Although extracellular calcium ionic concentration ([Ca](o) ) is known to increase during late gestation and to drop after parturition, little is known about the influence of [Ca](o) on fetal brain function. We have investigated the influence of [Ca](o) , calcium-sensing receptors/nonselective cation currents (CaSR/NSCC), and GABAergic inhibitions on maturation of brainstem-spinal motor activities: the primary low-frequency embryonic rhythm [LF; silent since embryonic day (E)16] and the fetal respiratory rhythm (RR; emerging at E14-E15). Using in vitro isolated brainstem-spinal cord preparations of mice at different fetal and postnatal (P) stages (E16-P1), we demonstrate that reducing fetal [Ca](o) from 1.2 mM to 0.7 mM at E16-E18 or blocking GABA(A) receptors at E16-P0 reactivates LF and reveals LF-related disturbance of RR at E16-E18. This LF is stopped by adding gadolinium or spermidine (CaSR/NSCC agonists) at E18-P0 or GABA(A) receptor agonists at E16-E18. In contrast, [Ca](o) -induced slowing of RR at E16-E18 is not reproduced by gadolinium and spermidine. We conclude that perinatal CaSR/NSCC and GABA(A) inhibition allow quiescence of the LF, thereby improving functional maturation of the RR.
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