During the assessment of long-term spatial memory at 99 weeks of age, GnRHa-Rec rams were found to be 1.5-fold slower than Controls in traversing the spatial maze. Interestingly this difference relative to the Controls is of the same magnitude as those reported when animals were receiving GnRHa-treatment (Hough et al., 2016). The maintenance of this difference in spatial performance, following the discontinuation of peripubertal GnRHa-treatment, demonstrated that the effects of peripubertal GnRHa on long-term spatial memory were not reversed and persisted into adulthood, despite the restoration of normal GnRH and gonadal steroid signaling. This result indicates that long-term spatial memory is dependent on changes that occurred during a critical window of development that is sensitive to alterations in GnRH signaling. These changes might be related to neural plasticity and endocrine signaling as suggested by Nuruddin et al. (2013b). Spatial memory can be subdivided into long-term spatial reference memory, which categorizes spatial information according to cues that remain the same between spatial tasks (Olton and Papas, 1979) and working spatial memory, which categorizes information based on the sequence of spatial cues (Olton and Papas, 1979). As the performance of the Control and GnRHa-Rec rams were comparable at 99 weeks of age in the novel maze, which effectively tests spatial working memory, it can be concluded that the observed permanent effects of peripubertal GnRHa-treatment on long-term spatial memory is specific to spatial reference memory. It is also reasonable to argue that the increase in circulating testosterone, which should have accompanied gonadal development in the GnRHa-Rec group, must have been sufficient to eliminate any effects of the peripubertal GnRHa-treatment on spatial working memory.