Developmental downregulation of low-voltage-activated Ca2+ channels in Cajal-Retzius cells of the mouse visual cortex.

Cajal-Retzius (CR) cells have been demonstrated to fulfil an important secretory function in the developing neocortex. On the other hand, the contribution of CR cell electrical activity during cortex development is still unclear. Using the whole-cell patch-clamp technique, we studied low-voltage-activated (LVA) Ca(2+) channels in CR cells in the layer I of the mouse visual cortex. CR cells were found to display a transient Ca(2+) current (I(T)) in response to a depolarization step from -100 mV to -40 mV. I(T) showed: (i) typical for LVA Ca(2+) channels voltage dependence of activation (half-activation at -55 mV) and inactivation (half-inactivation at -76 mV); (ii) fast activation and inactivation kinetics, with time constants of 1.4 and 28 ms, respectively, at -40 mV; (iii) fast recovery from steady-state inactivation (time constant: 290 ms); (iv) a complete block by 1 microm mibefradil; and (v) a partial block (to 55%) by 100 microm Ni(2+). The density of I(T) dramatically decreased between postnatal day (P) 1 and P9. Immunostaining demonstrated the presence and postnatal downregulation of the alpha(1G)-subunit of LVA Ca(2+) channels in CR cells. Experiments performed in the current-clamp mode revealed that mibefradil delayed an action potential generation in response to a suprathreshold depolarizing current at P1, but not at P8-9. We suggest that LVA Ca(2+) channels might influence CR cell excitability during the first postnatal week and thereby contribute to the shaping of synaptic connectivity in the neocortical layer I.