Using office hour appointment data to illustrate a decline in student-faculty interaction during and after COVID-19.

Student-faculty interaction (SFI) is an important indicator of student engagement that positively associates with academic achievement and retention. Quantitative information regarding the impact of emergency remote teaching (ERT) during COVID-19 on SFI is limited. This retrospective, observational cohort study tests the hypothesis that COVID-19 ERT negatively affected SFI in a gender-dependent manner. Electronic records of office hour (OH) appointments, used to measure SFI, for first-year medical students across three time periods, before, during and after COVID, were obtained and analyzed. A concerning, marked decline in SFI during and after the COVID-19 pandemic is noted. Before COVID, significantly more women (75.20%) made at least one OH appointment compared with men (40.54%). During COVID, the proportion of women making an OH appointment (69.71%) was statistically indistinguishable from women before COVID-19. In contrast, significantly fewer men during COVID (10.34%) than before COVID made an OH appointment. On return to face-to-face teaching, no rebound effect was observed. Compared with before COVID gender-matched peers, fewer men and women after COVID made OH appointments. Discipline-based analyses show that for all three time periods physiology emerged as the content area in which students made most OH appointments. The reduction in SFI observed, combined with the consistency with which the participants in our study indicated a need for assistance with the physiology discipline, emphasizes the importance of active promotion of faculty support and deliberate efforts to reconnect with students in the post-COVID context.NEW & NOTEWORTHY Applying readily available data, we quantify a persistent, negative impact of the shift to emergency remote teaching (ERT) on a measure of student-faculty interaction (SFI) among first-year medical students. A gender-based component to these effects is also discussed. Before, during, and after COVID, physiology emerged as the most engaged-with discipline as measured by office hour (OH) appointment volume.

Deficits in temporal order memory induced by interferon-alpha (IFN-α) treatment are rescued by aerobic exercise.

Patients receiving cytokine immunotherapy with IFN-α frequently present with neuropsychiatric consequences and cognitive impairments, including a profound depressive-like symptomatology. While the neurobiological substrates of the dysfunction that leads to adverse events in IFN-α-treated patients remains ill-defined, dysfunctions of the hippocampus and prefrontal cortex (PFC) are strong possibilities. To date, hippocampal deficits have been well-characterised; there does however remain a lack of insight into the nature of prefrontal participation. Here, we used a PFC-supported temporal order memory paradigm to examine if IFN-α treatment induced deficits in performance; additionally, we used an object recognition task to assess the integrity of the perirhinal cortex (PRH). Finally, the utility of exercise as an ameliorative strategy to recover temporal order deficits in rats was also explored. We found that IFN-α-treatment impaired temporal order memory discriminations, whereas recognition memory remained intact, reflecting a possible dissociation between recognition and temporal order memory processing. Further characterisation of temporal order memory impairments using a longitudinal design revealed that deficits persisted for 10 weeks following cessation of IFN-α-treatment. Finally, a 6 week forced exercise regime reversed IFN-α-induced deficits in temporal order memory. These data provide further insight into the circuitry involved in cognitive impairments arising from IFN-α-treatment. Here we suggest that PFC (or the hippocampo-prefrontal pathway) may be compromised whilst the function of the PRH is preserved. Deficits may persist after cessation of IFN-α-treatment which suggests that extended patient monitoring is required. Aerobic exercise may be restorative and could prove beneficial for patients treated with IFN-α.

Interferon-alpha-induced deficits in novel object recognition are rescued by chronic exercise.

The anti-viral drug interferon-alpha (IFN-alpha) is widely-known to induce psychiatric and cognitive effects in patients. Previous work has shown that physical exercise can have a positive effect against brain insult. We investigated the effects of a clinically-comparable treatment regime of IFN-alpha on cognitive function in male Wistar rats and assessed the impact of chronic treadmill running on the deficits generated by IFN-alpha. We found that IFN-alpha induced significant impairments in performance on both spatial novelty and object novelty recognition. Chronic forced exercise did not protect against IFN-alpha-induced learning deficits in reactivity to spatial change, but did restore the capacity for novel object recognition in IFN-alpha-treated animals.

Blockade of NMDA receptors pre-training, but not post-training, impairs object displacement learning in the rat.

Several forms of hippocampal-dependent learning rely upon activation of the N-methyl-d-aspartate (NMDA) subtype of glutamate receptor. Here we have investigated the effects of administration of the NMDA receptor antagonist (+/-)-3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP) on the performance of rats in an object displacement task and the possible role of extracellular signal-regulated kinase (ERK) in this form of learning. The data show that rats injected intraperitoneally with CPP (10 mg/kg) before, but not after, training in the object displacement task displayed impairments in spatial learning when compared with saline-injected controls. The NMDAR may thus be involved in the acquisition, but not the consolidation, of this type of memory. In addition, a significant positive correlation was observed between learning and the expression of activated ERK in the dentate gyrus. No such correlation was apparent in the rest of the hippocampal formation. This study implicates the NMDARs in the acquisition phase of spatial learning and provides evidence for a role for ERK in spatial learning in the dentate gyrus of the rat.

The widely-used anti-viral drug interferon-alpha induces depressive- and anxiogenic-like effects in healthy rats.

Interferon-alpha (IFN-alpha) is a naturally occurring human cytokine that is a key therapy in the treatment of several viral diseases and cancers. However, treatment can produce significant neuropsychiatric and neurotoxic adverse events, including depression and anxiety. Here we investigated the effects of a clinically-comparable treatment regime of IFN-alpha on depressive- and anxiety-like behaviour in rats; and also examined frontal-cortical and hippocampal BDNF levels. Rats treated with IFN-alpha for four weeks showed significant increases in depressive- and anxiety-like behaviour. Further experimental investigation revealed that hedonic dysregulation (stronger preference for a sweet solution) did not emerge until the second week of treatment, and became more persistent as treatment progressed. No significant IFN-alpha-induced changes in BDNF levels were found. These results indicate that the affective deficits seen in patients may be modelled in healthy animals. This model may represent a novel tool to investigate the extent of and mechanisms underlying the IFN-alpha psychiatric syndrome.

Aberrant gating of photic input to the suprachiasmatic circadian pacemaker of mice lacking the VPAC2 receptor.

VIP acting via the VPAC(2) receptor is implicated as a key signaling pathway in the maintenance and resetting of the hypothalamic suprachiasmatic nuclei (SCN) circadian pacemaker; circadian rhythms in SCN clock gene expression and wheel-running behavior are abolished in mice lacking the VPAC(2) receptor (Vipr2(-/-)). Here, using immunohistochemical detection of pERK (phosphorylated extracellular signal-regulated kinases 1/2) and c-FOS, we tested whether the gating of photic input to the SCN is maintained in these apparently arrhythmic Vipr2(-/-) mice. Under light/dark and constant darkness, spontaneous expression of pERK and c-FOS in the wild-type mouse SCN was significantly elevated during subjective day compared with subjective night; no diurnal or circadian variation in pERK or c-FOS was detected in the SCN of Vipr2(-/-) mice. In constant darkness, light pulses given during the subjective night but not the subjective day significantly increased expression of pERK and c-FOS in the wild-type SCN. In contrast, light pulses given during both subjective day and subjective night robustly increased expression of pERK and c-FOS in the Vipr2(-/-) mouse SCN. Although photic stimuli activate intracellular pathways within the SCN of Vipr2(-/-) mice, they do not engage the core clock mechanisms. The absence of photic gating, together with the general lack of overt rhythms in circadian output, strongly suggests that the SCN circadian pacemaker is completely dysfunctional in the Vipr2(-/-) mouse.