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Worldwide, parenthood remains a major driver for the reduced participation of women in the job market, where discrimination stems from people's biases against mothers, based on stereotypes and misconceptions surrounding the vision of motherhood in our society. In academia, parenthood may be perceived as negatively affecting scientists' commitment and dedication, especially women's. We conducted a survey amongst Brazilian scientists and found that mothers self-reported a higher prevalence of negative bias in their workplace when compared to fathers. The perception of a negative bias was influenced by gender and career status, but not by race, scientific field or number of children. Regarding intersections, mothers with less than 15 years of hiring reported having suffered a higher rate of negative bias against themselves. We discuss implications of these results and suggest how this negative bias should be addressed in order to promote an equitable environment that does not harm women in science.
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Maternal deprivation (MD) leads to long-lasting memory deficits. Conversely, maternal exercise could potently modify the offspring's cellular machinery. Here, we tested whether starting to run or reducing the intensity of running during pregnancy can protect prepubertal female offspring against MD-induced memory deficits. Female rats were divided into different groups submitted or not to MD: one started to run before pregnancy and reduced the intensity during the pregnancy (PGE); another started to run at the beginning of pregnancy (GE); and, finally, a control group (CT) was not submitted to exercise. All the rats but those of the CT ran on a treadmill until the delivery day (PND 0). Subsequently, MD was performed from PND 1 to 10. We assessed object recognition (OR) and spatial memory (SM) of female offspring after weaning (PND22, pre-pubertal stage). MD caused OR memory deficit; GE female offspring did not present this deficit, but PGE did. Both PGE and GE alone enhanced offspring spatial learning, but their combination with MD impaired it. MD promoted hippocampal lipid peroxidation increase, which both PGE and GE prevented. Total antioxidant capacity in the hippocampus was higher in both MD-exercised groups compared to all others. Although the antioxidant effects of exercise were similar in both MD exercise groups, we observed better results in the memory tests in the GE group than in the PGE group. These results suggest that starting to exercise during pregnancy is better than reducing the exercise intensity during pregnancy to prevent MD-induced memory deficits in female offspring.
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Privación Materna , Carrera , Embarazo , Ratas , Animales , Femenino , Trastornos de la Memoria/etiología , Trastornos de la Memoria/prevención & control , Aprendizaje Espacial , Percepción Visual , HipocampoRESUMEN
Memory extinction has been used in behavioral therapy to treat post-traumatic stress disorders. It was demonstrated that memory reactivation before extinction could facilitate this process. However, the mechanisms involved are still unclear. Here, we investigated the participation of two regions of the ventromedial prefrontal cortex (vmPFC), the infralimbic (IL) and prelimbic (PL), in the memory reactivation modulatory effect of fear extinction. We confirmed that the reactivation facilitates the fear extinction in an inhibitory aversive task; however, when the muscimol (a GABAergic agonist) is infused in IL or PL vmPFC after reactivation, extinction's facilitation was not observed. These findings support the idea that the reactivation can modulate the fear extinction process, facilitating it, and that this effect requires the activation of both IL and PL regions of vmPFC.
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Reacción de Prevención/fisiología , Extinción Psicológica/fisiología , Memoria/fisiología , Corteza Prefrontal/fisiología , Animales , Reacción de Prevención/efectos de los fármacos , Extinción Psicológica/efectos de los fármacos , Agonistas de Receptores de GABA-A/farmacología , Masculino , Memoria/efectos de los fármacos , Muscimol/farmacología , Corteza Prefrontal/efectos de los fármacos , Ratas , Ratas WistarRESUMEN
The coronavirus disease 2019 (COVID-19) pandemic is altering dynamics in academia, and people juggling remote work and domestic demands - including childcare - have felt impacts on their productivity. Female authors have faced a decrease in paper submission rates since the beginning of the pandemic period. The reasons for this decline in women's productivity need to be further investigated. Here, we analyzed the influence of gender, parenthood and race on academic productivity during the pandemic period based on a survey answered by 3,345 Brazilian academics from various knowledge areas and research institutions. Productivity was assessed by the ability to submit papers as planned and to meet deadlines during the initial period of social isolation in Brazil. The findings revealed that male academics - especially those without children - are the least affected group, whereas Black women and mothers are the most impacted groups. These impacts are likely a consequence of the well-known unequal division of domestic labor between men and women, which has been exacerbated during the pandemic. Additionally, our results highlight that racism strongly persists in academia, especially against Black women. The pandemic will have long-term effects on the career progression of the most affected groups. The results presented here are crucial for the development of actions and policies that aim to avoid further deepening the gender gap in academia.
