| Autor: |
Wanasuntronwong A; Department of Oral Biology, Faculty of Dentistry, Mahidol University, Bangkok 10400, Thailand., Wanakhachornkrai O; Department of Medical Sciences, Faculty of Science, Rangsit University, Pathum Thani 12000, Thailand., Phongphanphanee P; National Institute for Physiological Sciences, Okazaki 444-8585, Japan., Isa T; National Institute for Physiological Sciences, Okazaki 444-8585, Japan., Tantisira B; Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok 10330, Thailand., Tantisira MH; Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok 10330, Thailand.; Faculty of Pharmaceutical Sciences, Burapha University, Chonburi 20131, Thailand. |
| Abstrakt: |
GABAergic intercalated neurons of amygdala (ITCs) have recently been shown to be important in the suppression of fear-like behavior. Effects of ECa233 (a standardized extract of Centella asiatica ), previously demonstrated anxiolytic activity, were then investigated on ITCs. Cluster of GABAergic neurons expressing fluorescence of GFP was identified in GAD67-GFP knock-in mice. We found that neurons of medial paracapsular ITC were GABAergic neurons exhibiting certain intrinsic electrophysiological properties similar to those demonstrated by ITC neurons at the same location in C57BL/6J mice. Therefore, we conducted experiments in both C57BL/6J mice and GAD67-GFP knock-in mice. Excitatory postsynaptic currents (EPSCs) were evoked by stimulation of the external capsule during the whole cell patch-clamp recordings from ITC neurons in brain slices. ECa233 was found to increase the EPSC peak amplitude in the ITC neurons by about 120%. The EPSCs in ITC neurons were completely abolished by the application of an AMPA receptor antagonist. Morphological assessment of the ITC neurons with biocytin demonstrated that most axons of the recorded neurons innervated the central nucleus of the amygdala (CeA). Therefore, it is highly likely that anxiolytic activity of ECa233 was mediated by increasing activation, via AMPA receptors, of excitatory synaptic input to the GABAergic ITC leading to depression of CeA neurons. |
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