In response to the outbreak of the novel Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), pathogen of the new coronavirus disease (COVID-19), several sectors and social activities have been affected, including education. At first, it is explained that educators and students can feel fragile during and after the SARS-CoV-2 outbreak. Subsequently, it is discussed that their relationship ought to be carefully established given the triggering of psychological and neuropsychiatric effects arising from neural coding and plasticity processes, which result in the formation of positive and negative memories in the short to long term. Finally, it is pointed out that the SARS-CoV-2 pandemic generates a need for adequacy and adaptation for the significant attention to students during the re-starting of studies, given that possible disorders of sensory modulation and involvement of limbic brain areas triggered in situations of risk of death, potential or real threat, can happen. It is assumed that at times of the SARS-CoV-2 pandemic, in addition to preserving life, one of the challenges is the behavioural (re)organisation, which includes habits from the educational context that need to contemplate a scientific perspective, seeking to transform the consequences of the pandemic fear on opportunities to reinforcement of familiar links. In the context of modern rationality, the SARS-CoV-2 pandemic is also a period to think about the relationship between scientific knowledge and common sense. With this logic, neurosciences can develop a new format for the teaching-learning process, so that educators and students experiencing the pandemic threatening do not manifest psychological distress and secondary consequences. Therefore, education can be considered a central space in decision-making in the face of SARS-CoV-2 pandemic. In this sense, the urgency of a multidisciplinary strategies development is highlighted, connecting the synergy between neurosciences and education after the COVID-19 pandemic.

OBJETIVO: Estudar as conseqüências comportamentais, bioquímicas e histopatológicas da isquemia cerebral focal permanente e o possível efeito neuroprotetor do cetoprofeno. MÉTODO: Foram utilizados 103 ratos Wistar, divididos em grupos A e B, submetidos, respectivamente, a 48 horas e a 15 dias de isquemia. Cada grupo foi dividido em 4 subgrupos: isquêmico não tratado; isquêmico tratado; sham não tratado; sham tratado. Nos animais isquêmicos foi coagulada a artéria cerebral média esquerda. Os subgrupos tratados receberam cetoprofeno 15 minutos antes da oclusão ou manipulação arterial. RESULTADOS: Os animais isquêmicos reduziram a atividade exploratória e as evacuações nos primeiros dias pós-operatórios e mostraram alterações histopatológicas constantes em cada grupo. As concentrações do glutamato total 48 horas após a cirurgia foram maiores nos animais tratados. CONCLUSÃO: Não houve um paralelismo entre os achados comportamentais, bioquímicos e histopatológicos. O cetoprofeno não apresentou efeito protetor contra isquemia cerebral focal permanente, nos aspectos comportamentais e histopatológicos.

OBJECTIVE: To study the neurobehavioral, biochemical and histopathological consequences of permanent focal brain ischemia, and the putative neuroprotective action of ketoprofen. METHOD: One-hundred-and-three Wistar rats divided into groups A and B were respectively submitted to 48 hours and 15 days of ischemia. Each group was divided into 4 subgroups: ischemic not treated, ischemic treated, sham not treated, and sham treated. Ischemic animals had the left middle cerebral artery coagulated. Ketoprofen was administered to treated subgroups 15 minutes before arterial coagulation (manipulation in the sham group). RESULTS: Exploratory activity and defecation were reduced in all ischemic animals in the first postoperative days and constant histopathological changes were observed in each group. The total brain glutamate levels were higher in treated animals 48 hours after surgery. CONCLUSION: No clear parallelism among behavioral, biochemical and histopathological findings was observed. Ketoprofen demonstrated no neuroprotective effect on the behavioral or histopathological aspects of focal permanent brain ischemia.