Biology subjects

Goodman, A. M.

Publications and source records attributed to Goodman, A. M..

6 recordsLinked to original sources

bioRxiv2026

Contrasting Range and Demographic Histories in two Palearctic Dragonfly Species (Odonata: Anisoptera)

Climatic suitability is often used to infer historical range changes, yet whether suitable area predicts effective population size remains unexplored. We investigated this relationship in two Palearctic dragonflies with contrasting ecologies: Somatochlora arctica, a widespread peatland specialist, and S. meridionalis, a southern European species associated with shaded streams. We combined demographic reconstructions from individual reference genomes using the pairwise sequentially Markovian coalescent (PSMC), maximum entropy (MaxEnt) species distribution models projected across six paleoclimatic intervals spanning approximately 3.3 million years, and ancestral state reconstructions of peatland specialization. Predicted suitable area was consistently greater for S. arctica, reaching its greatest extent during the Last Glacial Maximum. However, its inferred effective population size was smaller than that of S. meridionalis for most of the last ~275,000 years. Ancestral reconstructions placed the most probable gain of peatland specialization in the S. arctica lineage (Clade I) during the late Miocene, with a median age of 9.4 million years, predating the modeled climatic intervals. These findings indicate a decoupling of climatic suitability and demographic history. Patchy breeding habitat, population structure, and the isolated Scottish origin of the sampled S. arctica may contribute to this mismatch. Combining genomic, ecological, and phylogenetic approaches provides complementary insights into historical biogeography and highlights the limitations of interpreting suitable climate as available breeding habitat or using individual genomes to characterize species-wide demographic histories.

genomics↗

bioRxiv2026

Sex in the City: Reproductive Behaviors of Dragonflies across an Urban Landscape

Anthropogenic cityscapes provide complex habitats that influence animal communication and movement patterns, which are generally understudied in aquatic and semi-aquatic organisms. Community science, referring to public participation in scientific research, is an important tool for recording occurrence records and behavioral observations of understudied urban species. Boise, Idaho (USA), one of the fastest-growing cities in North America, has a long-established community science program for documenting occurrences of the semi-aquatic insect order Odonata (dragonflies and damselflies), making the city an ideal study system for comparing behavioral observations from community science with observations recorded using AI driven iNaturalist. In this study, we test the accuracy of iNaturalist observations and volunteer surveys to characterize dragonfly reproductive behaviors (tandem flight and tandem perching, oviposition, and mating) in the city, and use these observations to determine which dragonflies are using the urban landscape as reproductive habitat. The total numbers of species observations by volunteers and on iNaturalist in Boise were strongly correlated, while reproductive observations showed a strong observational threshold, as reproductive behaviors were rarely identified in less-observed species. iNaturalist tended to underrepresent total occurrences of ''flyer'' species, which rarely perch, while volunteer surveys underrepresented occurrences and reproductive behaviors of a more cyclical species that did not appear to be abundant in the field season in which this study was conducted. Our findings suggest that Boise provides suitable breeding habitat for both migratory and resident dragonflies. Species distribution models of three migratory and three putatively migratory species further demonstrate that these species would be expected in southwestern Idaho regardless of the presence of a city, and have persisted through urban development. This research demonstrates the value of community science in conducting basic research on understudied urban-dwelling species, although findings must be considered alongside potential biases.

ecology↗

bioRxiv2025

Reducing ventral hippocampal CA1/subiculum hyperexcitability restores social memory and alleviates anxiety-related behavior in a mouse model of temporal lobe epilepsy

