Reproductive tactics, birth timing and the risk-resource trade-off in an income breeder.

In variable environments, habitats that are rich in resources often carry a higher risk of predation. As a result, natural selection should favour individuals that balance allocation of time to foraging versus avoiding predation through an optimal decision-making process that maximizes fitness. The behavioural trade-off between resource acquisition and risk avoidance is expected to be particularly acute during gestation and lactation, when the energetic demands of reproduction peak. Here, we investigated how reproductive female roe deer adjust their foraging activity and habitat use during the birth period to manage this trade-off compared with non-reproductive juveniles, and how parturition date constrains individual tactics of risk-resource management. Activity of reproductive females more than doubled immediately following parturition, when energy demand is highest. Furthermore, compared with non-reproductive juveniles, they increased their exposure to risk by using open habitat more during daytime and ranging closer to roads. However, these post-partum modifications in behaviour were particularly pronounced in late-parturient females who adopted a more risk-prone tactic, presumably to compensate for the growth handicap of their late-born offspring. In income breeders, individuals that give birth late may be constrained to trade risk avoidance for foraging during peak allocation to reproduction, with probable consequences for individual fitness.

Mature parvalbumin interneuron function in prefrontal cortex requires activity during a postnatal sensitive period.

In their seminal findings, Hubel and Wiesel identified sensitive periods in which experience can exert lasting effects on adult visual cortical functioning and behavior via transient changes in neuronal activity during development. Whether comparable sensitive periods exist for non-sensory cortices, such as the prefrontal cortex, in which alterations in activity determine adult circuit function and behavior is still an active area of research. Here, using mice we demonstrate that inhibition of prefrontal parvalbumin (PV)-expressing interneurons during the juvenile and adolescent period, results in persistent impairments in adult prefrontal circuit connectivity, in vivo network function, and behavioral flexibility that can be reversed by targeted activation of PV interneurons in adulthood. In contrast, reversible suppression of PV interneuron activity in adulthood produces no lasting effects. These findings identify an activity-dependent sensitive period for prefrontal circuit maturation and highlight how abnormal PV interneuron activity during development alters adult prefrontal circuit function and cognitive behavior.

Thalamocortical Development: A Neurodevelopmental Framework for Schizophrenia.

Adolescence is a period of increased vulnerability for the development of psychiatric disorders, including schizophrenia. The prefrontal cortex (PFC) undergoes substantial maturation during this period, and PFC dysfunction is central to cognitive impairments in schizophrenia. As a result, impaired adolescent maturation of the PFC has been proposed as a mechanism in the etiology of the disorder and its cognitive symptoms. In adulthood, PFC function is tightly linked to its reciprocal connections with the thalamus, and acutely inhibiting thalamic inputs to the PFC produces impairments in PFC function and cognitive deficits. Here, we propose that thalamic activity is equally important during adolescence because it is required for proper PFC circuit development. Because thalamic abnormalities have been observed early in the progression of schizophrenia, we further postulate that adolescent thalamic dysfunction can have long-lasting consequences for PFC function and cognition in patients with schizophrenia.

Adolescent thalamic inhibition leads to long-lasting impairments in prefrontal cortex function.

Impaired cortical maturation is a postulated mechanism in the etiology of neurodevelopmental disorders, including schizophrenia. In the sensory cortex, activity relayed by the thalamus during a postnatal sensitive period is essential for proper cortical maturation. Whether thalamic activity also shapes prefrontal cortical maturation is unknown. We show that inhibiting the mediodorsal and midline thalamus in mice during adolescence leads to a long-lasting decrease in thalamo-prefrontal projection density and reduced excitatory drive to prefrontal neurons. It also caused prefrontal-dependent cognitive deficits during adulthood associated with disrupted prefrontal cross-correlations and task outcome encoding. Thalamic inhibition during adulthood had no long-lasting consequences. Exciting the thalamus in adulthood during a cognitive task rescued prefrontal cross-correlations, task outcome encoding and cognitive deficits. These data point to adolescence as a sensitive window of thalamocortical circuit maturation. Furthermore, by supporting prefrontal network activity, boosting thalamic activity provides a potential therapeutic strategy for rescuing cognitive deficits in neurodevelopmental disorders.

Toward a Bias-Free and Inclusive Medical Curriculum: Development and Implementation of Student-Initiated Guidelines and Monitoring Mechanisms at One Institution.

As research and attention on implicit bias and inclusiveness in medical school is expanding, institutions need mechanisms for recognizing, reporting, and addressing instances of implicit bias and lack of inclusiveness in medical school curricular structures. These instances can come as a result of a lack of both awareness and communication around these sensitive issues. To identify and address cases of implicit bias in the medical school curriculum, a student-led initiative at Columbia University Vagelos College of Physicians and Surgeons (VP&S) developed guidelines and a bias-reporting process for educators and students. The guidelines, co-created by students and faculty, help educators identify and address implicit bias in the curriculum. Furthermore, to allow for continued development of the curriculum and the guidelines themselves, the group adapted an existing learning environment reporting and review process to identify and address instances of implicit bias. In the first year since their implementation, these tools have already had an impact on the learning climate at VP&S. They have led to enhanced identification of implicit bias in the curriculum and changes in instructional materials. The courage and inspiration of the students and the initial investment and commitment from the administration and faculty were crucial to this rapid effect. The authors present an approach and resources from which other institutions can learn, with the goal of reducing implicit bias and improving inclusiveness throughout medical education. In the long run, the authors hope that these interventions will contribute to better preparing future providers to care for all patients equitably.

