Role of astrocytes in depolarization-coupled release of glutamate in cerebellar cultures

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Role of astrocytes in depolarization-coupled release of glutamate in cerebellar cultures. / Bak, Lasse K; Waagepetersen, Helle S; Schousboe, Arne.

In: Neurochemical Research, Vol. 29, No. 1, 01.2004, p. 257-65.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Bak, LK, Waagepetersen, HS & Schousboe, A 2004, 'Role of astrocytes in depolarization-coupled release of glutamate in cerebellar cultures', Neurochemical Research, vol. 29, no. 1, pp. 257-65.

APA

Bak, L. K., Waagepetersen, H. S., & Schousboe, A. (2004). Role of astrocytes in depolarization-coupled release of glutamate in cerebellar cultures. Neurochemical Research, 29(1), 257-65.

Vancouver

Bak LK, Waagepetersen HS, Schousboe A. Role of astrocytes in depolarization-coupled release of glutamate in cerebellar cultures. Neurochemical Research. 2004 Jan;29(1):257-65.

Author

Bak, Lasse K ; Waagepetersen, Helle S ; Schousboe, Arne. / Role of astrocytes in depolarization-coupled release of glutamate in cerebellar cultures. In: Neurochemical Research. 2004 ; Vol. 29, No. 1. pp. 257-65.

Bibtex

@article{4b1854e176b447feb3b8b25ed09da412,
title = "Role of astrocytes in depolarization-coupled release of glutamate in cerebellar cultures",
abstract = "Release of preloaded D-[3H]aspartate in response to depolarization induced by high potassium, N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) or the endogenous agonist glutamate was studied using cultured glutamatergic cerebellar granule neurons, cerebellar astrocytes, and corresponding cocultures. Release from the vesicular and the cytoplasmic glutamate pools, respectively, was distinguished employing the competitive, non-transportable glutamate transport inhibitor DL-threo-beta-benzyloxyaspartate (DL-TBOA). The results indicate that the release in response to AMPA (30 microM) in the presence of cyclothiazide (50 microM) to block desensitization, was of a vesicular origin. Pulses of 55 mM K+ caused a DL-TBOA resistant efflux of preloaded D-[3H]aspartate from astrocytes, indicating that this release was not mediated by glutamate transporters. The results furthermore support the notion of an important function of the astrocytes in the uptake of released glutamate, because DL-TBOA caused a large, apparent increase in the depolarization-coupled release of preloaded D-[3H]aspartate in the cocultures, compared to neuronal monocultures.",
keywords = "Animals, Aspartic Acid, Astrocytes, Cells, Cultured, Cerebellum, Glutamic Acid, Mice, Nocodazole, alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid",
author = "Bak, {Lasse K} and Waagepetersen, {Helle S} and Arne Schousboe",
year = "2004",
month = jan,
language = "English",
volume = "29",
pages = "257--65",
journal = "Neurochemical Research",
issn = "0364-3190",
publisher = "Springer",
number = "1",

}

RIS

TY - JOUR

T1 - Role of astrocytes in depolarization-coupled release of glutamate in cerebellar cultures

AU - Bak, Lasse K

AU - Waagepetersen, Helle S

AU - Schousboe, Arne

PY - 2004/1

Y1 - 2004/1

N2 - Release of preloaded D-[3H]aspartate in response to depolarization induced by high potassium, N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) or the endogenous agonist glutamate was studied using cultured glutamatergic cerebellar granule neurons, cerebellar astrocytes, and corresponding cocultures. Release from the vesicular and the cytoplasmic glutamate pools, respectively, was distinguished employing the competitive, non-transportable glutamate transport inhibitor DL-threo-beta-benzyloxyaspartate (DL-TBOA). The results indicate that the release in response to AMPA (30 microM) in the presence of cyclothiazide (50 microM) to block desensitization, was of a vesicular origin. Pulses of 55 mM K+ caused a DL-TBOA resistant efflux of preloaded D-[3H]aspartate from astrocytes, indicating that this release was not mediated by glutamate transporters. The results furthermore support the notion of an important function of the astrocytes in the uptake of released glutamate, because DL-TBOA caused a large, apparent increase in the depolarization-coupled release of preloaded D-[3H]aspartate in the cocultures, compared to neuronal monocultures.

AB - Release of preloaded D-[3H]aspartate in response to depolarization induced by high potassium, N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) or the endogenous agonist glutamate was studied using cultured glutamatergic cerebellar granule neurons, cerebellar astrocytes, and corresponding cocultures. Release from the vesicular and the cytoplasmic glutamate pools, respectively, was distinguished employing the competitive, non-transportable glutamate transport inhibitor DL-threo-beta-benzyloxyaspartate (DL-TBOA). The results indicate that the release in response to AMPA (30 microM) in the presence of cyclothiazide (50 microM) to block desensitization, was of a vesicular origin. Pulses of 55 mM K+ caused a DL-TBOA resistant efflux of preloaded D-[3H]aspartate from astrocytes, indicating that this release was not mediated by glutamate transporters. The results furthermore support the notion of an important function of the astrocytes in the uptake of released glutamate, because DL-TBOA caused a large, apparent increase in the depolarization-coupled release of preloaded D-[3H]aspartate in the cocultures, compared to neuronal monocultures.

KW - Animals

KW - Aspartic Acid

KW - Astrocytes

KW - Cells, Cultured

KW - Cerebellum

KW - Glutamic Acid

KW - Mice

KW - Nocodazole

KW - alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid

M3 - Journal article

C2 - 14992285

VL - 29

SP - 257

EP - 265

JO - Neurochemical Research

JF - Neurochemical Research

SN - 0364-3190

IS - 1

ER -

ID: 152061244