Search bioRxiv⌕ Search

bioRxiv · 10.1101/2024.05.07.592876

Reorganisation of circadian activity and the pacemaker circuit under novel light regimes

Abstract

Many environmental features are cyclic, with predictable daily and yearly changes which vary across latitudes. Organisms cope with such change using internal timekeepers or circadian clocks which have evolved remarkable flexibility. This flexibility is evident in the waveforms of behavioural and underlying molecular rhythms. In todays world, many ecosystems experience artificial light at night, leading to unusual photoperiodic conditions. Additionally, occupational demands expose many humans to unconventional light cycles. Yet, practical means of manipulating activity waveforms for beneficial purposes are lacking. This requires an understanding of principles and factors governing waveform plasticity of activity rhythms. Even though waveform plasticity remains underexplored, few recent studies have used novel light regimes, inspired by shift work schedules, with alternating bright light and dim light (LDimLDim) to manipulate the activity waveform of nocturnal rodents. We undertook this study to understand what aspects of light regimes contribute to waveform flexibility and how the underlying neuronal circuitry regulates the behaviour by subjecting Drosophila melanogaster to novel light regimes. Using a range of LDimLDim regimes, we found that dim scotopic illumination of specific durations induces activity bifurcation in fruit flies, similar to mammals. Thus, we suggest evolutionarily conserved effects of features of the light regime on waveform plasticity. Further, we demonstrate that the circadian photoreceptor CRYPTOCHROME is necessary for activity bifurcation. We also find evidence for circadian reorganisation of the pacemaker circuit wherein the evening neurons regulate the timing of both bouts of activity under novel light regimes. Thus, such light regimes can be explored further to understand the dynamics and coupling within the circadian circuit. The conserved effects of specific features of the light regime open up the possibility of designing other regimes to test their physiological impact and leverage them for waveform manipulation to minimise the ill effects of unusual light regimes. Author SummaryIt is thought that the appropriate timing of physiological and behavioural rhythms of organisms with respect to the environmental cycle confers an adaptive advantage. Endogenous timekeepers or circadian clocks regulate such rhythms. To optimally time biological rhythms, its waveform must be plastic and respond to changes in external cycles. Changes in external cycles may be natural, as seen across latitudes or seasons, or anthropogenic, such as artificial light induced changes in photoperiod or shiftwork driven novel light/dark cycles. Previous studies using a nocturnal rodent model showed that novel light regimes (LDimLDim) caused locomotor activity to bifurcate such that mice showed two bouts of activity restricted to the dimly lit phases. Here, we first demonstrate that conserved features of the light regime - dim scotopic illumination of specific light durations induce activity bifurcation in the fly model. We leverage the genetic toolkit of the Drosophila model to also show evidence for the reorganisation of the circadian pacemaker neuronal network upon exposure to novel light regimes. Our findings indicate that conserved effects of specific features of the environmental regimes can be exploited to design light regimes that ease the waveform into synchronising with challenging conditions such as during shift work, jetlag, and photoperiodic changes.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Sharma, P., Sheeba, V.. 2024-05-08. Reorganisation of circadian activity and the pacemaker circuit under novel light regimes. https://doi.org/10.1101/2024.05.07.592876

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

The Unreasonable Effectiveness of Cell Types in Describing Neuronal Physiological Features

Single-cell RNA sequencing (scRNA-seq) captures detailed gene expression profiles at scale, while patch-clamp recordings measure intrinsic neuronal electrophysiological properties. Modeling the relations between these two modalities remains a challenge. Here, we compare how well electrophysiological features can be predicted by traditional transcriptomic cell type classification, representations derived from a foundational model (scGPT) pretrained on large-scale scRNA-seq datasets, ion channel-coding genes, and highly variable genes. Using paired transcriptomic and electrophysiological patch-sequencing data from 495 human neurons from neurosurgical tissue, we find that cluster-level cell type representations consistently outperform highly variable gene selection, ion channel gene selection, and context-enriched scGPT embeddings. Notably, performance varies across model architectures and initializations, and the best results are obtained by combining the outputs of separate cell type and scGPT-based models. Together, these findings suggest that traditional discrete cellular classification is highly effective in predicting physiological features. For maximum performance it can be complemented by pretrained transformer models.

neuroscience↗

A nonlinear inhibition pathway underlying cortical responses to tuned holographic optogenetic perturbations

Optogenetics enables causal manipulation of cortical activity. Perturbation responses can be counterintuitive due to network interactions, making theory essential for predicting them. Existing approaches often rely on linear approximations, which fail for many biologically relevant perturbations. Here we develop a nonlinear theory of responses to holographic perturbations in cell-type-specific recurrent networks with structured connectivity. We fit a nonlinear model to mouse V1 data, which shows cotuned-ensemble suppression: perturbing spatially clustered neurons with similar preferred orientations yields markedly stronger short-range suppression than perturbing untuned ensembles. We show that cotuned-ensemble suppression arises from a feature-tuned, nonlinear inhibition pathway implicating somatostatin-positive (SST) interneurons. The theory predicts that cotuned ensembles suppress parvalbumin-positive (PV) neurons but facilitate SST neurons, and links the degree of cotuned-ensemble suppression or facilitation to the variance of the SST response. This framework identifies mechanisms by which nonlinear inhibition sculpts cortical dynamics and establishes a predictive basis for targeted optogenetic interventions.

neuroscience↗

Proteomic signatures of APOE ε4 across human tissues and cell types in Alzheimers disease

The apolipoprotein E {varepsilon}4 (APOE {varepsilon}4) allele is the strongest genetic risk factor for late-onset Alzheimers disease (AD). However, the underlying molecular mechanisms remain unclear. This study included 1691 participants from the Religious Orders Study and Rush Memory and Aging Project (ROSMAP), 1226 participants from the Accelerating Medicines Partnership - Alzheimers Disease (AMP-AD) Diverse Cohorts Study, and 735 participants from the Alzheimers Disease Neuroimaging Initiative (ADNI). To characterise APOE {varepsilon}4 molecular effects, we analysed proteomic data from plasma, cerebrospinal fluid (CSF), and induced pluripotent stem cell (iPSC)-derived astrocytes and neurons, as well as transcriptomic and proteomic data from multiple brain regions. The association of APOE {varepsilon}4 with AD neuropathology was also examined. APOE {varepsilon}4 carriers shared a plasma proteomic signature enriched for immune processes, irrespective of AD diagnosis. A machine learning classifier trained on this signature discriminated APOE {varepsilon}4 carriers from non-carriers in an independent cohort using CSF proteomics. APOE {varepsilon}4 carriage was associated with higher Braak stages and Consortium to Establish a Registry for Alzheimers Disease (CERAD) score. However, only limited APOE {varepsilon}4-associated transcriptomic and proteomic changes were observed in bulk brain tissue, with poor cross-layer concordance. Proteomic analyses of iPSC-derived astrocytes and neurons further revealed cell-type-specific APOE {varepsilon}4-associated changes. APOE {varepsilon}4 is associated with a consistent proteomic signature across plasma and CSF. Its molecular effects in the brain differ across cell types, brain regions and molecular layers. These findings support the need for cell-type-resolved multi-omic studies to elucidate how APOE {varepsilon}4 confers AD risk.

neuroscience↗