BackgroundInterictal cognitive and affective comorbidities in temporal lobe epilepsy (TLE) often remain refractory to seizure-directed therapies. We tested the causal role of ventral hippocampal CA1/subiculum (vCA1/Sub) hyperexcitability in social memory failure and anxiety-related behavior, and whether normalizing principal-cell excitability restores function. MethodsIn pilocarpine-treated mice we combined blinded behavioral assays (social approach/discrimination, open field, olfaction), whole-cell recordings from mCherry-labeled vCA1/Sub principal neurons, alveus stimulation to assay synaptic inhibition/excitation, immunohistochemistry for parvalbumin (PV) and somatostatin (SST) interneurons, and chemogenetic control of excitability (hM3Dq in controls; hM4Di and KORD in epileptic mice). Missing behavioral outcomes were handled by multiple imputation with bootstrapping; pooled analyses used ANOVA, mixed-effects models, and logistic regression. ResultsEpileptic mice showed preserved social approach but impaired social discrimination, with intact detection of social odors. Regular-spiking and bursting vCA1/Sub neurons exhibited depolarized resting membrane potential and reduced synaptically driven hyperpolarizations during alveus stimulation, indicating disinhibition; PV and SST interneuron densities were reduced in stratum oriens. Chemogenetic manipulation bidirectionally tuned excitability: bath CNO depolarized hM3Dq-expressing cells, whereas it hyperpolarized hM4Di-expressing cells by [~]5 mV and decreased current-evoked spiking. In vivo, inhibiting vCA1/Sub principal cells (hM4Di or KORD activation) increased the probability of successful social discrimination in epileptic mice without altering investigation time; neither CNO nor salvinorin B affected unDREADDed animals. In the open field, epileptic mice displayed reduced center preference and high-velocity bouts; vCA1/Sub inhibition normalized center preference and movement toward control values. Center preference predicted social discrimination in DREADDed epileptic mice, linking anxiety-related behavior to vCA1/Sub excitability. ConclusionsvCA1/Sub hyperexcitability drives interictal social memory and anxiety-related deficits in chronic TLE. Reducing principal-cell excitability restores behavior despite interneuron loss, supporting a model in which ventral hippocampal output can be retuned to rescue cognition. These results nominate neuromodulation of vCA1/Sub as a strategy to improve quality of life in epilepsy.

neuroscience↗

bioRxiv2021

DENTATE GRANULE CELLS ARE HYPEREXCITABLE IN THE TGF344-AD RAT MODEL OF ALZHEIMER'S DISEASE

The dentate gyrus is both a critical gatekeeper for hippocampal signal processing and one of the first regions to dysfunction in Alzheimers disease (AD). Accordingly, the appropriate balance of excitation and inhibition through the dentate is a compelling target for mechanistic investigation and therapeutic intervention of early AD. Previously, we reported increased LTP magnitude at medial perforant path-dentate granule cell (MPP-DGC) synapses in slices from TgF344-AD rats compared to Wt as early as 6 months. We next determined that the enhanced LTP magnitude was due to heightened function of {beta}-ARs leading us to ask if dentate granule cells (DGCs) also have modified passive or active membrane properties which may also contribute to hyperexcitability or aberrant hippocampal processing. Although there was no detectable difference in spine density and presynaptic release probability, dentate granule cells (DGCs) themselves might have increased electrical response to synaptic input during LTP induction, which was measured as a significant increase in charge transfer during high-frequency stimulation. In this study, we found passive membrane properties and active membrane properties are altered, leading to increased TgF344-AD DGC excitability. Specifically, TgF344-AD DGCs have an increased input resistance and decreased rheobase, decreased sag, and increased action potential (AP) spike accommodation. Importantly, we find that the voltage response increased in DGCs from TgF344-AD compared to Wt accompanied by decreased delay to fire the first AP, indicating that for the same amount of depolarizing current injection TgF344-AD DGCs membranes are more excitable. Taken together, DGCs of TgF344-AD rats are more excitable, but due to heightened accommodation, may be unable to discharge at high frequency for longer durations of time, compared to their Wt littermates.

neuroscience↗

bioRxiv2020

Heightened β-adrenergic receptor function in the TgF344-AD rat model drives synaptic potentiation and supports learning and memory

