Numerous studies suggest that endogenous GABA_A receptor (GABA_AR) activation is involved in neocortical development including migration. Those studies used GABA_AR blockers by assuming endogenous agonist is GABA. We performed in utero electroporation of mRFP gene to mice in which GABA synthesizing enzyme (GAD67) gene (Gad1) is replaced by GFP gene (GAD67^GFP/GFP, GAD67^GFP/+ and GAD67^+/+). Thus we could label (mRFP) cortical plate cells born on E14.5 under different ambient GABA levels. There were no differences in migration or GABA response of labeled cells among genotypes. However, continuous blockade of GABA_AR accelerated radial migration. This GABA_AR blockade in GAD67^GFP/GFP mice suggested an existence of alternative endogenous GABA_AR agonists. Thus, we tested a role for taurine, which is derived from maternal blood, but abundant in the fetal brain. Taurine-evoked currents in labeled cells were mediated by GABA_AR. Taurine uptake was blocked by the taurine transporter inhibitor GES, and release of taurine was blocked by the volume-sensitive anion channel blocker DCPIB, as studied with HPLC in acute neocortical slices. GES increased extracellular taurine concentration and induced an inward shift of I_hold, which was reversed by a GABA_AR antagonist. In embryonic taurine deficient model by maternal i.p. injection of optical isomer of taurine precursor (D-cysteinesulfinic acid), GABA_AR-mediated tonic currents decreased and radial migration was accelerated. As tonic currents were equivalent among genotypes of GAD67-GFP knock-in mice, taurine rather than GABA might be an endogenous agonist of embryonic tonic GABA_AR conductance. Thus, taurine may have agonistic effects on tonic GABA_AR, to work as a stop signal for radially migrating cortical plate cells.