Medial prefrontal lesions impair performance in an operant delayed nonmatch to sample working memory task.

Cognitive functions, such as working memory, are disrupted in most psychiatric disorders. Many of these processes are believed to depend on the medial prefrontal cortex (mPFC). Traditionally, maze-based behavioral tasks, which have a strong exploratory component, have been used to study the role of the mPFC in working memory in mice. In maze tasks, mice navigate through the environment and require a significant amount of time to complete each trial, thereby limiting the number of trials that can be run per day. Here, we show that an operant-based delayed nonmatch to sample (DNMS) working memory task, with shorter trial lengths and a smaller exploratory component, is also mPFC-dependent. We created excitotoxic lesions in the mPFC of mice and found impairments in both the acquisition of the task, with no delay, and in the performance with delays introduced. Importantly, we saw no differences in trial length, reward collection, or lever-press latencies, indicating that the difference in performance was not due to a change in motivation or mobility. Using this operant DNMS task will facilitate the analysis of working memory and improve our understanding of the physiology and circuit mechanisms underlying this cognitive process. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

Accelerating across the landscape: The energetic costs of natal dispersal in a large herbivore.

Dispersal is a key mechanism enabling species to adjust their geographic range to rapid global change. However, dispersal is costly and environmental modifications are likely to modify the cost-benefit balance of individual dispersal decisions, for example, by decreasing functional connectivity. Dispersal costs occur during departure, transience and settlement, and are levied in terms of energy, risk, time and lost opportunity, potentially influencing individual fitness. However, to the best of our knowledge, no study has yet quantified the energetic costs of dispersal across the dispersal period by comparing dispersing and philopatric individuals in the wild. Here, we employed animal-borne biologgers on a relatively large sample (N = 105) of juvenile roe deer to estimate energy expenditure indexed using the vector of dynamic body acceleration and mobility (distance travelled) in an intensively monitored population in the south-west of France. We predicted that energy expenditure would be higher in dispersers compared to philopatric individuals. We expected costs to be (a) particularly high during transience, (b) especially high in the more fragmented areas of the landscape and (c) concentrated during the night to avoid disturbance caused by human activity. There were no differences in energy expenditure between dispersers and philopatric individuals during the pre-dispersal phase. However, dispersers expended around 22% more energy and travelled around 63% further per day than philopatric individuals during transience. Differences in energy expenditure were much less pronounced during the settlement phase. The costs of transience were almost uniquely confined to the dawn period, when dispersers spent 23% more energy and travelled 112% further than philopatric individuals. Finally, the energetic costs of transience per unit time and the total distance travelled to locate a suitable settlement range were higher in areas of high road density. Our results provide strong support for the hypothesis that natal dispersal is energetically costly and indicate that transience is the most costly part of the process, particularly in fragmented landscapes. Further work is required to link dispersal costs with fitness components so as to understand the likely outcome of further environmental modifications on the evolution of dispersal behaviour.

Adult-born neurons boost odor-reward association.

Olfaction is an important sensory modality driving fundamental behaviors. During odor-dependent learning, a positive value is commonly assigned to an odorant, and multiple forms of plasticity are involved when such odor-reward associations are formed. In rodents, one of the mechanisms underlying plasticity in the olfactory bulb consists in recruiting new neurons daily throughout life. However, it is still unknown whether adult-born neurons might participate in encoding odor value. Here, we demonstrate that exposure to reward-associated odors specifically increases activity of adult-born neurons but not preexisting neurons. Remarkably, adult-born neuron activation during rewarded odor presentation heightens discrimination learning and enhances the ability to update the odor value during reversal association. Moreover, in some cases, activation of this interneuron population can trigger olfactory learning without sensory stimulation. Taken together, our results show a specific involvement of adult-born neurons in facilitating odor-reward association during adaptive learning.

Monosodium iodoacetate-induced osteoarthritis produces pain-depressed wheel running in rats: implications for preclinical behavioral assessment of chronic pain.

Pain stimulates some behaviors (e.g., withdrawal responses) and depresses other behaviors (e.g., feeding and locomotion). We are developing methods for testing candidate analgesics using measurements of pain-depressed behaviors. Such assays may model important aspects of clinical pain and complement traditional procedures that measure pain-stimulated behaviors. The present study characterized the effects of a chronic pain manipulation (monosodium iodoacetate (MIA)-induced osteoarthritis) on wheel running in rats. Rats had 24 h voluntary access to running wheels. Duration of running wheel acquisition was manipulated such that rats had either 21 or 7 days of running wheel access prior to MIA administration. Wheel running was monitored for an additional 21 days following MIA administration. MIA produced concentration- and acquisition length-dependent decreases in wheel running. Parallel experiments demonstrated that MIA produced concentration-dependent tactile allodynia and shifts in hind limb weight bearing. MIA was differentially potent across assays with a potency rank: weight-bearing≥von Frey>running wheel. MIA produced greater depression of wheel running in rats with relatively high baseline running rates compared to rats with relatively low baseline running rates. The differential potency of MIA across assays and apparent rate-dependent effects in running wheels may impact our traditional interpretations of preclinical nociceptive and antinociceptive testing.