Understanding the intricate interplay between dendritic, cytoskeletal organization, and synaptic compartmentalization is crucial in deciphering neuronal function. While much is known about the role of actin filaments and microtubules in excitatory neurons, their organization in inhibitory GABAergic neurons remains relatively understudied. This research delves into the distinct cytoskeletal organization within aspiny GABAergic Parvalbumin-positive neurons, particularly focusing on their dendritic microtubule arrangement and its interaction with postsynaptic sites. Unlike excitatory neurons where actin patches typically localize to dendritic spines, Parvalbumin neurons exhibit a prominent mesh of cortical actin outlining the dendritic membrane. Moreover, postsynaptic densities of excitatory synapses in Parvalbumin neurons are directly located on the dendritic shaft, in close proximity to microtubules. Investigating these features under physiological conditions and in a mouse model of Autism spectrum disorder, we uncover insights into the intricate synaptic-cytoskeletal interactions. Notably, a global knockout of a synaptic protein implicated in Autism spectrum disorder results in an Autism-related phenotype, mirroring outcomes achieved by specific knockout in GABAergic or Parvalbumin-expressing neurons. This suggests that Autism dysfunction may predominantly stem from within interneuronal populations. Our findings illuminate the distinctive cytoskeletal organization in GABAergic neurons and propose a role for the ASD-associated mutation in altering synaptic-cytoskeletal interactions, potentially disrupting molecular trafficking pathways.