GABA triggers a Cl− efflux from cultured mouse oligodendrocytes

Hoppe, D.; Kettenmann, Helmut

doi:10.1016/0304-3940(89)90620-4

Cited by 57 publications

(31 citation statements)

References 8 publications

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“…It is possible that subtypes of GABAA receptors with different channel properties exist, since individual GABA receptor subunits can be differentially expressed (Shivers et al 1989;Zhang, Makoto & Tohyama, 1991) and the combination of subunits expressed in GABA receptors can control their channel properties (Verdoorn, Draguhn, Ymer, Seeburg & Sakmann, 1990 Kopito, 1990) driven by the production of CO2/HCO3-inside the cell; or by a Cl--cation transporter driven by the transmembrane gradient of Na+. Consistent with this idea, the Cl-transport inhibitor frusemide can reduce GABAevoked depolarizations in guinea-pig hippocampal neurons and in mouse oligodendrocytes (Misgeld et al 1986;Hoppe & Kettenmann, 1989 Physiol. 476.3 419 the picrotoxin-sensitive Cl--permeable channel.…”

Section: Mechanism Of Depolarizationmentioning

confidence: 74%

Mechanisms of GABA and glycine depolarization‐induced calcium transients in rat dorsal horn neurons.

Reichling

Kyrozis

Wang

et al. 1994

The Journal of Physiology

253

181

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1. The mechanisms and effects of GABA-and glycine-evoked depolarization were studied in cultured rat dorsal horn neurons using indo-1 recordings of [Ca2+]i and patch clamp recordings in conventional whole-cell or perforated-patch mode.2. Application of GABA to unclamped neurons caused [Ca2+]i increases that were dose dependent and exhibited GABAA receptor pharmacology. Calcium entered the neurons via high-threshold voltage-gated calcium channels (conotoxin and nimodipine sensitive). 3. In perforated-patch recordings employing cation-selective ionophores, GABAA receptor activation depolarized 123 of 132 cells to membrane potentials as depolarized as -33 mV (mean -50 mV in all 132 cells, + 12 mV above resting potential). The ionic basis of the depolarization was determined by extracellular ion substitution; increased anionic conductance could account fully for the results. 4. Glycine, acting at a strychnine-sensitive receptor, also caused Ca2+ entry into these neurons through voltage-gated Ca2" channels. Glycine and GABA both evoked [Ca2+]i responses in the same cells and the responses were highly correlated in amplitude. Glycine also depolarized all five cells tested with perforated recording. Each of the five cells was also depolarized by muscimol to a value similar to that obtained for glycine.5. Both the depolarization and the increases in [Ca21]i caused by GABA and glycine could potentially play a role in processes of development and differentiation and sensory transmission in the spinal cord dorsal horn.

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Section: Mechanism Of Depolarizationmentioning

confidence: 74%

Mechanisms of GABA and glycine depolarization‐induced calcium transients in rat dorsal horn neurons.

Reichling

Kyrozis

Wang

et al. 1994

The Journal of Physiology

253

181

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“…Activation of GABAA receptors, therefore, results in a profound efflux of C1-since the normal resting membrane potential of astrocytes is negative (rp = -80 mV in 5 mM [K+l,J (Burnard et al, 1990). In agreement, ionsensitive electrodes have revealed a C1-efflux from glial cells following GABA application (Hoppe and Kettenmann, 1989).…”

Section: Gaba Receptorsmentioning

confidence: 89%

Astrocytic GABA receptors

Fraser

Mudrick‐Donnon

MacVicar

1994

Glia

106

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GABA receptors are distributed widely throughout the central nervous system on a variety of cell types. It has become increasingly clear that astrocytes, both in cell culture and tissue slices, express abundant GABAA receptors. In astrocytes, GABA activates Cl(-)-specific channels that are modulated by barbiturates and benzodiazepines; however, the neuronal inverse agonist methyl-4-ethyl-6, 7-dimethoxy-beta-carboline-3-carboxylate enhances the current in a subpopulation of astrocytes. The properties of astrocytic GABAA receptors, therefore, are remarkably similar to their neuronal counterparts, with only a few pharmacological exceptions. In stellate glial cells of the pituitary pars intermedia, GABA released from neuronal terminals activates postsynaptic potentials directly. The physiological significance of astrocytic GABAA-receptor activation remains unknown, but it may be involved in extracellular ion homeostasis and pH regulation. At present, there is considerably less evidence for the presence of GABAB receptors on astrocytes. The data that have emerged, however, indicate a prominent role for second-messenger regulation by this receptor.

