Swimming behaviour and post-swimming activity in Vitamin D receptor knockout mice

Animal experiments have shown that Vitamin D plays a role in both brain development and adult brain function. The adult Vitamin D receptor null mutant mouse (VDR -/-) is reported to be less active and more anxious than wild-type litter mate controls and to have poor swimming ability. However, an anxious behavioural phenotype is inferred from differences in locomotor behaviour. This is a general problem in behavioural phenotyping where a neurological phenotype is inferred from changes in locomotion which will be affected by non-neurological factors, such as muscle fatigue. In this study of VDR -/-, we conducted a detailed examination of one form of motor behaviour, swimming, compared to wildtype littermate controls. Swimming was assessed using a forced swim test, a laneway swimming test and a watermaze test using a visible platform. Post-swimming activity was assessed by comparing grooming and rearing behaviour before, and 5 min after, the forced swimming test. We replicated previous findings in which VDR -/- mice demonstrate more sinking episodes than wildtype controls in the forced swim test but they were similar to controls in the time taken to swim a 1 m laneway, and in the time taken to reach a visible platform in the watermaze. Thus, the VDR -/- mice were able to swim but were not able to float. Grooming and rearing behaviour of the VDR -/- mice was similar to wildtype controls before the forced swim but the VDR -/- were much less active after the swim compared with wildtype mice which displayed high levels of grooming and rearing. We conclude that VDR -/- mice have muscular and motor impairments that do not affect their ability to swim but significantly alters the ability to float as well as their post-swimming activity. Differences in muscle strength may confound tests of activity that are used to infer an anxious phenotype. (c) 2005 Elsevier Inc. All rights reserved.

Spatially localized distortions of event time

A fundamental question about the perception of time is whether the neural mechanisms underlying temporal judgements are universal and centralized in the brain or modality specific and distributed []. Time perception has traditionally been thought to be entirely dissociated from spatial vision. Here we show that the apparent duration of a dynamic stimulus can be manipulated in a local region of visual space by adapting to oscillatory motion or flicker. This implicates spatially localized temporal mechanisms in duration perception. We do not see concomitant changes in the time of onset or offset of the test patterns, demonstrating a direct local effect on duration perception rather than an indirect effect on the time course of neural processing. The effects of adaptation on duration perception can also be dissociated from motion or flicker perception per se. Although 20 Hz adaptation reduces both the apparent temporal frequency and duration of a 10 Hz test stimulus, 5 Hz adaptation increases apparent temporal frequency but has little effect on duration perception. We conclude that there is a peripheral, spatially localized, essentially visual component involved in sensing the duration of visual events.