GABA-A receptor pharmacology evaluated in overexpressing HEK cells and primary astrocytes on QPatch




Kim Boddum1, Kadla Røskva Rosholm1, Linda Blomster2, Hervør Lykke Olsen, Naja Møller Sørensen1, Göran Mattsson1



The major inhibitory neurotransmitter of the central nervous system is γ-aminobutyric acid (GABA) and GABA is exerting its effect by binding to GABA receptors. The central role of GABA in the nervous system is underscored by the devastating consequences of pathophysiological changes in GABA signalling. Conversely, manipulation of GABA receptors can offer relief of a large group of neurological and psychiatric disorders. Pharmacological manipulation of GABAA has a large potential and ligands increasing the current will typically have anxiolytic, anticonvulsant, amnesic, sedative, hypnotic, euphoriant, and muscle relaxant effects1–4.
GABAA receptors are ligand-gated ion channels, permeable to Cl- ions, consisting of 5 membrane-spanning subunits5,6. 16 different subunits are identified in humans (α1-6, β1-3, γ1-3, δ, ε, θ, π) and the cellular GABA response is hence composed by a population of GABA receptors with significant different pharmacology7. Here we demonstrate pharmacological GABA receptor evaluation in both a stably-transfected cell line containing only α5β3γ2 receptors and a primary cell culture of rat hippocampal astrocytes with a diverse GABA receptor population.

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