Biology subjects

Giannoni-Guzman, M. A.

Publications and source records attributed to Giannoni-Guzman, M. A..

3 recordsLinked to original sources

bioRxiv2020

The Role of Temperature on the Development of Circadian Rhythms in Honey Bee Workers

Circadian rhythms in honey bees are involved in various processes that impact colony survival. For example, young nurses take care of the brood constantly throughout the day and lack circadian rhythms, while foragers use the circadian clock to remember and predict food availability in subsequent days. Previous studies suggested that development of circadian rhythms both in the field and the laboratory began around 7-9 days of age. However, not much is understood about the postembryonic development of circadian rhythms in honey bees. In the current study, we examine the effects of socially regulated colony temperature on the ontogeny of circadian rhythms of young workers under controlled laboratory conditions. We hypothesized that temperature plays a key role in the development of circadian rhythmicity in young workers. Our results show that young workers kept at 35{degrees}C develop circadian rhythmicity faster and in greater proportion than bees kept at 25{degrees}C. In addition, we examine if the effect of colony temperature during the first 48 hours after emergence is enough to observe effects on the rate and proportion of development of circadian rhythmicity. We observed that twice as many individuals that were exposed to 35{degrees}C during the first 48 hours develop circadian rhythms compared to individuals kept at 25{degrees}C. In addition, we observed differences in the average endogenous period length consistent with temperature compensation of the circadian rhythms between the 25{degrees}C and 35{degrees}C cohorts. We also observed differences in the degree of period length variation between the 25{degrees}C and 35{degrees}C cohorts, which combined with the proportion of arrhythmic individuals and survival data suggest that development of circadian rhythms is incomplete in individuals exposed to 25{degrees}C adult emergence. This study shows that temperature, which is socially regulated inside the hive, is a key factor that influences the ontogeny of circadian rhythmicity of workers.

animal behavior and cognition↗

bioRxiv2020

Circadian photoperiod alters TREK-1 channel function and expression in dorsal raphe serotonergic neurons

Seasonal daylength has been linked to the development and prevalence of mood disorders, however, the neural mechanisms underlying this relationship remain unknown. Previous work in our laboratory has shown that developmental exposure to seasonal photoperiods has enduring effects on the activity of mouse dorsal raphe serotonergic neurons, their intrinsic electrical properties, as well as on depression and anxiety-related behaviors. Here we focus on the possible ionic mechanisms that underlie the observed photoperiodic programming of the electrophysiological properties of serotonin neurons, focusing on the twin-pore K+ channels TREK-1 and TASK-1 that set resting membrane potential and regulate excitability. Using multielectrode array recordings in ex vivo dorsal raphe slices, we examined the effects of pharmacological inhibition of these channels on the spike rates of serotonin neurons of mice from different photoperiods. Pharmacological inhibition of TREK-1 significantly increased spike frequency in Short and Equinox photoperiod cohorts, but did not further elevate the firing rate in slices from Long photoperiod mice, suggesting that TREK-1 function is reduced in Long photoperiods. In contrast, inhibition of TASK-1 resulted in increases in firing rates across all photoperiods, suggesting that it contributes to setting excitability, but is not regulated by photoperiod. To examine if photoperiod impacts transcriptional regulation of TREK-1, we quantified Kcnk2 mRNA levels specifically in dorsal raphe 5-HT neurons using triple-label RNAscope. We found that Long photoperiod significantly reduced levels of Kcnk2 in serotonin neurons co-expressing Tph2, and Pet-1, Photoperiodic effects on the function and expression of TREK-1 were blocked in melatonin 1 receptor knockout (MT-1KO) mice, consistent with previous findings that MT-1 signaling is necessary for photoperiodic programming of dorsal raphe 5-HT neurons. Taken together these results indicate that photoperiodic regulation of TREK-1 expression and function plays a key role in photoperiodic programming the excitability of dorsal raphe 5-HT neurons.

neuroscience↗

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↗