Calcium transient activity in cultured murine neural crest cells is regulated at the IP3 receptor

Marc B. Carey, Steven Matsumoto

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

In a previous study we have shown that cultured neural crest cells exhibit spontaneous calcium transients and that these events are required for neurogenesis. In this study, we examine the mechanism that generates these calcium transients. Extracellular Ca2+ modulates calcium transient activity. Lanthanum (La3+), a general calcium channel antagonist and zero extracellular Ca2+, reduces the percentage of cells exhibiting calcium transients (26.2 and 40.5%, respectively) and decreases calcium spiking frequency (4.5 to 1.0 and 2.5 to 1.0 spikes/30 min, respectively). Intracellular calcium stores also contribute to the generation of calcium transients. Depleting the calcium stores of the endoplasmic reticulum (ER) reduces the percentage of active cells (15.7%) and calcium spiking frequency (2.8 to 1.5 spikes/30 min). Ryanodine (100 μM), which blocks calcium release regulated by the ryanodine receptor (RyR), had no effect on calcium transient activity. Blocking inositol 1,4,5-triphosphate receptor (IP3R)-dependent calcium release, with elevated extracellular Mg2+ (20 mM), abolished calcium transient activity. Mg2+ did not block caffeine-sensitive calcium release (RyR-dependent) or voltage dependent calcium channels. Mg2+ also suppressed thimerosal-induced calcium oscillations (IP3R-dependent). Small increases in the intracellular calcium concentration ([Ca2+](i)), increases the percentage of active cells and the calcium spiking frequency, while larger increases in [Ca2+](i) block the transients. Reducing intracellular IP3 levels reduces the percentage of active cells and the calcium spiking frequency. We conclude that the mechanism for generating spontaneous calcium transients in cultured neural crest cells fits the model for IP3R-dependent calcium excitability of the ER. Theme: A: Development and regeneration: Topics: Genesis of neurons and glia. Copyright (C) 2000 Elsevier Science B.V.

Original languageEnglish (US)
Pages (from-to)201-210
Number of pages10
JournalBrain Research
Volume862
Issue number1-2
DOIs
StatePublished - Apr 17 2000

Fingerprint

Inositol 1,4,5-Trisphosphate Receptors
Neural Crest
Calcium
Ryanodine Receptor Calcium Release Channel
Endoplasmic Reticulum
Thimerosal
Lanthanum
Ryanodine

Keywords

  • Excitability
  • Inositol 1,4,5-triphosphate
  • Intracellular calcium
  • Spontaneous calcium transients

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Calcium transient activity in cultured murine neural crest cells is regulated at the IP3 receptor. / Carey, Marc B.; Matsumoto, Steven.

In: Brain Research, Vol. 862, No. 1-2, 17.04.2000, p. 201-210.

Research output: Contribution to journalArticle

@article{d4e0c04ef76f4938b32c3d3b41422b72,
title = "Calcium transient activity in cultured murine neural crest cells is regulated at the IP3 receptor",
abstract = "In a previous study we have shown that cultured neural crest cells exhibit spontaneous calcium transients and that these events are required for neurogenesis. In this study, we examine the mechanism that generates these calcium transients. Extracellular Ca2+ modulates calcium transient activity. Lanthanum (La3+), a general calcium channel antagonist and zero extracellular Ca2+, reduces the percentage of cells exhibiting calcium transients (26.2 and 40.5{\%}, respectively) and decreases calcium spiking frequency (4.5 to 1.0 and 2.5 to 1.0 spikes/30 min, respectively). Intracellular calcium stores also contribute to the generation of calcium transients. Depleting the calcium stores of the endoplasmic reticulum (ER) reduces the percentage of active cells (15.7{\%}) and calcium spiking frequency (2.8 to 1.5 spikes/30 min). Ryanodine (100 μM), which blocks calcium release regulated by the ryanodine receptor (RyR), had no effect on calcium transient activity. Blocking inositol 1,4,5-triphosphate receptor (IP3R)-dependent calcium release, with elevated extracellular Mg2+ (20 mM), abolished calcium transient activity. Mg2+ did not block caffeine-sensitive calcium release (RyR-dependent) or voltage dependent calcium channels. Mg2+ also suppressed thimerosal-induced calcium oscillations (IP3R-dependent). Small increases in the intracellular calcium concentration ([Ca2+](i)), increases the percentage of active cells and the calcium spiking frequency, while larger increases in [Ca2+](i) block the transients. Reducing intracellular IP3 levels reduces the percentage of active cells and the calcium spiking frequency. We conclude that the mechanism for generating spontaneous calcium transients in cultured neural crest cells fits the model for IP3R-dependent calcium excitability of the ER. Theme: A: Development and regeneration: Topics: Genesis of neurons and glia. Copyright (C) 2000 Elsevier Science B.V.",
keywords = "Excitability, Inositol 1,4,5-triphosphate, Intracellular calcium, Spontaneous calcium transients",
author = "Carey, {Marc B.} and Steven Matsumoto",
year = "2000",
month = "4",
day = "17",
doi = "10.1016/S0006-8993(00)02128-4",
language = "English (US)",
volume = "862",
pages = "201--210",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",
number = "1-2",

}

TY - JOUR

T1 - Calcium transient activity in cultured murine neural crest cells is regulated at the IP3 receptor

AU - Carey, Marc B.

