Activity-dependent structural plasticity (ADSP) plays a significant role in the homeostatic regulation of neuronal connectivity and activity in developing neuronal networks. This process involves intricate activity-dependent interaction between neuronal growth and migration, which shapes synaptic connections and results in network architectures with varying levels of clustering and modularity, influenced by the initial conditions. While excitatory interactions are essential for early network formation, the timely maturation of inhibition is also considered essential for stable activity dynamics that support normal brain function. In fact, GABAergic signaling in the developing brain undergoes a switch from depolarizing to hyperpolarizing, introducing excitatory/inhibitory (E/I) interactions that could interact with ADSP during network formation. Yet, how E/I signaling interacts with ADSP in regulating connectivity and activity in developing networks remains poorly understood. The extent of inhibition depends on the proportion of inhibitory neurons (IN), synaptic interaction strength, and embedding of INs in the mesoscale organization of the network. To disentangle interactions among neuronal growth, migration, and inhibition, we utilize computational growth models that capture many aspects exhibited in cultured neuronal networks. In simulations, we investigated the impact of different IN fractions on network structure stabilization and spatial distribution of neurons. Additionally, we explored how varying the strength and maturation delay of inhibitory signaling affects the local spatial embedding of INs. Our simulations suggest that asymmetric interactions between E/I neurons crucially impact on the development of network architectures. The presence of inhibition prolonged the phase of neuronal growth and migration, delaying the developmental time-course until network stability was attained. Increasing inhibitory synaptic strength crucially influenced the spatial embedding of INs. This phenomenon was most pronounced in networks with rapidly migrating neurons, where excitatory neurons (ENs) formed well-defined clusters, while INs tended to be excluded. In contrast, delaying the maturation of inhibition led to a more random integration of INs into clusters. Our results indicate that the timing of inhibitory maturation may significantly influence the developmental embedding of INs into neuronal networks.