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Antioxidant supplementation and physical exercise have been discussed as strategies to minimize neurodegeneration in Alzheimer's disease (AD). We investigated the neuroprotective effects of strength exercise (StrEx) and green tea (GT) supplementation, combined or not, on memory impairments induced by ß-amyloid characterizing an AD-like condition in rats. Wistar rats were submitted to 8 weeks of StrEx, GT supplementation, or StrEx and GT combined. AD-like condition was induced by injection of Aß (25-35) in the hippocampus. We evaluate object recognition (OR) and social recognition (SR) memory, and removed the rats' hippocampus for biochemical analysis. StrEx improved OR and SR. StrEx combined with GT improved OR and did not improve SR. GT reduced antioxidant capacity and improved acetylcholinesterase activity. Both strength exercise and green tea are neuroprotective against impairments resultant of ß-amyloid, but benefits do not add up when the two interventions are associated.
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Enfermedad de Alzheimer , Fármacos Neuroprotectores , Entrenamiento de Fuerza , Enfermedad de Alzheimer/prevención & control , Péptidos beta-Amiloides/metabolismo , Animales , Modelos Animales de Enfermedad , Hipocampo/metabolismo , Humanos , Trastornos de la Memoria/prevención & control , Fármacos Neuroprotectores/farmacología , Estrés Oxidativo , Fragmentos de Péptidos/farmacología , Ratas , Ratas Wistar , TéRESUMEN
Alzheimer's disease (AD) is the leading cause of dementia in the world, accounting for 50-75% of cases. Currently, there is limited treatment for AD. The current pharmacological therapy minimizes symptom progression but does not reverse brain damage. Studies focused on nonpharmacological treatment for AD have been developed to act on brain plasticity and minimize the neurotoxicity caused by the amyloid-beta (Aß) peptide. Using a neurotoxicity model induced by Aß in rats, the present study shows that physical (PE) and cognitive exercise (CE) reverse recognition memory deficits (with a prominent effect of long-term object recognition memory), decrease hippocampal lipid peroxidation, restore the acetylcholinesterase activity altered by Aß neurotoxicity, and seems to reverse, at least partially, hippocampal tissue disorganization.
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Alzheimer's disease is a progressive neurodegenerative pathological process that causes memory loss and cognitive impairment. One of the pathological characteristics of Alzheimer's disease is the amyloid-ß protein aggregation on the brain. The regular practice of physical exercise is a consolidated strategy on the prevention of cognitive deficits; however, little is known about the effects of acute exercise on memory. We hypothesize that one physical exercise session could act as a modulator of learning. Here we investigated the effects of one single session of running (aerobic) or strength (anaerobic) exercise on memory deficits related to neurotoxicity induced by amyloid-ß. Male Wistar rats were submitted to stereotaxic surgery to intrahippocampal infusion of amyloid-ß protein or saline (control). Ten days after the surgery the rats were submitted to the object recognition (OR) memory task. Immediately after the OR learning session, some rats were submitted to one treadmill running or strength exercise session. Then, the animals were submitted to memory tests 24 h, 7, and 14 days after the OR learning. We demonstrated that one physical exercise session, both aerobic as anaerobic, performed after learning improves learning and memory, promoting memory persistence in control rats and memory consolidation in rats submitted to amyloid-ß neurotoxicity model. Notably, the effects of the aerobic exercise session seem to be more prominent, since they also reflect in an improvement of object discrimination index for 7 days in control animals. We verified that the mechanisms involved in the effects of aerobic exercise include the dopaminergic system activation. The mechanisms involved in the anaerobic exercise effects seem to be others since no alterations on hippocampal dopamine or noradrenaline levels were detected.
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Enfermedad de Alzheimer , Péptidos beta-Amiloides/toxicidad , Trastornos del Conocimiento/inducido químicamente , Condicionamiento Físico Animal/fisiología , Reconocimiento en Psicología/fisiología , Animales , Masculino , Condicionamiento Físico Animal/métodos , Ratas , Ratas WistarRESUMEN
Previously we demonstrated that a single physical exercise session promotes the persistence of object recognition (OR) memory and this effect involves the activation of the noradrenergic system. Here, using adult male Wistar rats (3 months old) we confirm that an aerobic single physical exercise session (30 min of treadmill running at an intensity of 60-70 % of indirect VO2 max.) after OR learning promotes memory persistence. We also demonstrate that this effect involves the dopaminergic system, since it is blocked when a D1-family receptor antagonist (SCH-23390, 1µg/µl) is infused into the hippocampus after the physical exercise session. Additionally, through HPLC experiments we demonstrate that a physical exercise session increases the hippocampal dopamine levels. Taken together, our results demonstrate that acute post-learning physical exercise is able to promote the persistence of OR memory, inducing the release of dopamine in hippocampus, which is necessary for the modulation of memory persistence. This work brings new evidences on the benefit of a single physical exercise session to memory, as well as suggests that catecholaminergic mechanisms are behind this effect.
