In the embryonic brain, post‐mitotic cortical neurons migrate from their place of origin to their final location. Various external factors such as hormones, neurotransmitters or peptides regulate their migration. To date, however, only a few studies have investigated the effects of these external factors on the electrical properties of the newly formed embryonic cortical neurons. The aim of the present study was to determine whether glutamate and brain‐derived neurotrophic factor (BDNF), known to regulate neuronal cell migration, could modulate currents through voltage‐gated calcium channels (I_Ca) in cortical neurons isolated from embryonic day 13 (E13) mouse foetuses. Whole cell recordings of I_Ca showed that E13 cortical cells kept 1 day in vitro expressed functional low‐ and high‐voltage activated (LVA and HVA) Ca²⁺ channels of T‐, L‐ and N‐types. A 1‐day glutamate treatment non‐specifically inhibited LVA and HVA I_Ca whereas BDNF down‐regulated HVA with N‐type I_Ca being more depressed than L‐type I_Ca. The glutamate‐induced I_Ca inhibition was mimicked by NMDA. BDNF exerted its action by recruiting trkB receptors and SKF‐96365‐sensitive channels. BAPTA prevented the glutamate‐ and the BDNF‐dependent inhibition of I_ca, indicating a Ca²⁺‐dependent mechanism of action. It is proposed that an influx of Ca²⁺ through NMDA receptors depresses the expression of LVA and HVA Ca²⁺ channels whereas a Ca²⁺ influx through SKF‐96365‐sensitive TRPC (transient receptor potential protein of C subtype) channels preferentially inhibits the expression of HVA Ca²⁺ channels. Glutamate and BDNF appear as potent modulators of the electrical properties of early post‐mitotic neurons. By down‐regulating I_Ca they could exert a neuroprotective action on embryonic cortical neurons.