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Functional GABA[sub A] receptors on human glioma cells.

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Title: Functional GABA[sub A] receptors on human glioma cells.
Authors: Labrakakis, Charalampos, Patt, Stephan, Hartmann, Jana, Kettenmann, Helmut
Source: European Journal of Neuroscience. Jan1998, Vol. 10 Issue 1. 1 Chart, 10 Graphs.
Subjects: GABA receptors, Gliomas, Calcium channels
Abstract: Glioma cells in acute slices and in primary culture, and glioma-derived human cell lines were screened for the presence of functional GABA[sub A] receptors. Currents were measured in whole-cell voltage clamp in response to γ-aminobutyric acid (GABA). While cells from the most malignant glioma, the glioblastoma multiforme, did not respond to GABA, an inward current (under our experimental conditions with high Cl[sup -] concentration in the pipette) was induced in gliomas of lower grades, namely in 71% of oligodendroglioma cells and in 62% of the astrocytoma cells. Glioma cell lines did not express functional GABA[sub A] receptors, irrespective of the malignancy of the tumour they originate from. The currents elicited by application of GABA were due to activation of GABA[sub A] receptors; the specific agonist muscimol mimicked the response, the antagonists bicuculline and picrotoxin blocked the GABA-activated current and the benzodiazepine receptor agonist flunitrazepam augmented the GABA-induced current and the benzodiazepine inverse agonist DMCM decreased the GABA current. Cells were heterogeneous with respect to the direction of the current flow as tested in gramicidin perforated patches: in some cells GABA hyperpolarized the membrane, while in the majority it triggered a depolarization. Moreover, GABA triggered an increase in [Ca[sup 2+]][sub i] in the majority of the tumour cells due to the activation of Ca[sup 2+] channels. Our results suggest a link between the expression of GABA receptors and the growth of glioma cells as the disappearance of functional GABA[sub A] receptors parallels unlimited growth typical for malignant tumours and immortal cell lines. [ABSTRACT FROM AUTHOR]
Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: Functional GABA[sub A] receptors on human glioma cells.
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  Data: <searchLink fieldCode="AR" term="%22Labrakakis%2C+Charalampos%22">Labrakakis, Charalampos</searchLink><br /><searchLink fieldCode="AR" term="%22Patt%2C+Stephan%22">Patt, Stephan</searchLink><br /><searchLink fieldCode="AR" term="%22Hartmann%2C+Jana%22">Hartmann, Jana</searchLink><br /><searchLink fieldCode="AR" term="%22Kettenmann%2C+Helmut%22">Kettenmann, Helmut</searchLink>
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  Data: <searchLink fieldCode="JN" term="%22European+Journal+of+Neuroscience%22">European Journal of Neuroscience</searchLink>. Jan1998, Vol. 10 Issue 1. 1 Chart, 10 Graphs.
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  Data: <searchLink fieldCode="DE" term="%22GABA+receptors%22">GABA receptors</searchLink><br /><searchLink fieldCode="DE" term="%22Gliomas%22">Gliomas</searchLink><br /><searchLink fieldCode="DE" term="%22Calcium+channels%22">Calcium channels</searchLink>
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  Label: Abstract
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  Data: Glioma cells in acute slices and in primary culture, and glioma-derived human cell lines were screened for the presence of functional GABA[sub A] receptors. Currents were measured in whole-cell voltage clamp in response to γ-aminobutyric acid (GABA). While cells from the most malignant glioma, the glioblastoma multiforme, did not respond to GABA, an inward current (under our experimental conditions with high Cl[sup -] concentration in the pipette) was induced in gliomas of lower grades, namely in 71% of oligodendroglioma cells and in 62% of the astrocytoma cells. Glioma cell lines did not express functional GABA[sub A] receptors, irrespective of the malignancy of the tumour they originate from. The currents elicited by application of GABA were due to activation of GABA[sub A] receptors; the specific agonist muscimol mimicked the response, the antagonists bicuculline and picrotoxin blocked the GABA-activated current and the benzodiazepine receptor agonist flunitrazepam augmented the GABA-induced current and the benzodiazepine inverse agonist DMCM decreased the GABA current. Cells were heterogeneous with respect to the direction of the current flow as tested in gramicidin perforated patches: in some cells GABA hyperpolarized the membrane, while in the majority it triggered a depolarization. Moreover, GABA triggered an increase in [Ca[sup 2+]][sub i] in the majority of the tumour cells due to the activation of Ca[sup 2+] channels. Our results suggest a link between the expression of GABA receptors and the growth of glioma cells as the disappearance of functional GABA[sub A] receptors parallels unlimited growth typical for malignant tumours and immortal cell lines. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1046/j.1460-9568.1998.00036.x
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        Text: English
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        Type: general
      – SubjectFull: Gliomas
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      – SubjectFull: Calcium channels
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              Text: Jan1998
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