Pkd2l1 deletion inhibits the neurogenesis of cerebrospinal fluid-contacting neurons and impedes spinal cord injury repair.

Adult neural stem cells (NSCs) offer a promising avenue for restoring spinal cord injury (SCI). However, their precise identity in the mammalian spinal cord remains unclear. Our previous research demonstrated that Pkd2l1-positive cerebrospinal fluid-contacting neurons (CSF-cNs) possess the NSC properties. Furthermore, understanding the role and molecular mechanisms of CSF-cNs as endogenous NSCs in spinal cord repair is crucial for developing effective treatments. This study utilizes a Pkd2l1(-/-) transgenic mouse model to investigate the role of CSF-cNs in SCI repair. We found that the CSF-cN population was almost absent in Pkd2l1(-/-) mice. Following SCI, these mice exhibited a significant reduction in the number of NSCs surrounding the central canal. Notably, Pkd2l1(-/-) mice showed impaired neuronal regeneration and compromised motor function recovery post-SCI. These findings highlight the potential importance of Pkd2l1 as a target for treating SCI by focusing on endogenous NSCs.