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Rogers, N.

Publications and source records attributed to Rogers, N..

6 recordsLinked to original sources

Context-dependent effects of microglial MyD88 removal on voluntary ethanol consumption in mice

Neuroimmune signaling is increasingly implicated in alcohol use disorder (AUD). Microglia, the brains resident immune cells, signal in part through the adaptor protein myeloid differentiation primary response 88 (MyD88), a key mediator of innate immune responses. Here, we investigated whether microglial-specific MyD88 signaling regulates voluntary alcohol consumption in adulthood, as whole-body loss of MyD88 was previously shown to increase drinking. We further determined if alcohol altered parvalbumin-expressing interneurons (PVIs) and microglia within the pre-frontal cortex, based on our previously described role for MyD88 signaling on perineuronal net (PNN) deposition on PVIs in several brain regions, and the well characterized role of inhibitory signaling in alcohol use disorders. Loss of microglial-MyD88 had minimal effects on voluntary alcohol intake and anxiety-like behaviors. Alcohol exposure did not modify observed MyD88-dependent changes in PVIs/PNNs, despite altering microglial morphology in the male prefrontal cortex independent of genotype. The addition of an early life endotoxin challenge was sufficient to induce an increase in adult alcohol consumption in both MyD88-deficient and control males. However, injection of saline alone also induced an increase in adult drinking in MyD88-deficient males. These findings suggest that microglial-MyD88 signaling does not strongly regulate alcohol intake under baseline conditions in a one-bottle, voluntary binge-drinking paradigm, however there may be a role for microglial-MyD88 signaling in modulating the impact of developmental environmental contexts, such as stress, in later-life male drinking behavior. This work highlights the importance of developmental context, such as stress or inflammatory history, in understanding underlying microglia signaling mechanisms in conferring AUD risk.

neuroscience↗

Earlier leaf out and loss of cold tolerance for northeastern U.S. trees in response to winter warming events and early springs

O_LIWinter warming events and early springs can advance spring phenology of trees. However, these events can also decrease cold tolerance, leaving them vulnerable to subsequent refreezing. The goal of this study was to determine how spring phenology and cold tolerance of ten tree species in the northeastern U.S. responded to warming events of different timing and duration. C_LIO_LIWe exposed 300 tree seedlings of ten species to six different warming treatments. We assessed budburst, leaf out, vigor, and freezing damage on a weekly basis and measured the cold tolerance of species exposed to warming. C_LIO_LIThe timing of leaf out varied among species, and generally warming treatments advanced leaf out 5 - 41 days. Leaf out was best predicted by photoperiod for deciduous trees and thermal time for evergreen trees. Cold tolerance was reduced for most species (5 - 29 {degrees}C) when exposed to only two weeks of warming, reducing their safety margin from freezing damage. C_LIO_LIWinter warming events and early springs will drive species-specific and foliar habit responses in phenology and cold tolerance that are likely to shape competitive forest dynamics, especially at forest ecotones. C_LI

plant biology↗

Climate-linked biogeography of mycorrhizal fungal spore traits

Climate-driven variation in microbial traits is crucial for predicting ecological responses to environmental change, yet global patterns remain understudied. Using global datasets of arbuscular mycorrhizal (AM) fungal observations linked to spore morphology, we show that climate gradients shape spore trait variation and functional diversity. Temperature and precipitation emerged as key drivers, influencing species range size and trait-environment relationships through trade-offs. Larger spore volumes were more prevalent in warm, wet, stable climates but were associated with smaller species range sizes, suggesting a trade-off between persistence and dispersal potential. Spores with ornamentation were also more prevalent in warm, wet climates and linked to restricted range sizes, possibly reflecting specialization to specific environmental conditions. Cell wall investment decreased in warmer, wetter climates, and was the strongest predictor of species range size, with intermediate investment associated with broader geographic distributions. Spore shape and color also exhibited climate-driven patterns, with spherical spores and greater pigmentation more common in warm, wet climates. Phylogenetic analyses revealed high trait conservatism for spore ornamentation, moderate for volume, low for color, and none for shape and cell wall investment. Additionally, functional diversity analyses revealed that warm, wet environments promote within-community trait richness but lower trait divergence, while broader climatic variability drives higher beta diversity. These findings highlight the role of climate in shaping microbial trait biogeography and suggest that evolutionary history constrains some traits while others are adaptable, suggesting that ongoing climate change may restructure AM fungal distributions, impacting plant-fungal interactions, nutrient cycling, and ecosystem stability. Significance statementA trait-based approach in microbial ecology helps explain how the environment shapes microbial traits, yet global patterns remain largely unknown. This study provides the first global assessment of climate influence on arbuscular mycorrhizal (AM) fungal spore traits. We identify key trade-offs between trait persistence and species range size, demonstrating that temperature and precipitation are primary drivers of spore volume, ornamentation, cell wall investment, shape, and color. These findings highlight the role of broad climatic patterns in shaping microbial communities and suggest that ongoing environmental change may alter AM fungal distributions, potentially disrupting plant-fungal interactions, soil health, and ecosystem stability.

