The interaction between the hippocampus and parahippocampal region is essential for the processing and storage of episodic memories. Spatial memory is a form of episodic memory, which entails the details of the what, when and where components of experienced events. The medial entorhinal cortex (MEC) is anatomically located as an interface between neocortex and hippocampus and it is considered to be a hub in the distributed network for spatial navigation. The area of interest for spatial memory is the medial entorhinal cortex(MEC), which is found to be essential for spatial navigation and memory. Stable spatial representations are essential in order to recall and discriminate between similar memories. Recently it has been proposed that a specialized form of condensed extracellular matrix molecules called perineuronal nets (PNNs) stabilize neural connections and restrict adult brain plasticity. In the adult neocortex, PNNs tightly enwrap the parvalbumin-positive (PV+) neurons, a major subclass of interneurons found in cortex including the MEC. This tightly encasing structure of PNNs restricts plasticity in adult animals, but can be dissolved by the enzyme chondroitinase ABC (chABC). The role PNNs have for acquiring and maintaining spatial memory have never been investigated. I investigated the effects of degradation of the PNNs in the MEC for acquisition, consolidation and plasticity of spatial memory. This was done by performing microinjections of chABC into the medial entorhinal cortex of rats, and testing their performance in a Morris watermaze. The results from this study suggest that degrading PNNs in MEC does not affect spatial learning in the watermaze task. During the acquisition phase, all groups performed well and showed a steep learning curve. By the end of the training week they had in general halved the amount of time to find the escape platform (escape latency). However, the chABC treated group needed one more day that the other groups to acquire an escape latency below 60 seconds. This behaviour was also seen during the second trial week, by the group treated with the enzyme between the two trial weeks. Treatment with chABC prior to a remote memory test did not appear to affect recall of spatial memory. The three groups did not show significant differences when remote memory was tested. Finally, I tested the rats ability to learn a new platform location when the salient cues in the room was changed. The daily probe trials revealed that the group treated with chABC prior to trial week two took quickly to the new platform location in the trials. Both the sham treated animals and the latter group showed erratic behaviour judged by the latency measure from the probe trials. The conclusion from my study is limited by the low number of animals in each group, and future studies will test whether the effects were caused by the enzymatic treatment, chance variations or other unknown influence.