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Conducta Animal/fisiología , Antagonistas de Dopamina/farmacología , Hipocampo/metabolismo , Condicionamiento Físico Animal/fisiología , Receptores de Dopamina D1/antagonistas & inhibidores , Reconocimiento en Psicología/fisiología , Animales , Conducta Animal/efectos de los fármacos , Benzazepinas/farmacología , Antagonistas de Dopamina/administración & dosificación , Hipocampo/efectos de los fármacos , Masculino , Ratas , Ratas Wistar , Reconocimiento en Psicología/efectos de los fármacosRESUMEN
Aversive memory is essential for survival, but in some situations its exacerbation can be potentially dangerous. There are several ways to modulate memory, among them, through stress-related hormones physiological release or administration of exogenous substances analogous to them. Recently, our group shown that a chronic treatment with a low dose of methylprednisolone (MP) is able to promote memory persistence in rats. Herein, we evaluate if a single intraperitoneal (IP) dose of MP (5 mg/kg) is able to modulate aversive memory consolidation and promote memory persistence and extinction in rats. For this, two experiments were carried out. In the first one, we demonstrated that a single IP MP administration in specific times after inhibitory avoidance (IA) training improved memory consolidation and persistence. In the second experiment, we verified that a single IP MP administration 2 h after IA extinction training promoted memory extinction. This results suggest a possible new clinical applicability for MP on the aversive memory disorders, as post-traumatic stress.
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The generalization of aversive memory can be defined as the phenomenon in which a situation similar to (but distinctive from) a previous aversive event triggers an avoidance response. This phenomenon has been suggested to play a role in several psychological disorders. In this study, we investigate the effects of novelty on the generalization of fear memories, and the involvement of noradrenergic and dopaminergic systems in this process. For this study we used male Wistar rats (3 months old, 300-400â¯g). The participation of each neurotransmitter system was evaluated separately (two set of experiments). In each experimental set, the animals were divided in groups (8 animals each): (i) control, (ii) novelty, and, (iii) antagonistâ¯+â¯novelty group (timolol, a ß-adrenergic antagonist, or SCH23390, a D1/D5 dopaminergic antagonist, in the first and in the second set of experiments, respectively). Additionaly, to investigate whether novelty exposure increases the levels of noradrenaline and/or dopamine in the hippocampus fifteen animals were divided in three groups (5 animals each).: (i) naïve, (ii) control; and, (iii) novelty. To examine aversive memory, and generalization of aversive memory, we trained adult male Wistar rats in an inhibitory avoidance (IA) memory task and after in a modified inhibitory avoidance (MIA). Before the MIA training some of the animals were exposed to environmental novelty (open field). Immediately before this novelty exposure, some animals received intrahippocampal infusion of timolol (ß-adrenergic antagonist), SCH23390 (D1/D5 antagonist) or vehicle to evaluate the involvement of noradrenergic and dopaminergic systems. Finally, to evaluate aversive memory and generalization of aversive memory respectively, half of the animals in each group were tested on IA and half on MIA. We confirmed that the exposure to novelty blocks the generalization of aversive memory, but moreover, demonstrated that this process involves activation of ß-adrenergic and dopaminergic D1/D5 pathways. We additionally observed that exposure to novelty raises hippocampal levels of noradrenaline and dopamine. This suggests that these neurotransmitters not only influence long-term memory (LTM) as such, but also aversive memory generalization.