ecology↗

The clock transcription factor BMAL1 is a key regulator of extracellular matrix homeostasis and cell fate in the intervertebral disc

The circadian clock in mammals temporally coordinates physiological and behavioural processes to anticipate daily rhythmic changes in their environment. Chronic disruption to circadian rhythms (e.g., through ageing or shift work) is thought to contribute to a multitude of diseases, including degeneration of the musculoskeletal system. The intervertebral disc (IVD) in the spine contains circadian clocks which control [~]6% of the transcriptome in a rhythmic manner, including key genes involved in extracellular matrix (ECM) homeostasis. However, it remains largely unknown to what extent the local IVD molecular clock is required to drive rhythmic gene transcription and IVD physiology. In this work, we identified profound age-related changes of ECM microarchitecture and an endochondral ossification-like phenotype in the annulus fibrosus (AF) region of the IVD in the Col2a1-Bmal1 knockout mice. Circadian time series RNA-Seq of the whole IVD in Bmal1 knockout revealed loss of circadian patterns in gene expression, with an unexpected emergence of 12-hour ultradian rhythms, including FOXO transcription factors. Further RNA sequencing of the AF tissue identified region-specific changes in gene expression, evidencing a loss of AF phenotype markers and a dysregulation of ECM and FOXO pathways in Bmal1 knockout mice. Consistent with an up-regulation of FOXO1 mRNA and protein levels in Bmal1 knockout IVDs, inhibition of FOXO1 in AF cells suppressed their osteogenic differentiation. Collectively, these data highlight the importance of the local molecular clock mechanism in the maintenance of the cell fate and ECM homeostasis of the IVD. Further studies may identify potential new molecular targets for alleviating IVD degeneration.

physiology↗

Imaging through Windansee electrode arrays reveals a small fraction of local neurons following surface MUA

Prior studies have shown that neuronal spikes can be recorded with microelectrode arrays placed on the cortical surface. However, the etiology of these spikes remains unclear. Because the top cortical layer (layer 1) contains very few neuronal cell bodies, it has been proposed that these spikes originate from neurons with cell bodies in layer 2. To address this question, we combined two-photon calcium imaging with electrophysiological recordings from the cortical surface in awake mice using chronically implanted PEDOT:PSS electrode arrays on transparent parylene C substrate. Our electrode arrays (termed Windansee) were integrated with cortical windows offering see-through optical access while also providing measurements of local field potentials (LFP) and multiunit activity (MUA) from the cortical surface. To enable longitudinal data acquisition, we have developed a mechanical solution for installation, connectorization, and protection of Windansee devices aiming for an unhindered access for high numerical aperture microscope objectives and a lifetime of several months while worn by a mouse. Contrary to the common notion, our measurements revealed that only a small fraction of layer 2 neurons from the sampled pool (~13%) faithfully followed MUA recorded from the surface above the imaging field-of-view. Surprised by this result, we turned to computational modeling for an alternative explanation of the MUA signal. Using realistic modeling of neurons with back-propagating dendritic properties, we computed the extracellular action potential at the cortical surface due to firing of local cortical neurons and compared the result to that due to axonal inputs to layer 1. Assuming the literature values for the cell/axon density and firing rates, our modeling results show that surface MUA due to axonal inputs is over an order of magnitude larger than that due to firing of layer 2 pyramidal neurons. Thus, a combination of surface MUA recordings with two-photon calcium imaging can provide complementary information about the input to a cortical column and the local circuit response. Cortical layer I plays an important role in integration of a broad range of cortico-cortical, thalamocortical and neuromodulatory inputs. Therefore, detecting their activity as MUA while combining electrode recording with two-photon imaging using optically transparent surface electrode arrays would facilitate studies of the input/output relationship in cortical circuits, inform computational circuit models, and improve the accuracy of the next generation brain-machine interfaces.

neuroscience↗

Microscale physiological events on the human cortical surface detected with PEDOT:PSS Electrodes

Despite ongoing advancements in our understanding of the local single-cellular and network-level activity of neuronal populations in the human brain, extraordinarily little is known about their intermediate microscale local circuit dynamics. Here, we utilized ultrahigh density microelectrode arrays and a rare opportunity to perform intracranial recordings across multiple cortical areas in human participants to discover three distinct classes of cortical activity that are not locked to ongoing natural brain rhythmic activity. The first included fast waveforms similar to extracellular single unit activity. The other two types were discrete events with slower waveform dynamics and were found preferentially in upper layers of the grey matter. They were also observed in rodents, non-human primates, and semi-chronic recordings in humans via laminar and Utah array microelectrodes. The rates of all three events were selectively modulated by auditory and electrical stimuli, pharmacological manipulation, and cold saline application and had small causal co-occurrences. These results suggest that with the proper combination of high resolution microelectrodes and analytic techniques it is possible to capture neuronal dynamics that lay between somatic action potentials and aggregate population activity and that understanding these intermediate microscale dynamics may reveal important details of the full circuit behavior in human cognition.

neuroscience↗