Perineuronal nets (PNNs) are dense extracellular matrix around a subset of neurons, mostly parvalbumin neurons (PVNs), regulating plasticity. The sulfation pattern of chondroitin sulfate chains within PNNs is key to their functions. Chondroitin 4 sulfate (C4S) levels rise with brain maturation and then slowly toward late ageing. The shift toward increased C4S/C6S ratio observed at the end of critical period and ageing was proposed as the plasticity limiting factor and could potentially prevent aberrant plasticity. Knockout of chondroitin sulfotransferase 11 (Chst11), an enzyme for C4S sulfation, has shown to increase plasticity and enhance memory. Unlike plasticity enhancment strategy in adult nervous system where functional recovery was observed, hyperplasticity from development and throughout life may induce adverse consequence, such as schizophrenia (SZ). SZ is a debilitating disease, often manifesting with reduced behavioral flexibility and cognitive control, increased anxiety, and impaired social behavior. Here, we investigated whether the developmental deletion of Chst11 in PVNs leads to behavioural abnormalities as observed in SZ animal models. Chst11 knockout (KO) mice exhibited heightened freezing behavior in the zero maze, reduced prepulse inhibition, and learning deficits in the Carousel maze task. Interestingly, they showed unimpaired spatial memory in water maze and even superior memory in novel object recognition. Moreover, the Chst11 KO showed an impaired sociability but well-preserved social memory. The results suggests that C4S depletion in PVNs manifests plasticity-induced memory enhancement and perserverance. A link between aberrant PNN development in PVNs and SZ-like behaviour is on-going. This work was supported by GACR grant 23-05540S.