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Hemingway, C.

Publications and source records attributed to Hemingway, C..

4 recordsLinked to original sources

Bees attend primarily to costs, not benefits, to avoid exploitation by floral mimics

Animals are expected to weigh costs and benefits when making foraging decisions. Flowering plants often offer floral food rewards to pollinators, but also frequently deceive pollinators into visiting without providing rewards. Although floral mimicry, in which rewardless flowers mimic rewarding (model) flowers is common, it remains unclear whether pollinators evaluate the relative costs and benefits of visiting each. Using a signal detection theory (SDT) framework, we investigated how bumble bee decisions respond to experimental manipulations of costs and benefits within an intersexual floral mimicry system in which unrewarding female flowers imperfectly mimic pollen-rewarding male flowers (models). Using a fully factorial design, we increased the cost of visiting mimics (by adding quinine), increased the benefit of visiting models (by adding pollen), increased both simultaneously, and made no changes (control). As predicted by SDT, increasing mimic costs led to a conservative bias: bees made more correct rejections, but fewer correct detections. Contradicting SDT predictions, enhancing model reward did not elicit a liberal bias and decision performance remained unchanged. Our findings suggest that bees prioritize avoiding costly errors under uncertainty, even when this limits potential gains. Such conservative foraging decisions may help stabilize deceptive systems by allowing mimics to persist despite moderate costs.

animal behavior and cognition↗

Nest attributes influence choice accuracy, but not decision speed in acorn ants

Decision making can have significant fitness consequences across various aspects of animal life. For acorn ants, Temnothorax curvispinosus, choosing a new nest quickly and accurately can affect the survival and fitness of the whole colony. When emigrating, ants consider several nest attributes such as cavity shape, thickness, and brightness. Ants may benefit from having more attributes differentiating potential nests only if they can quickly and accurately assess all possible attributes and make well-informed decisions. Here, we asked if the number and type of attributes differentiating potential nests affect the accuracy and latency of colony decision-making. We used pair-wise tests, where potential nests differed in 1-3 attributes, with one nest within the pair considered less optimal. We recorded the nest the colonies chose and the time it took to make the decision. We found that the degree of difference did not affect the decision-making latency, suggesting that ant colonies searching for a new nest might be constrained temporally when selecting a new nest site. We also found that accuracy increased with the number of attributes, particularly when nest brightness was manipulated, indicating that increasing the number of attributes may help facilitate nest-site selection.

animal behavior and cognition↗

Perinatal serotonin signalling dynamically influences the development of cortical GABAergic circuits with consequences for lifelong sensory encoding

Serotonin plays a prominent role in neurodevelopment, regulating processes from cell division to synaptic connectivity1,2. Clinical studies suggest that alterations in serotonin signalling such as genetic polymorphisms3-5 or antidepressant exposure during pregnancy6,7 are risk factors for neurodevelopmental disorders. However, an understanding of how dysfunctional neuromodulation alters systems level activity over neocortical development is lacking. Here, we use a longitudinal imaging approach to investigate how genetics, pharmacology, and aversive experience disrupt state-dependent serotonin signalling with pathological consequences for sensory processing. We find that all three factors lead to increased neocortical serotonin levels during the initial postnatal period. Genetic deletion of the serotonin transporter or antidepressant dosing results in a switch from hypo- to hyper-cortical activity that arises as a consequence of altered cortical GABAergic microcircuitry. However, the trajectories of these manipulations differ with postnatal exposure to antidepressants having effects on adult sensory encoding. The latter is not seen in the genetic model despite a similar early phenotype, and a distinct influence of maternal genotype on the development of supragranular layers. These results reveal the dynamics and critical nature of serotonin signalling during perinatal life; pharmacological targeting of which can have profound life-long consequences for cognitive development of the offspring.

neuroscience↗

SEQUIN multiscale imaging of mammalian central synapses reveals loss of synaptic microconnectivity resulting from diffuse traumatic brain injury

The complex microconnectivity of the mammalian brain underlies its computational abilities, and its vulnerability to injury and disease. It has been challenging to illuminate the features of this synaptic network due in part to the small size and exceptionally dense packing of its elements. Here we describe a rapid and accessible super-resolution imaging and image analysis workflow--SEQUIN--that identifies, quantifies, and characterizes central synapses in animal models and in humans, enabling automated volumetric imaging of mesoscale synaptic networks without the laborious production of large histological arrays. Using SEQUIN, we identify delayed cortical synapse loss resulting from diffuse traumatic brain injury. Similar synapse loss is observed in an Alzheimer disease model, where SEQUIN mesoscale mapping of excitatory synapses across the hippocampus identifies region-specific synaptic vulnerability to neurodegeneration. These results establish a novel, easily implemented and robust nano-to-mesoscale synapse quantification and molecular characterization method. They furthermore identify a mechanistic link--synaptopathy--between Alzheimer neurodegeneration and its best-established epigenetic risk factor, brain trauma.

neuroscience↗