Synaptically activated Ca2+ release from internal stores in CNS neurons

William N. Ross, Takeshi Nakamura, Shigeo Watanabe, Matthew Larkum, Nechama Lasser-Ross

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

1. Synaptically activated postsynaptic [Ca2+] i increases occur through three main pathways: Ca2+ entry through voltage-gated Ca2+ channels, Ca2+ entry through ligand-gated channels, and Ca2+ release from internal stores. The first two pathways have been studied intensively; release from stores has been the subject of more recent investigations. 2. Ca2+ release from stores in CNS neurons primarily occurs as a result of IP3 mobilized by activation of metabotropic glutamatergic and/or cholingergic receptors coupled to PLC. Ca2+ release is localized near spines in Purkinje cells and occurs as a wave in the primary apical dendrites of pyramidal cells in the hippocampus and cortex. The amplitude of the [Ca2+]i increase can reach several micromolar, significantly larger than the increase due to backpropagating spikes. 3. The large amplitude, long duration, and unique location of the [Ca2+]i increases due to Ca2+ release from stores suggests that these increases can affect specific downstream signaling mechanisms in neurons.

Original languageEnglish
Pages (from-to)283-295
Number of pages13
JournalCellular and Molecular Neurobiology
Volume25
Issue number2
DOIs
Publication statusPublished - 2005 Apr
Externally publishedYes

Fingerprint

Neurons
Ligand-Gated Ion Channels
Pyramidal Cells
Purkinje Cells
Programmable logic controllers
Dendrites
Hippocampus
Spine
Chemical activation
Electric potential

Keywords

  • Calcium
  • Dendrite
  • IP
  • Pyramidal neuron

ASJC Scopus subject areas

  • Neuroscience(all)
  • Clinical Biochemistry
  • Cell Biology
  • Genetics

Cite this

Ross, W. N., Nakamura, T., Watanabe, S., Larkum, M., & Lasser-Ross, N. (2005). Synaptically activated Ca2+ release from internal stores in CNS neurons. Cellular and Molecular Neurobiology, 25(2), 283-295. https://doi.org/10.1007/s10571-005-3060-0

Synaptically activated Ca2+ release from internal stores in CNS neurons. / Ross, William N.; Nakamura, Takeshi; Watanabe, Shigeo; Larkum, Matthew; Lasser-Ross, Nechama.

In: Cellular and Molecular Neurobiology, Vol. 25, No. 2, 04.2005, p. 283-295.

Research output: Contribution to journalArticle

Ross, WN, Nakamura, T, Watanabe, S, Larkum, M & Lasser-Ross, N 2005, 'Synaptically activated Ca2+ release from internal stores in CNS neurons', Cellular and Molecular Neurobiology, vol. 25, no. 2, pp. 283-295. https://doi.org/10.1007/s10571-005-3060-0
Ross, William N. ; Nakamura, Takeshi ; Watanabe, Shigeo ; Larkum, Matthew ; Lasser-Ross, Nechama. / Synaptically activated Ca2+ release from internal stores in CNS neurons. In: Cellular and Molecular Neurobiology. 2005 ; Vol. 25, No. 2. pp. 283-295.
@article{f3403cc332ba499fa86dde392e1119af,
title = "Synaptically activated Ca2+ release from internal stores in CNS neurons",
abstract = "1. Synaptically activated postsynaptic [Ca2+] i increases occur through three main pathways: Ca2+ entry through voltage-gated Ca2+ channels, Ca2+ entry through ligand-gated channels, and Ca2+ release from internal stores. The first two pathways have been studied intensively; release from stores has been the subject of more recent investigations. 2. Ca2+ release from stores in CNS neurons primarily occurs as a result of IP3 mobilized by activation of metabotropic glutamatergic and/or cholingergic receptors coupled to PLC. Ca2+ release is localized near spines in Purkinje cells and occurs as a wave in the primary apical dendrites of pyramidal cells in the hippocampus and cortex. The amplitude of the [Ca2+]i increase can reach several micromolar, significantly larger than the increase due to backpropagating spikes. 3. The large amplitude, long duration, and unique location of the [Ca2+]i increases due to Ca2+ release from stores suggests that these increases can affect specific downstream signaling mechanisms in neurons.",
keywords = "Calcium, Dendrite, IP, Pyramidal neuron",
author = "Ross, {William N.} and Takeshi Nakamura and Shigeo Watanabe and Matthew Larkum and Nechama Lasser-Ross",
year = "2005",
month = "4",
doi = "10.1007/s10571-005-3060-0",
language = "English",
volume = "25",
pages = "283--295",
journal = "Cellular and Molecular Neurobiology",
issn = "0272-4340",
publisher = "Springer New York",
number = "2",

}

TY - JOUR

T1 - Synaptically activated Ca2+ release from internal stores in CNS neurons

AU - Ross, William N.

AU - Nakamura, Takeshi

AU - Watanabe, Shigeo

AU - Larkum, Matthew

AU - Lasser-Ross, Nechama

PY - 2005/4

Y1 - 2005/4

N2 - 1. Synaptically activated postsynaptic [Ca2+] i increases occur through three main pathways: Ca2+ entry through voltage-gated Ca2+ channels, Ca2+ entry through ligand-gated channels, and Ca2+ release from internal stores. The first two pathways have been studied intensively; release from stores has been the subject of more recent investigations. 2. Ca2+ release from stores in CNS neurons primarily occurs as a result of IP3 mobilized by activation of metabotropic glutamatergic and/or cholingergic receptors coupled to PLC. Ca2+ release is localized near spines in Purkinje cells and occurs as a wave in the primary apical dendrites of pyramidal cells in the hippocampus and cortex. The amplitude of the [Ca2+]i increase can reach several micromolar, significantly larger than the increase due to backpropagating spikes. 3. The large amplitude, long duration, and unique location of the [Ca2+]i increases due to Ca2+ release from stores suggests that these increases can affect specific downstream signaling mechanisms in neurons.

AB - 1. Synaptically activated postsynaptic [Ca2+] i increases occur through three main pathways: Ca2+ entry through voltage-gated Ca2+ channels, Ca2+ entry through ligand-gated channels, and Ca2+ release from internal stores. The first two pathways have been studied intensively; release from stores has been the subject of more recent investigations. 2. Ca2+ release from stores in CNS neurons primarily occurs as a result of IP3 mobilized by activation of metabotropic glutamatergic and/or cholingergic receptors coupled to PLC. Ca2+ release is localized near spines in Purkinje cells and occurs as a wave in the primary apical dendrites of pyramidal cells in the hippocampus and cortex. The amplitude of the [Ca2+]i increase can reach several micromolar, significantly larger than the increase due to backpropagating spikes. 3. The large amplitude, long duration, and unique location of the [Ca2+]i increases due to Ca2+ release from stores suggests that these increases can affect specific downstream signaling mechanisms in neurons.

KW - Calcium

KW - Dendrite

KW - IP

KW - Pyramidal neuron

UR - http://www.scopus.com/inward/record.url?scp=20044366566&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=20044366566&partnerID=8YFLogxK

U2 - 10.1007/s10571-005-3060-0

DO - 10.1007/s10571-005-3060-0

M3 - Article

VL - 25

SP - 283

EP - 295

JO - Cellular and Molecular Neurobiology

JF - Cellular and Molecular Neurobiology

SN - 0272-4340

IS - 2

ER -