McMahon, D. G. | bioRxiv Science

bioRxiv2020

Neonicotinoids Disrupt Circadian Rhythms and Sleep in Honey Bees

Honey bees are critical pollinators in ecosystems and agriculture, but their numbers have significantly declined. Declines in pollinator populations are thought to be due to multiple factors including habitat loss, climate change, increased vulnerability to disease and parasites, and pesticide use. Neonicotinoid pesticides are agonists of insect nicotinic cholinergic receptors, and sub-lethal exposures are linked to reduced honey bee hive survival. Honey bees are highly dependent on circadian clocks to regulate critical behaviors, such as foraging orientation and navigation, time-memory for food sources, sleep, and learning/ memory processes. Because circadian clock neurons in insects receive light input through cholinergic signaling we tested for effects of neonicotinoids on honey bee circadian rhythms and sleep. Neonicotinoid ingestion by feeding over several days results in neonicotinoid accumulation in the bee brain, disrupts circadian rhythmicity in many individual bees, shifts the timing of behavioral circadian rhythms in bees that remain rhythmic, and impairs sleep. Neonicotinoids and light input act synergistically to disrupt bee circadian behavior, and neonicotinoids directly stimulate wake-promoting clock neurons in the fruit fly brain. Neonicotinoids disrupt honey bee circadian rhythms and sleep, likely by aberrant stimulation of clock neurons, to potentially impair honey bee navigation, time-memory, and social communication.

animal behavior and cognition↗

bioRxiv2020

Distinct components of photoperiodic light are differentially encoded by the mammalian circadian clock

Seasonal light cycles influence multiple physiological functions and are mediated through photoperiodic encoding by the circadian system. Despite our knowledge of the strong connection between seasonal light input and downstream circadian changes, less is known about the specific components of seasonal light cycles that are encoded and induce persistent changes in the circadian system. Using combinations of three T cycles (23, 24, 26 hr.) and two photoperiods per T cycle (Long and Short, with duty cycles scaled to each T cycle), we investigate after-effects of entrainment to these six light cycles. We measure locomotor behavior duration (), period ({tau}), and entrained phase angle ({Psi}) in vivo, and SCN phase distribution ({sigma}{phi}), {tau}, and {Psi} ex vivo in order to refine our understanding of critical light components for influencing particular circadian properties. We find that photoperiod and T cycle length both drive determination of in vivo {Psi} but differentially influence after-effects in and {tau}, with photoperiod driving changes in and photoperiod length and T cycle length combining to influence {tau}. Using skeleton photoperiods, we demonstrate that in vivo {Psi} is determined by both parametric and non-parametric components, while changes in are driven non-parametrically. Within the ex vivo SCN, we find that {Psi} and {sigma}{phi} of the PER2::LUCIFERASE rhythm follow closely with their likely behavioral counterparts ({Psi} and of the locomotor activity rhythm), while also confirming previous reports of {tau} after-effects of gene expression rhythms showing negative correlations with behavioral {tau} after-effects in response to T cycles. We demonstrate that within-SCN {sigma}{phi} changes, thought to underly changes in vivo, are induced primarily non-parametrically. Taken together, our results demonstrate distinct components of seasonal light input differentially influence {Psi}, , and {tau}, and suggest the possibility of separate mechanisms driving the persistent changes in circadian behaviors mediated by seasonal light.

neuroscience↗