Contextual fear conditioning is enhanced in mice lacking functional sphingosine kinase 2.

In this study we investigated the consequences of global SphK2 knockout (SphK2(-/-)) on basic motor capabilities, anxiety, learning, and memory in mice, using a range of tests including the elevated plus maze, the cheeseboard, contextual and cued fear conditioning, and fear extinction. Loss of SphK2 resulted in an 85-90% reduction in brain S1P levels, and was associated with a notably higher freezing response in a novel context. SphK2 knockout mice also exhibited increased contextual fear conditioning but the extinction of contextual fear memory was similar to control mice. SphK2(-/-) mice, contrary to their control littermates, did not respond to cue presentation with increased freezing. Anxiety measures in the elevated plus maze were not different between SphK2(-/-) mice and control littermates. Also, knockout mice showed no deficits in neurological reflexes or motor functions, and performed as well as their control littermates in the spatial memory test. Our findings demonstrate that SphK2 is responsible for the vast majority of S1P synthesis in the brain, and plays a role in freezing responses as evaluated in the fear conditioning paradigm. PMID: 28625547 [PubMed - as supplied by publisher]
Source: Behavioural Brain Research - Category: Neurology Authors: Tags: Behav Brain Res Source Type: research