Biology subjects

Giannoni-Guzman, M. A.

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

5 recordsLinked to original sources

bioRxiv2025

Gut microbiota as a modulator of circadian neural development in the honey bee model.

Disruption in gut microbiota during the early postnatal period can disrupt normal neural development and result in long-term behavioral alterations1. Similar to other neural systems, the circadian clock mechanism continues to mature after birth2, yet how microbial disturbances in the early period influence the onset of circadian rhythms and the development of central clock mechanisms remains poorly understood. Here we studied whether early-life gut dysbiosis affects the ontogeny of behavioral circadian rhythms and the maturation of clock neurons using the honey bee (Apis mellifera), a model organism that shares features of postnatal development of behavioral circadian rhythm and clock system3-5 with humans6. Our findings demonstrate that antibiotic-treated and gnotobiotic-reared bees display reduced rhythmicity compared to controls. These treatments also impair the development of the circadian pacemaker, marked by fewer Pigment-Dispersing Factor (PDF)-expressing neurons. Additionally, antibiotic exposure increased the expression of the Insulin-like Growth Factor Binding Protein Acid Labile Subunit (IGFALS) in early ages, which stabilizes the IGF-1/27, a hormone important for neurodevelopmental processes42. Together, these results identify gut microbiota as a modulator of circadian development. Our work provides an understanding of how early-life microbial disruptions influence the development of circadian rhythms, providing information that may extend to other animals, including humans.

neuroscience↗

bioRxiv2024

SCN gene expression plasticity in response to photoperiod

Seasonal daylength, or circadian photoperiod, is a pervasive environmental signal that profoundly influences physiology and behavior. In mammals, the central circadian clock resides in the suprachiasmatic nuclei (SCN) of the hypothalamus where it receives retinal input and synchronizes, or entrains, organismal physiology and behavior to the prevailing light cycle. The process of entrainment induces sustained plasticity in the SCN, but the molecular mechanisms underlying SCN plasticity are incompletely understood. Entrainment to different photoperiods persistently alters the timing, waveform, period, and light resetting properties of the SCN clock and its driven rhythms. To elucidate novel molecular mechanisms of photoperiod plasticity, we performed RNAseq on whole SCN dissected from mice raised in Long (LD 16:8) and Short (LD 8:16) photoperiods. Fewer rhythmic genes were detected in Long photoperiod and in general the timing of gene expression rhythms was advanced 4-6 hours. However, a few genes showed significant delays, including Gem. There were significant changes in the expression clock-associated gene Timeless and in SCN genes related to light responses, neuropeptides, GABA, ion channels, and serotonin. Particularly striking were differences in the expression of the neuropeptide signaling genes Prokr2 and Cck, as well as convergent regulation of the expression of three SCN light response genes, Dusp4, Rasd1, and Gem. Transcriptional modulation of Dusp4 and Rasd1, and phase regulation of Gem, are compelling candidate molecular mechanisms for plasticity in the SCN light response through their modulation of the critical NMDAR-MAPK/ERK-CREB/CRE light signaling pathway in SCN neurons. Modulation of Prokr2 and Cck may critically support SCN neural network reconfiguration during photoperiodic entrainment. Our findings identify the SCN light response and neuropeptide signaling gene sets as rich substrates for elucidating novel mechanisms of photoperiod plasticity.

neuroscience↗

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↗