Statement of Partnership and Humility: A Structural Intervention to Improve Equity and Justice in Medical Education.

PROBLEM: Due to generational exposure to the Black Lives Matter movement, other anti-bias social movements, and diverse peer advocacy groups, health professions students are often more knowledgeable than their teachers about ways in which systemic racism and bias have led to scientific inaccuracies that contribute to health inequities. However, traditional hierarchies and concerns about retaliation may limit educational communities from benefiting maximally from students' contributions. APPROACH: In spring 2021, faculty and students at the Vagelos College of Physicians and Surgeons, Columbia University, designed a structural innovation to engage faculty and students in partnership toward decreasing bias in medical education. This article discusses development and implementation of a Statement of Partnership and Humility (SPH) disclosure slide on which faculty acknowledge consideration of potential teaching biases and invite student feedback. OUTCOMES: The initial primary goal of the SPH slide was to increase faculty awareness and engagement in anti-bias topics; however, the unexpected dividends of decreasing faculty anxiety about receiving student feedback and promoting student engagement have proven equally powerful in promoting a healthy, inclusive learning environment. NEXT STEPS: Next steps include gathering qualitative and quantitative data to elicit both faculty and student perspectives on the use of the SPH slide, particularly with regard to psychological safety and openness to feedback.

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).