Exp Neurobiol 2014; 23(2): 163-168
Published online June 30, 2014
© The Korean Society for Brain and Neural Sciences
Junsung Woo1,2, Suengmok Cho3 and C. Justin Lee1,2*
1Center for Neural Science and Functional Connectomics, Korea Institute of Science and Technology (KIST), Seoul 136-791, 2Neuroscience Program, University of Science and Technology (UST), Daejeon 305-350, 3Korea Food Research Institute, Seongnam 463-746, Korea
Correspondence to: *To whom correspondence should be addressed.
TEL: 82-2-958-6940, FAX: 82-2-958-7219
Isoliquiritigenin (ILTG) is a chalcone compound and shows various pharmacological properties, including antioxidant and anti-inflammatory activities. In recent study, we have reported a novel role of ILTG in sleep through a positive allosteric modulation of gamma-aminobutyric acid type A (GABAA)-benzodiazepine (BZD) receptors. However, the effect of ILTG in GABAAR-mediated synaptic response in brain has not been tested yet. Here we report that ILTG significantly prolonged the decay of spontaneous inhibitory postsynaptic currents (sIPSCs) mediated by GABAAR in mouse hippocampal CA1 pyramidal neurons without affecting amplitude and frequency of sIPSCs. This enhancement was fully inhibited by flumazenil (FLU), a specific GABAA-BZD receptor antagonist. These results suggest a potential role of ILTG as a modulator of GABAergic synaptic transmission.
Keywords: Isoliquiritigenin, GABAA-BZD receptor, sIPSC