiu¹,

Zong²,

Fu³

et al. 2009

TOPHYJ

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Ginsenoside Rg1, the main active ingredient of Ginseng Radix which is a famous Chinese medicine, is widely used as an anti-stress, anti-aging and neurological performance improving agent. In this study, we used calcium imaging and whole-cell patch clamp techniques to investigate the effect of Ginsenoside Rg1 on spontaneous and synchronous Ca 2+ oscillations and the possible mechanisms in primarily cultured hippocampal neuronal networks. We found that Ginsenoside Rg1 could decrease the frequencies of spontaneous and synchronous Ca 2+ oscillations and inhibit the amplitude of high-voltage activated calcium channel currents. These results provided the experimental evidence for the clinical application of Rg1 as a neuroprotector on the cellular level, and enriched the theoretical system of Chinese medicine.

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Mechanism of synchronized Ca2+ oscillations in cortical neurons

Cited by 84 publications

References 26 publications

Expression of Human Amyloid Precursor Protein in Rat Cortical Neurons Inhibits Calcium Oscillations

Expression of Human Amyloid Precursor Protein in Rat Cortical Neurons Inhibits Calcium Oscillations

Control of Electrical Activity in Central Neurons by Modulating the Gating of Small Conductance Ca2+-activated K+ Channels

Ginsenoside Rg1 Modulates Spontaneous Synchronous Ca2+ Oscillations of Cultured Hippocampal Neurons

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