Extracellular calcium induces quiescence of the low-frequency embryonic motor rhythm in the mouse isolated brainstem.

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.

Oestradiol rapidly enhances spontaneous glycinergic synaptic inhibition of hypoglossal motoneurones.

Whereas oestradiol is well-known to facilitate excitatory glutamatergic synaptic transmission, its effects on fast inhibitory neurotransmission are not as well established. Possible acute modulation of the spontaneous glycinergic synaptic activity by oestradiol was investigated in voltage-clamped hypoglossal motoneurones by whole-cell patch-clamp recording in rat brainstem slices. The spontaneous glycinergic synaptic activity was continuously recorded in each neurone under control conditions, during 12-20 min of perfusion with 17beta-oestradiol and during washing.