In the developing hippocampus, once generated, the pyramidal neurons migrate along radial glia processes to form the complex CA regions. Therefore, it is critical to understand the mechanisms controlling neuronal motility, leading to coordinated neuronal function. Doublecortin (DCX) shows mutations in human lissencephaly and heterotopia associated with epilepsy and intellectual disability. In the Dcx mouse mutant, the CA3 pyramidal region in the hippocampus forms an abnormal double layer, typical of heterotopia. Consequently, the mutant mouse presents an increased susceptibility to epilepsy. Since Dcx is a microtubule associated protein (MAP), the altered cytoskeletal dynamics are thought to constitute the primary cause of the neuronal heterotopia phenotype. But recent evidence shows that already at birth (P0), mitochondria in CA3 neurons are abnormal: is the neuronal phenotype at least in part due also to metabolism defects? Preliminary data suggest the importance of the metabolism regulation as a key element during neuronal migration and outgrowth: 1) Mitochondrial morphology is altered at P0 in Dcx mutant neurons. Preliminary electron microscopy data also show alterations in the interactions between mitochondria and the endoplasmic reticulum (mitochondria associated membranes, MAMs). 2) Super-resolution live imaging (SIM microscopy) analyzing mitochondria motility within mutant immature neurons shows a reduced speed. 3) Transcriptomic data comparing control and mutant neuronal layers reveal disrupted mitochondrial gene expression data. Different gene candidates are currently being tested contributing to these phenotypes. These data will help us understand how altered functional mitochondrial activity during development can impact the correct formation of neural circuits in the adult hippocampus.