Dendritic branching mechanisms are precisely controlled during brain development, as dendritic architecture provides the specificity and capacity of the synaptic input. Integrin receptors on the neuronal membrane are critical regulators of when and where the dendritic arborization will take place during neuronal differentiation. Integrin activity is not solely dictated by external ligand binding – the receptor's shape and function are also fine-tuned by intracellular binding proteins, including actin-binding protein Filamin A (FlnA). By combining in vitro mouse neuronal cultures with genetic and pharmacological manipulations, our study reveals that altering FlnA expression in hippocampal neurons can significantly enhance dendritic arborization, and this response is critically dependent on the extracellular matrix (ECM). Detailed analyses of FlnA knockdown and overexpression models revealed that the observed dendritic hypertrophy phenotypes are mediated by integrin activity and actin cytoskeleton modelling, respectively. Intriguingly, we also observed that silencing FlnA leads to aberrant Akt activity in neurons, potentially contributing to the observed dendritic morphology under the influence of integrin receptors. Supported by the German Research Foundation (STO488/4-1, STO488/8-1, CRC779 TPB05 and RTG2413 SynAGE).