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. Author manuscript; available in PMC: 2015 Apr 1.
Published in final edited form as: Biochem Soc Trans. 2014 Apr;42(2):461–467. doi: 10.1042/BST20140027

Figure 1. MG is an endogenous, partial agonist at neuronal GABAA receptors.

Figure 1

(A) The application of 100 μM MG to hippocampal neurons evokes Cl− currents through GABAA receptors that are ~ ⅓ the magnitude of those evoked by 100 μM GABA in the same cells. The EC50 of the currents evoked by MG was 9.5 ± 1 μM and the physiological concentration of MG in rodent brain was measured at 5 μM. MG has a similar efficacy when applied to cerebellar granule neurons. (B) MG evoked currents in hippocampal neurons are augmented by co-application of classical anxiolytics that act as positive allosteric modulators of GABAARs, such as the benzodiazapenes diazepam and midazolam and the imidazopyridine zolpidem. Scale bars represent 1 nA and 10 s. Adapted from Distler et al., (2012)[7].