GABAA receptor
Extracellular ligand-gated chloride channel
(Alternative nomenclature: ClGABA-A, iGABAR)
GABAA Receptor is a neurotransmitter-gated ion channel that mediates post-synaptic inhibition. The main neurotransmitter is γ-amino-butyric acid (GABA). It is a hetero-pentamer composed of 4-TM subunits. GABA binding to the receptor leads to an increase in the chloride conductance which causes hyperpolarization (inhibition of neuronal firing).
Localization:
CNS neurons and glial cells, peripheral nervous system.
Information links:
http://www.expasy.org/cgi-bin/niceprot.pl?Q16445
QPatch recordings for GABAA receptor currents:
Whole-cell GABAA receptor currents in response to increasing concentrations of GABA (0.4-50 μM for 8000 ms). Green cursors define interval in which peak currents are identified. Expression system HEK-293. 
Concentration-response relationship for GABA based on whole-cell currents shown above. IC50 = 9.4 μM.
Pharmacological profiling:
Antagonists: Bicuculline
Agonists: Chlordizepoxide
Modulators: steroids, barbiturates, benzodiazepines
(The list is not intended to be complete)
QPatch concentration response analysis:
Whole-cell GABAA receptor currents in the presence of increasing concentrations of the antagonist bicuculline (50 nM – 50 μM). The currents were elicited by applications of 10 μM GABA for 2000 ms. Expression system HEK-293.
Concentration-response relationship for bicuculline based on whole-cell currents shown above. IC50 = 1.2 μM.
Pathophysiology: epilepsy, Angleman or Prader-Willi
QPatch written material:
Application reports:
Targeting ligand-gated ion channels by QPatch 16 (339 kB)
PrecisIONTM GABA-A a1/b3/g2 HEK* from Millipore
Posters:
Assessing Functional Properties of Ligand-gated Ion Channels with Automated Whole-Cell Patch-Clamp Technology, The BiophysicalSociety Annual Meeting 2006 (920 kB)
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