The axon initial segment (AIS) is a site of action potential generation containing a large number of different ion channels clustering at high concentrations. Some of these channels, like voltage-gated potassium channels Kv7.2/7.3 (encoded by KCNQ2/3 genes), or voltage-gated sodium channel Nav1.2 (gene SCN2A) have been associated with benign forms of neonatal seizures, starting within the first days (KCNQ2/3) or first days to months of life (SCN2A) and remitting spontaneously after weeks to months. Whereas the observed loss-of-function caused by Kv7.2/7.3 epilepsy mutations or gain-of-function proposed for the Nav1.2 mutations can explain the hyperexcitability of the AIS and the generation of seizures, the mechanisms underlying their spontaneous remission remain unclear. We analyzed the expression of these channels at AIS in mouse brain by performing immunofluorescent stainings of frozen sections obtained at postnatal (P) days P1-P40. Nav and Kv7 channel subunits exhibited different expression patterns during development, and showed a distinctive localization within the initial segments, with Nav1.6 and Kv7.2 lying more distally compared to Nav1.2 and Kv7.3. We could further show that gephyrin, a protein important for postsynaptic clustering of GABA(A) receptors within inhibitory synapses, is upregulated at the AIS of pyramidal hippocampal neurons after P15, together with gamma2 and beta3 subunits of this receptor. These results suggest a clearly dynamic developmental reorganization taking place within the initial segment, indicating that the observed ion channel rearrangements in the AIS may account for the transient epileptic phenotypes.