AU - Matsumoto, Steven

PY - 2000/4/17

Y1 - 2000/4/17

N2 - In a previous study we have shown that cultured neural crest cells exhibit spontaneous calcium transients and that these events are required for neurogenesis. In this study, we examine the mechanism that generates these calcium transients. Extracellular Ca2+ modulates calcium transient activity. Lanthanum (La3+), a general calcium channel antagonist and zero extracellular Ca2+, reduces the percentage of cells exhibiting calcium transients (26.2 and 40.5%, respectively) and decreases calcium spiking frequency (4.5 to 1.0 and 2.5 to 1.0 spikes/30 min, respectively). Intracellular calcium stores also contribute to the generation of calcium transients. Depleting the calcium stores of the endoplasmic reticulum (ER) reduces the percentage of active cells (15.7%) and calcium spiking frequency (2.8 to 1.5 spikes/30 min). Ryanodine (100 μM), which blocks calcium release regulated by the ryanodine receptor (RyR), had no effect on calcium transient activity. Blocking inositol 1,4,5-triphosphate receptor (IP3R)-dependent calcium release, with elevated extracellular Mg2+ (20 mM), abolished calcium transient activity. Mg2+ did not block caffeine-sensitive calcium release (RyR-dependent) or voltage dependent calcium channels. Mg2+ also suppressed thimerosal-induced calcium oscillations (IP3R-dependent). Small increases in the intracellular calcium concentration ([Ca2+](i)), increases the percentage of active cells and the calcium spiking frequency, while larger increases in [Ca2+](i) block the transients. Reducing intracellular IP3 levels reduces the percentage of active cells and the calcium spiking frequency. We conclude that the mechanism for generating spontaneous calcium transients in cultured neural crest cells fits the model for IP3R-dependent calcium excitability of the ER. Theme: A: Development and regeneration: Topics: Genesis of neurons and glia. Copyright (C) 2000 Elsevier Science B.V.

AB - In a previous study we have shown that cultured neural crest cells exhibit spontaneous calcium transients and that these events are required for neurogenesis. In this study, we examine the mechanism that generates these calcium transients. Extracellular Ca2+ modulates calcium transient activity. Lanthanum (La3+), a general calcium channel antagonist and zero extracellular Ca2+, reduces the percentage of cells exhibiting calcium transients (26.2 and 40.5%, respectively) and decreases calcium spiking frequency (4.5 to 1.0 and 2.5 to 1.0 spikes/30 min, respectively). Intracellular calcium stores also contribute to the generation of calcium transients. Depleting the calcium stores of the endoplasmic reticulum (ER) reduces the percentage of active cells (15.7%) and calcium spiking frequency (2.8 to 1.5 spikes/30 min). Ryanodine (100 μM), which blocks calcium release regulated by the ryanodine receptor (RyR), had no effect on calcium transient activity. Blocking inositol 1,4,5-triphosphate receptor (IP3R)-dependent calcium release, with elevated extracellular Mg2+ (20 mM), abolished calcium transient activity. Mg2+ did not block caffeine-sensitive calcium release (RyR-dependent) or voltage dependent calcium channels. Mg2+ also suppressed thimerosal-induced calcium oscillations (IP3R-dependent). Small increases in the intracellular calcium concentration ([Ca2+](i)), increases the percentage of active cells and the calcium spiking frequency, while larger increases in [Ca2+](i) block the transients. Reducing intracellular IP3 levels reduces the percentage of active cells and the calcium spiking frequency. We conclude that the mechanism for generating spontaneous calcium transients in cultured neural crest cells fits the model for IP3R-dependent calcium excitability of the ER. Theme: A: Development and regeneration: Topics: Genesis of neurons and glia. Copyright (C) 2000 Elsevier Science B.V.

KW - Excitability

KW - Inositol 1,4,5-triphosphate

KW - Intracellular calcium

KW - Spontaneous calcium transients

UR - http://www.scopus.com/inward/record.url?scp=0034678805&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034678805&partnerID=8YFLogxK

U2 - 10.1016/S0006-8993(00)02128-4

DO - 10.1016/S0006-8993(00)02128-4

M3 - Article

C2 - 10799686

AN - SCOPUS:0034678805

VL - 862

SP - 201

EP - 210

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 1-2

ER -