The central noradrenergic (NA) system is critical for maintenance of attention, behavioral flexibility, spatial navigation, and learning and memory, those cognitive functions lost first in early Alzheimers disease (AD). In fact, the locus coeruleus (LC), the sole source of norepinephrine (NE) for >90% of the brain, is the first site of pathological tau accumulation in human AD with axon loss throughout forebrain, including hippocampus. The dentate gyrus (DG) is heavily innervated by LC-NA axons, where released norepinephrine (NE) acts on {beta}-adrenergic receptors (ARs) at excitatory synapses from entorhinal cortex (EC) to facilitate long-term synaptic plasticity and memory formation. These synapses dysfunction in early AD prior to cognitive impairment. In the TgF344-AD rat model, degeneration of LC-NA axons in hippocampus recapitulates human AD, providing a preclinical model to investigate synaptic and behavioral consequences. Using immunohistochemistry, Western blot analysis, and brain slice electrophysiology in 6-9 month old wild type and TgF344-AD rats, we discovered that loss of LC-NA axons co-insides with heightened {beta}-AR function at medial perforant path-dentate granule cell synapses (MPP-DCG) that is responsible for the increase in LTP magnitude at these synapses. Furthermore, novel object recognition is facilitated in TgF344-AD rats that requires {beta}-ARs, and pharmacological blockade of {beta}-ARs unmasks a deficit in extinction learning only in TgF344-AD rats, indicating a greater reliance on {beta}-ARs in both behaviors. Thus, a compensatory increase in {beta}-AR function during prodromal AD in TgF344-AD rats heightens synaptic plasticity and preserves some forms of learning and memory. Significance StatementThe locus coeruleus (LC), a brain region located in the brainstem which is responsible for attention and arousal, is damaged first by Alzheimers disease pathology. The LC sends axons to hippocampus where released norepinephrine (NE) modulates synaptic function required for learning and memory. How degeneration of LC axons and loss of NE in hippocampus in early AD impacts synaptic function and learning and memory is not well understood despite the importance of LC in cognitive function. We used a transgenic AD rat model with LC axon degeneration mimicking human AD and found that heightened function of {beta} adrenergic receptors in the dentate gyrus increased synaptic plasticity and preserved learning and memory in early stages of the disease.

neuroscience↗

bioRxiv2019

Alpha1-Adrenergic Receptor Mediated Long-Term Depression at CA3-CA1 Synapses Can be Induced via Accumulation of Endogenous Norepinephrine and is Preserved Following Noradrenergic Denervation

Locus coeruleus (LC) provides the sole source of noradrenergic (NA) innervation to hippocampus, and it undergoes significant degeneration early in Alzheimers disease (AD). Norepinephrine (NE) modulates synaptic transmission and plasticity at hippocampal synapses which likely contributes to hippocampus dependent learning and memory. We previously reported that pharmacological activation of 1 adrenergic receptors (1ARs) induces long-term depression (LTD) at CA3-CA1 synapses. Here we investigated whether accumulation of endogenous NE via pharmacological blockade of NE transporters (NET) and the NE degradative enzyme, monoamine oxidase (MAO), can induce 1AR LTD, as these inhibitors are used clinically. Further, we sought to determine how degeneration of hippocampal NA innervation, as occurs in AD, impacts 1AR function and 1AR LTD. Bath application of NET and MAO inhibitors in slices from control rats reliably induced 1AR LTD when {beta} adrenergic receptors were inhibited. To induce degeneration of LC-NA innervation, rats were treated with the specific NA neurotoxin DSP-4 and recordings performed 1-3 weeks later when NA axon degeneration had stabilized. Even with 85% loss of hippocampal NA innervation, 1AR LTD was successfully induced using either the 1AR agonist phenylephrine or the combined NET and MAO inhibitors, and importantly, the LTD magnitude was not different from saline-treated control. These data suggest that despite significant decreases in NA input to hippocampus, the mechanisms necessary for the induction of 1AR LTD remain functional. Furthermore, we posit that 1AR activation could be a viable therapeutic target for pharmacological intervention in AD and other diseases involving malfunctions of NA neurotransmission.

neuroscience↗