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Reacción de Prevención/fisiología , Conducta Exploratoria/fisiología , Generalización Psicológica/fisiología , Amígdala del Cerebelo/metabolismo , Animales , Reacción de Prevención/efectos de los fármacos , Benzazepinas/farmacología , Encéfalo/metabolismo , Condicionamiento Clásico/efectos de los fármacos , Dopamina/metabolismo , Antagonistas de Dopamina/farmacología , Conducta Exploratoria/efectos de los fármacos , Miedo/efectos de los fármacos , Hipocampo/metabolismo , Masculino , Memoria/fisiología , Norepinefrina/metabolismo , Ratas , Ratas Wistar , Receptores de Dopamina D1/metabolismoRESUMEN
Here we described two activities related to Women in Science: one main conference and one symposium, both developed during the Annual Congress of the Brazilian Physiological Society, which were held within the XXXIII Annual Meeting of the Federation of Brazilian Experimental Biology Societies, from September 3-6, 2018, in Campos do Jordão (SP/Brazil). This conference and the symposium were among the most popular activities of the congress. This is important because the activities addressed important issues, including the fact that only 29% of the worlds' researchers are women, and women have difficulty progressing in a scientific career. Our report discusses why and which strategies could change this reality. We believe this symposium has not only contributed to advance and bring insights to physiological sciences, but, more importantly, it inspired and motivated physiologists to think about gender balance and the contribution and participation of women in physiological science.
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Selección de Profesión , Congresos como Asunto , Identidad de Género , Fisiología/economía , Fisiología/métodos , Sociedades Científicas , Brasil , Congresos como Asunto/tendencias , Femenino , Humanos , Fisiología/tendencias , Sociedades Científicas/tendenciasRESUMEN
Aerobic exercise induces neuroprotection, but few studies investigated whether strength training has similar potential. Here we examine whether effects of strength training differ from those of running training concerning cognitive symptomatology, oxidative stress and cholinergic status in a model of AD-like cognitive impairment induced by intrahippocampal infusion of a mix of ß-amyloid peptides (Aß) in rats. Male Wistar rats were submitted to 8â¯weeks of running exercise (RunEx; 40â¯min sessions at 70% of indirect VO2 max, 3 times/week) or strength exercise (StrEx; 3 sessions/week, 12 repetitions in 8 sets, 2 sets with repetitions at 50%, 2 at 75%, 2 at 90% and 2 at 100% of the maximum load), followed by Aß infusion in the dorsal hippocampus. Short-term (STM) and long-term (LTM) object recognition (OR) and social recognition (SR) memories were evaluated. Hippocampal oxidative status was determined by quantification of reactive oxygen species, lipid peroxidation by thiobarbituric acid reactive substance test, total antioxidant capacity by ferric reducing/antioxidant power, and acetylcholinesterase enzyme activity (AChE). Aß infusion impaired STM and LTM and resulted in higher hippocampal oxidative damage and impaired AChE activity. StrEx results in better neuroprotection than RunEx by preventing deficits in OR and SR memories, prevents increases in lipid peroxidation, and decreases in AChE activity. RunEx elicits neuroprotection only for SR memory deficits, prevents increase in ROS and lipid peroxidation, and preserves the total antioxidant capacity. While RunEx effects are related to oxidative status, only StrEx shows potential to also influence the cholinergic system.
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Enfermedad de Alzheimer/prevención & control , Memoria/fisiología , Neuroprotección/fisiología , Condicionamiento Físico Animal/fisiología , Entrenamiento de Fuerza , Carrera/fisiología , Acetilcolinesterasa/metabolismo , Enfermedad de Alzheimer/metabolismo , Enfermedad de Alzheimer/patología , Péptidos beta-Amiloides/farmacología , Animales , Modelos Animales de Enfermedad , Conducta Exploratoria/fisiología , Hipocampo/metabolismo , Hipocampo/patología , Masculino , Actividad Motora/fisiología , Estrés Oxidativo/fisiología , Ratas , Ratas Wistar , Especies Reactivas de Oxígeno/metabolismoRESUMEN
Alzheimer's disease (AD) is characterized by the presence of amyloid-ß (Aß), oxidative damage and neuronal degeneration, which, together with other pathological events, promote progressive memory loss and cognitive decline. Non-pharmacological strategies have been study to provide some protection against the development of AD. Considering that physical exercise neuroprotective effects on prevention of cognitive deficits are well elucidate, it is important clarify the effects of cognitive training, and verify if they are similar or comparable to those observed for physical exercise. Here we divided male adult Wistar rats in six groups: control, which rats were not submitted to any intervention; Aß, which rats were submitted to hippocampal infusion of Aß; physical exercise (PE), which rats were submitted to 4 weeks of PE training; PE + Aß, which rats were submitted to 4 weeks of PE training followed by hippocampal infusion of Aß; cognitive exercise (CE), which rats were submitted to 4 weeks of CE training; and, CE + Aß, which rats were submitted to 4 weeks of CE training followed by hippocampal infusion of Aß. Ten days after Aß infusion, short (STM) and long-term (LTM) object recognition memory, as well as hippocampal oxidative stress (ROS levels by DCFH test), lipid peroxidation (TBARS), total antioxidant capacity (FRAP) and hippocampal histology were evaluated. Both PE and CE were effective in protect cognitive function against memory deficits related to Aß neurotoxicity, preventing oxidative stress and damage and hippocampal cellular disorganization. So, cognitive training seems to be as good as physical training in the prevention of memory deficits related to Aß and seems to share some mechanisms of actions, as oxidative stress prevention.
