Cerebrospinal fluid-contacting neurons (CSF-cNs) are spinal sensory cells that detect chemical and mechanical stimuli via PKD2L1 channels located on a primary cilium, as established in aquatic vertebrates like zebrafish. The mechanosensory mechanism in mammals, however, has remained unclear due to the absence of definitive evidence for cilia on their apical processes (ApPrs). Here we show that mouse CSF-cN ApPrs lack cilia but instead possess drebrin-stabilized filopodia enriched with F-actin. Mechanical stimulation of these cilia-free ApPrs elicits robust, PKD2L1-dependent inward currents, that are sufficient to drive neuronal firing, confirming a novel, cilia-independent mechanosensory mechanism. Comparative analyses indicate an evolutionary divergence from ciliary mechanotransduction, with mice adopting a direct, actin-associated mechanism. These findings advance our understanding of the cellular basis of spinal mechanosensation in mammals and reveal a specialized adaptation for monitoring central canal dynamics, with implications for spinal sensory integration and evolution.