Aquaporin 4 (AQP4) is a predominant water channel protein in mammalian brains, localized in the astrocyte plasma membrane. The regulation of AQP4 is believed to be important for the homeostasis of water in the brain, but the AQP4 regulatory mechanisms are not yet known. In this study, we investigate
Effect of steroids on γ-aminobutyrate-induced currents in cultured rat astrocytes
✍ Scribed by A. Chvátal; H. Kettenmann
- Publisher
- Springer
- Year
- 1991
- Tongue
- English
- Weight
- 417 KB
- Volume
- 419
- Category
- Article
- ISSN
- 0031-6768
No coin nor oath required. For personal study only.
✦ Synopsis
Cultured astrocytes from rat cortex respond to the inhibitory neurotransmitter y-aminobutyric acid (GABA) by the activation of C1-channels [Bormann J, Kettenmann H (1988) Proc Natl Acad Sci USA 85:9336-9340]. The glial response shares many pharmacological properties with those mediated by neuronal GABAA receptors, but differs in its sensitivity to inverse benzodiazepine agonists [Backus KH, Kettenmann H, Schachner M (1988) Glia 1:132-140]. To compare glial GABA receptors further with their neuronal counterparts, we analysed the effect of steroids, which have recently been shown to modulate neuronal GABAA-rece ptor-mediated responses, on GABA-induced currents in astrocytes. The agonist allotetrahydrodeoxycorticosterone (THDOC) at concentrations of 100 nM and 1 ~tM enhanced GABA-evoked (with 10 ~M GABA) currents up to 115~ and 162.4~ of controls respectively. The antagonist dehydroisoandrosterone 3-sulphate (DHEAS) at concentrations of 1 gM, 10 gM and 100 IxM depressed GABA-evoked (10txM) currents to 72070, 42.80/0 and 21.4% of controls respectively. The steroids were less effective at higher GABA concentrations. 100 gM DHEAS directly elicited a membrane current, while THDOC (1 gM) did not exert any direct response. This study demonstrates that steroids modulate GABA-evoked currents and thus may interfere with any of the functions of glial GABA receptors that are at present under discussion.
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