bioRxiv Science⌕ Search

Biology subjects

Ayres, A. I.

Publications and source records attributed to Ayres, A. I..

2 recordsLinked to original sources

Standard touchscreen test procedures shift circadian rhythms in mice: a modified protocol to minimize circadian confounds

Touchscreen based cognitive testing for rodents offers considerable experimental benefits, including a semi automated battery approach and the use of appetitive rather than aversive reinforcement. However, food reward and touchscreen illumination introduce potential confounds, as both food and light can shift, entrain, or disrupt circadian rhythms, which in turn can affect learning and memory. The potential for the test apparatus to impact endogenous circadian rhythms is particularly problematic when probing relationships between sleep, circadian disruption, and cognitive performance. After observing phase shifting of circadian rhythms in nocturnal mice tested using standard touchscreen test procedures, which include testing during the active period (early lights off), we evaluated the relative contributions of the illuminated screen and the appetitive food reward. Our results indicate that light emitted by the touchscreen chambers is responsible for the circadian phase shifting effects, with standard screen conditions inducing a ~3.5 h phase delay in daily activity rhythms when training is conducted early in the dark period for 7 consecutive days. We then modified lighting in the test environment and the home cage to identify parameters that would minimize circadian shifting without impairing visual discrimination or performance on a widely used cognitive test (Trial Unique Nonmatching to Location, TUNL). From the 10 conditions tested, we offer specific recommendations for modifying touchscreen test protocols to minimize circadian confounds, without impacting task acquisition or performance.

animal behavior and cognition↗

Gap junctions in the C. elegans nervous system regulate ageing and lifespan

The nervous system is a central regulator of longevity, but how neuronal communication interfaces with ageing pathways is not well understood. Gap junctions are key conduits that allow voltage and metabolic signal transmission across cellular networks, yet it has remained unexplored whether they play a role in regulating ageing and longevity. We show that the innexin genes encoding gap junction subunits in Caenorhabditis elegans have extensive and diverse impacts on lifespan. Loss of the neural innexin unc-9 increases longevity by a third and also strongly benefits healthspan. Unc-9 acts specifically in a glutamatergic circuit linked to mechanosensation. Absence of unc-9 depends on a functional touch-sensing machinery to regulate lifespan and alters the age-dependent decline of mechanosensory neurons. The life extension produced by removal of unc-9 requires reactive oxygen species. Our work reveals for the first time that gap junctions are important regulators of ageing and lifespan.

physiology↗