Sodium coupled neutral amino acid transporter 10 (SNAT10), which is also known as solute carrier 38a10 (Slc38a10), is a class of transporter which has previously been identified to have a transceptor function, which means it can also cause signal-cascades in their cells. The SNAT10 protein has earlier been identified to transport different amino acids which take part in the glutamate/GABA-glutamine cycle (GGGC). The GGGC is interesting as it is known from previous studies that a disruption in the GGGC homeostasis can lead to cognitive dysfunctions and is believed to have a key role in the processes which contribute to neurodegenerative diseases. The aim of this study was to analyze a previously performed mouse study where SNAT10 deficient mice (SNAT10-/-) were put in a Barnes Maze (BM) to evaluate their spatial-memory function and afterwards evaluate their performance against the control group (SNAT10+/+). To test this hypothesis, the mice were put in the BM, where they were lowered onto a platform with circular holes distributed close to the edge, on which they must learn to navigate to an escape box that will shield them from the open and aversive environment. A histological analysis of the brain between the two genotypes with Nissl-staining were also performed, to analyze any differences in brain structure, specifically the hippocampus region. The result from BM showed a few differences in the parameters between the genotypes. It is possible that Slc38a10 protein is involved in mechanisms in the body which affects spatial memory function, but the result also showed that there must be a compensatory mechanism which is strong enough to compensate for the removal of Slc38a10s function. The result from the Nissl-staining showed no differences but the result is neither accurate nor reliable due to the population size and the different brain-sections used.