Transitioning from Faculty-Written Examinations to National Board of Medical Examiners Custom Examinations in Medical Education.

Purpose: A challenge for medical educators is choosing a method that best evaluates preclinical students' performance in preparation for Step 1. In previous years, block directors (BDs) of the 2nd year (MS2) neuroscience course at Texas Tech University Health Sciences Center School of Medicine issued faculty-written (FW) examinations during the course. In 2022, BDs replaced FW examinations with National Board of Medical Examiners (NBME) custom examinations. The rationale being that the customized NBME exams would better reflect the national neuroscience curriculum and enhance student preparedness for taking standardized exams. Methods: FW examinations (2021) were created by the faculty in the neuroscience course and reviewed by BDs. In contrast, questions that best aligned with the material covered for the 2022 course were selected by BDs using MyNBMESM Services Portal. The custom questions selected are assigned a "difficulty" score by NBME, generating a predicted national average score. At the end of the course, undergraduate medical students in the School of Medicine at Texas Tech University Health Sciences Center completed an online Qualtrics questionnaire to compare the transition of assessment type. Results: Participants reported greater satisfaction in their neuroscience education and block organization with NBME examinations. For example, there was a nearly twofold (1.83) increase in the number of students that strongly agreed with the statement "Overall, I am satisfied with the quality of my neuroscience education in this block." They were also less likely to report the workload as being "much too heavy." Overall, students expressed a preference for the customized NBME exams as opposed to faculty generated exams (88.1%). Conclusions: From the student perspective, building customized assessments through MyNBMESM Services Portal was found to be useful and preferable for evaluating student performance. From block directors' perspective, it is noted that time is saved assisting faculty in writing valid questions, time defending/justifying FW questions, and time expended generating exams. The only perceived negative regarding the NBME exams is the cost.

Tectal CRFR1 receptor involvement in avoidance and approach behaviors in the South African clawed frog, Xenopus laevis.

Animals in the wild must balance food intake with vigilance for predators in order to survive. The optic tectum plays an important role in the integration of external (predators) and internal (energy status) cues related to predator defense and prey capture. However, the role of neuromodulators involved in tectal sensorimotor processing is poorly studied. Recently we showed that tectal CRFR1 receptor activation decreases food intake in the South African clawed frog, Xenopus laevis, suggesting that CRF may modulate food intake/predator avoidance tradeoffs. Here we use a behavioral assay modeling food intake and predator avoidance to test the role of CRFR1 receptors and energy status in this tradeoff. We tested the predictions that 1) administering the CRFR1 antagonist NBI-27914 via the optic tecta will increase food intake and feeding-related behaviors in the presence of a predator, and 2) that prior food deprivation, which lowers tectal CRF content, will increase food intake and feeding-related behaviors in the presence of a predator. Pre-treatment with NBI-27914 did not prevent predator-induced reductions in food intake. Predator exposure altered feeding-related behaviors in a predictable manner. Pretreatment with NBI-27914 reduced the response of certain behaviors to a predator but also altered behaviors irrelevant of predator presence. Although 1-wk of food deprivation altered some non-feeding behaviors related to energy conservation strategy, food intake in the presence of a predator was not altered by prior food deprivation. Collectively, our data support a role for tectal CRFR1 in modulating discrete behavioral responses during predator avoidance/foraging tradeoffs.

Neuroendocrine modulation of predator avoidance/prey capture tradeoffs: Role of tectal NPY2R receptors.

The optic tectum rapidly inhibits food intake when a visual threat is present. Anatomical and electrophysiological evidence support a role for neuropeptide Y (NPY), originating from cells in the thalamus, in the tectal inhibition of prey capture. Here we test the hypothesis that tectal NPY receptor type 2 (NPY2R) influences prey-capture and predator-avoidance responses in the African clawed frog, Xenopus laevis. We tested two questions: 1) Does tectal NPY administration decrease food intake and alter prey-capture behavior? 2) Does tectal administration of a NPY2R antagonist increase food intake, alter prey-capture behavior, and alter predator avoidance behavior? NPY microinjected bilaterally into the tecta failed to significantly alter food intake at any dose tested, although predator presence significantly reduced food intake. However, NPY differentially altered discrete components of prey capture including increasing the latency to contact food and reducing the amount of time in contact with food. These effects were blocked by the NPY2R antagonist BIIE0246. Additionally, BIIE0246 elevated food intake on its own after bilateral tectal microinjection. Furthermore, BIIE0246 reversed the reduction of food intake caused by exposure to a predator. Overall, these findings indicate that tectal NPY2R activation causes frogs to consume food more quickly, which may be adaptive in predator-rich environments. Blocking tectal NPY2R increases baseline food intake and reduces or eliminates predator-induced changes in prey capture and food intake.

Tectal CRFR1 receptors modulate food intake and feeding behavior in the South African clawed frog Xenopus laevis.

The optic tectum and superior colliculus rapidly inhibit food intake when a visual threat is present. Previous work indicates that CRF, acting on CRFR1 receptors, may play a role in tectal inhibition of feeding behavior and food intake. Here we test the hypothesis that tectal CRFR1 receptors modulate food intake and feeding behavior in juvenile Xenopus laevis. We performed five experiments to test the following questions: 1) Does tectal CRF injection decrease food intake/feeding behavior? 2) Does a selective CRFR1 antagonist block CRF effects on feeding/feeding behavior? 3) Does a reactive stressor decrease food intake/feeding behavior? 4) Does a selective CRFR1 antagonist block reactive stress-induced decrease in feeding/feeding behavior? 5) Does food deprivation increase food intake/feeding behavior? Tectal CRF injections reduced food intake and influenced exploratory behavior, hindlimb kicks, and time in contact with food. These effects were blocked by the selective R1 antagonist NBI-27914. Exposure to a reactive stressor decreased food intake and this effect was blocked by NBI-27914. Neither food intake or feeding behavior changed following 1 wk of food deprivation. Overall, we conclude that activation of tectal CRFR1 inhibits food intake in juvenile X. laevis. Furthermore, tectal CRFR1 receptors appear to be involved in the reduction of food intake that occurs in response to a reactive stressor.

Tectal corticotropin-releasing factor (CRF) neurons respond to fasting and a reactive stressor in the African Clawed Frog, Xenopus laevis.

It is well established that hypothalamic neurons producing the peptide corticotropin-releasing factor (CRF) play a key role in stress adaptation, including reduction of food intake when a threat or stressor is present. We have previously reported on the presence of an intrinsic CRF signaling system within the optic tectum (OT), a brain area that plays a key role in visually guided prey capture/predator avoidance decisions. To better understand the potential role of tectal CRF neurons in regulating adaptive behavior and energy balance during stress we examined evidence for modulation of tectal CRF neuronal activity after stressor exposure and food deprivation in the African clawed frog Xenopus laevis. We tested two predictions, 1) that exposure to categorically distinct stressors (ether vapors and shaking) will reduce food intake and modulate the activity of tectal CRF cells, and 2) that food deprivation will modulate the activity of tectal CRF cells. Exposure to ether increased tectal content of CRF and CRF transcript, but lowed CRFR1 transcript abundance. Two weeks of food deprivation reduced total fat stores in frogs and decreased tectal content of CRF content while having no effect on CRF and CRFR1 transcript abundance. Our data are consistent with a role for tectal CRF neurons in modulating food intake in response to certain stressors.