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Enfermedad de Alzheimer/terapia , Cognición/fisiología , Condicionamiento Físico Animal/fisiología , Enfermedad de Alzheimer/patología , Péptidos beta-Amiloides/metabolismo , Animales , Cognición/efectos de los fármacos , Trastornos del Conocimiento/patología , Modelos Animales de Enfermedad , Hipocampo/metabolismo , Peroxidación de Lípido/efectos de los fármacos , Masculino , Aprendizaje por Laberinto/efectos de los fármacos , Trastornos de la Memoria/tratamiento farmacológico , Memoria a Largo Plazo/efectos de los fármacos , Fármacos Neuroprotectores/farmacología , Estrés Oxidativo/efectos de los fármacos , Ratas , Ratas Wistar , Reconocimiento en Psicología/efectos de los fármacosRESUMEN
Aluminum (Al), which is omnipresent in human life, is a potent neurotoxin. Here, we have tested the potential for Egg White Hydrolysate (EWH) to protect against changes in cognitive function in rats exposed to both high and low levels of Al. Indeed, EWH has been previously shown to improve the negative effects induced by chronic exposure to heavy metals. Male Wistar rats received orally: Group 1) Low aluminum level (AlCl3 at a dose of 8.3 mg/kg b.w. during 60 days) with or without EWH treatment (1 g/kg/day); Group 2) High aluminum level (AlCl3 at a dose of 100 mg/kg b.w. during 42 days) with or without EWH treatment (1 g/kg/day). After 60 or 42 days of exposure, rats exposed to Al and EWH did not show memory or cognitive dysfunction as was observed in Al-treated animals. Indeed, co-treatment with EWH prevented catalepsy, hippocampal oxidative stress, cholinergic dysfunction and increased number of activated microglia and COX-2-positive cells induced by Al exposure. Altogether, since hippocampal inflammation and oxidative damage were partially prevented by EWH, our results suggest that it could be used as a protective agent against the detrimental effects of long term exposure to Al.
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Aluminio/toxicidad , Disfunción Cognitiva/inducido químicamente , Disfunción Cognitiva/prevención & control , Clara de Huevo , Alimentos Funcionales , Hidrolisados de Proteína/uso terapéutico , Acetilcolinesterasa/metabolismo , Animales , Antioxidantes/metabolismo , Conducta Animal , Peso Corporal , Ciclooxigenasa 2/metabolismo , Hipocampo/efectos de los fármacos , Hipocampo/metabolismo , Masculino , Memoria a Largo Plazo/efectos de los fármacos , Memoria a Corto Plazo/efectos de los fármacos , Microglía/efectos de los fármacos , Fármacos Neuroprotectores/uso terapéutico , Estrés Oxidativo , Ratas , Ratas Wistar , Especies Reactivas de Oxígeno/metabolismoRESUMEN
Fear generalization is defined as the transferring of fear experienced during a traumatic event to safe conditions resembling or not the traumatic event. It has been related to several psychological disorders. Here we set out to determine whether novelty exposure can be effective to avoid fear generalization. We evaluated the effect of a novelty exposure on fear memory generalization using an aversive memory task, the inhibitory avoidance (IA). Male Wistar rats were trained in IA (day 1) and 24 h after (day 2) they were exposed to a new context similar to the original (modified IA - MIA), with some rats being exposed to a novelty just before the exposure to the MIA, while others were not (controls). On day 3, retention tests for IA and MIA contexts were performed. The control rats generalized the memory, expressing aversive behavioral in both contexts whereas rats exposed to novelty only expressed aversion on IA. Furthermore, both anisomycin, an inhibitor of ribosomal protein synthesis, and rapamycin, an inhibitor of mTOR-mediated protein synthesis, injected in the CA1 region of dorsal hippocampus blocked the novelty effect, promoting memory generalization. We conclude that novelty exposure hinders aversive memory generalization depending on hippocampal protein synthesis.