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“…Thus, adenosine, glutamate, GABA, and ATP can modulate the proliferation, differentiation, and migration of OPC as well as OLG survival and myelination (e.g., Gallo et al, 1996;Gudz et al, 2006;Ishibashi et al, 2006;Domercq et al, 2010;Etxeberria et al, 2010;Wake et al, 2011;Zonouzi et al, 2015). In particular, both OPCs and mature OLGs express the two main subtypes of GABA receptors: GABA A (Hoppe and Kettenmann 1989;Von Blankenfeld et al, 1991;Berger et al, 1992;Cahoy et al, 2008) and GABA B (Luyt et al, 2007). Sensitivity to GABA in mature OLGs is greatly reduced (Berger et al, 1992), which suggests a specific role for GABA signaling in the development of the oligodendroglial lineage and during the initial stages of myelination and/or axon recognition (Vélez-Fort et al, 2012;Zonouzi et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Axon-to-Glia Interaction Regulates GABA_AReceptor Expression in Oligodendrocytes

Arellano¹,

Sánchez‐Gómez²,

Alberdi³

et al. 2015

Mol Pharmacol

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Myelination requires oligodendrocyte-neuron communication, and both neurotransmitters and contact interactions are essential for this process. Oligodendrocytes are endowed with neurotransmitter receptors whose expression levels and properties may change during myelination. However, only scant information is available about the extent and timing of these changes or how they are regulated by oligodendrocyte-neuron interactions. Here, we used electrophysiology to study the expression of ionotropic GABA, glutamate, and ATP receptors in oligodendrocytes derived from the optic nerve and forebrain cultured either alone or in the presence of dorsal root ganglion neurons. We observed that oligodendrocytes from both regions responded to these transmitters at 1 day in culture. After the first day in culture, however, GABA sensitivity diminished drastically to less than 10%, while that of glutamate and ATP remained constant. In contrast, the GABA response amplitude was sustained and remained stable in oligodendrocytes cocultured with dorsal root ganglion neurons. Immunochemistry and pharmacological properties of the responses indicated that they were mediated by distinctive GABA A receptors and that in coculture with neurons, the oligodendrocytes bearing the receptors were those in direct contact with axons. These results reveal that GABA A receptor regulation in oligodendrocytes is driven by axonal cues and that GABA signaling may play a role in myelination and/or during axonglia recognition.

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GABA triggers a Cl− efflux from cultured mouse oligodendrocytes

Cited by 57 publications

References 8 publications

Mechanisms of GABA and glycine depolarization‐induced calcium transients in rat dorsal horn neurons.

Mechanisms of GABA and glycine depolarization‐induced calcium transients in rat dorsal horn neurons.

Astrocytic GABA receptors

Axon-to-Glia Interaction Regulates GABA_AReceptor Expression in Oligodendrocytes

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GABA triggers a Cl− efflux from cultured mouse oligodendrocytes

Cited by 57 publications

References 8 publications

Mechanisms of GABA and glycine depolarization‐induced calcium transients in rat dorsal horn neurons.

Mechanisms of GABA and glycine depolarization‐induced calcium transients in rat dorsal horn neurons.

Astrocytic GABA receptors

Axon-to-Glia Interaction Regulates GABAAReceptor Expression in Oligodendrocytes

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Axon-to-Glia Interaction Regulates GABA_AReceptor Expression in Oligodendrocytes