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TL;DR
Researchers used a genetic knockout model (Crtl1-KO mice) lacking the Crtl1 protein, which selectively disrupts the aggregation of chondroitin sulfate proteoglycans in PNNs.
Molecular Neurobiology · 10 authors, 4 centres
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Researchers used a genetic knockout model (Crtl1-KO mice) lacking the Crtl1 protein, which selectively disrupts the aggregation of chondroitin sulfate proteoglycans in PNNs.
Researchers used a genetic knockout model (Crtl1-KO mice) lacking the Crtl1 protein, which selectively disrupts the aggregation of chondroitin sulfate proteoglycans in PNNs. Following fear conditioning, Crtl1-KO mice exhibited accelerated fear extinction, with reduced freezing levels appearing as early as the third block of conditioned stimulus presentations, compared to wild-type mice. This accelerated extinction was confirmed using pupillometry. Critically, Crtl1-KO mice also showed significantly reduced spontaneous recovery and fear renewal of fear memories at 7 and 42 days post-extinction, indicating persistent erasure rather than temporary suppression. Immunohistochemical analysis revealed reduced neuronal activation (Zif268+ cells) in the basolateral amygdala, lateral amygdala, and central amygdala of Crtl1-KO mice after extinction, compared to wild-type mice. The findings suggest that the developmental condensation of CSPGs into PNNs is a key factor in determining whether fear memories become persistent.