Abstract
Depolarization of cultured astrocytes by KCl stimulated γ-aminobutyric acid (GABA) release in a dose-dependent manner. At 60 mM KCl, the stimulatory effect was calcium- and sodium- independent, and was not altered by the presence of β-alanine. The potassium-evoked GABA release was inhibited by furosemide and 4-acetamido-4'-isothiocyano-2,2'-stilbene disulfonic acid (SITS), blockers of the chloride transporter across the plasma membrane, as well by chloride ion replacement with glucuronate. Other depolarizing agents, such as veratridine and ouabain, decreased basal GABA release; ouabain also inhibited the stimulatory effect of 60 mM KCl. The high K+-induced GABA release may affect CNS excitability and may represent an important aspect of glial-neuronal interactions.
| Original language | English |
|---|---|
| Pages (from-to) | 169-175 |
| Number of pages | 7 |
| Journal | Acta Neurobiologiae Experimentalis |
| Volume | 58 |
| Issue number | 3 |
| State | Published - Oct 1 1998 |
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Keywords
- Calcium
- Chloride
- Cortical astrocytes
- Depolarizing agents
- GABA release
- Sodium
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Potassium-stimulated GABA release is a chloride-dependent but sodium- and calcium-independent process in cultured astrocytes. / Albrecht, Jan; Bender, Alex S.; Norenberg, Michael D.
In: Acta Neurobiologiae Experimentalis, Vol. 58, No. 3, 01.10.1998, p. 169-175.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Potassium-stimulated GABA release is a chloride-dependent but sodium- and calcium-independent process in cultured astrocytes
AU - Albrecht, Jan
AU - Bender, Alex S.
AU - Norenberg, Michael D
PY - 1998/10/1
Y1 - 1998/10/1
N2 - Depolarization of cultured astrocytes by KCl stimulated γ-aminobutyric acid (GABA) release in a dose-dependent manner. At 60 mM KCl, the stimulatory effect was calcium- and sodium- independent, and was not altered by the presence of β-alanine. The potassium-evoked GABA release was inhibited by furosemide and 4-acetamido-4'-isothiocyano-2,2'-stilbene disulfonic acid (SITS), blockers of the chloride transporter across the plasma membrane, as well by chloride ion replacement with glucuronate. Other depolarizing agents, such as veratridine and ouabain, decreased basal GABA release; ouabain also inhibited the stimulatory effect of 60 mM KCl. The high K+-induced GABA release may affect CNS excitability and may represent an important aspect of glial-neuronal interactions.
AB - Depolarization of cultured astrocytes by KCl stimulated γ-aminobutyric acid (GABA) release in a dose-dependent manner. At 60 mM KCl, the stimulatory effect was calcium- and sodium- independent, and was not altered by the presence of β-alanine. The potassium-evoked GABA release was inhibited by furosemide and 4-acetamido-4'-isothiocyano-2,2'-stilbene disulfonic acid (SITS), blockers of the chloride transporter across the plasma membrane, as well by chloride ion replacement with glucuronate. Other depolarizing agents, such as veratridine and ouabain, decreased basal GABA release; ouabain also inhibited the stimulatory effect of 60 mM KCl. The high K+-induced GABA release may affect CNS excitability and may represent an important aspect of glial-neuronal interactions.
KW - Calcium
KW - Chloride
KW - Cortical astrocytes
KW - Depolarizing agents
KW - GABA release
KW - Sodium
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UR - http://www.scopus.com/inward/citedby.url?scp=0031714754&partnerID=8YFLogxK
M3 - Article
C2 - 9803010
AN - SCOPUS:0031714754
VL - 58
SP - 169
EP - 175
JO - Acta Neurobiologiae Experimentalis
JF - Acta Neurobiologiae Experimentalis
SN - 0065-1400
IS - 3
ER -