Acute physical exercise prevents memory amnesia caused by protein synthesis inhibition in rats' hippocampus.

The benefits of physical exercise (PE) on memory consolidation have been well-documented in both healthy and memory-impaired animals. However, the underlying mechanisms through which PE exerts these effects are still unclear. In this study, we aimed to investigate the role of hippocampal protein synthesis in memory modulation by acute PE in rats. After novel object recognition (NOR) training, rats were subjected to a 30-min moderate-intensity acute PE on the treadmill, while control animals did not undergo any procedures. Using anisomycin (ANI) and rapamycin (RAPA), compounds that inhibit protein synthesis through different mechanisms, we manipulated protein synthesis in the CA1 region of the hippocampus to examine its contribution to memory consolidation. Memory was assessed on days 1, 7, and 14 post-training. Our results showed that inhibiting protein synthesis by ANI or RAPA impaired NOR memory consolidation in control animals. However, acute PE prevented this impairment without affecting memory persistence. We also evaluated brain-derived neurotrophic factor (BDNF) levels after acute PE at 0.5h, 2h, and 12h afterward and found no differences in levels compared to animals that did not engage in acute PE or were only habituated to the treadmill. Therefore, our findings suggest that acute PE could serve as a non-pharmacological intervention to enhance memory consolidation and prevent memory loss in conditions associated with hippocampal protein synthesis inhibition. This mechanism appears not to depend on BDNF synthesis in the early hours after exercise.

Acute physical exercise enhances memory persistence in female rats.

Memory is a complex cognitive process with distinct stages, such as acquisition, consolidation, and retrieval. The hippocampus plays a crucial role in memory consolidation and retrieval. Physical exercise (PE) has been shown to enhance memory and cognitive functions, but the available research is mainly developed with males. So, there is limited knowledge about acute PE's effects on females' memory. This study aimed to investigate the impact of acute PE on memory in female rats and explore potential sex differences in PE memory modulation. Forty-two female Wistar rats were subjected to a novel object recognition (NOR) task, with half of them undergoing a single session of 30 min of PE after the learning session (memory acquisition). Behavioral assessments showed that acute PE improved memory persistence in female rats, with increased discrimination of novel objects. Biochemical analysis revealed elevated noradrenaline levels in the hippocampus following acute PE and NOR training. Notably, the positive effects of acute PE on female rats' memory were similar to those previously observed in male rats. These findings suggest that acute PE can enhance memory in female rats and underscore the importance of considering sex differences in cognitive research. PE may offer a non-invasive strategy to promote cognitive health in both males and females.

Acute physical exercise improves recognition memory via locus coeruleus activation but not via ventral tegmental area activation.

Both animals and humans have been studied to explore the impact of acute physical exercise (PE) on memory. In rats, a single session of PE enhances the persistence of novel object recognition (NOR) memory, which depends on dopamine and noradrenaline activity in the hippocampus. However, limited research has examined the involvement of other brain regions in this phenomenon. In this study, we investigated the role of the ventral tegmental area (VTA) and locus coeruleus (LC) in modulating the persistence of NOR memory induced by acute PE. After NOR training, some animals underwent a 30 min treadmill PE session, followed by infusion of either vehicle (VEH) or muscimol (MUS) in either the VTA or LC. Other animals did not undergo PE and only received VEH, MUS, or NMDA within the same time window. We evaluated memory recall 1, 7, and 14 days later. Acute PE promoted memory persistence for up to 14 days afterward, similar to NMDA glutamatergic stimulation of the VTA or LC. Moreover, only the LC region was required for the memory improvement induced by acute PE since blocking this region with MUS impaired NOR encoding. Our findings suggest that acute PE can improve learning within a closed time window, and this effect depends on LC, but not VTA, activity.

Novelty facilitates the persistence of aversive memory extinction by dopamine regulation in the hippocampus and ventral tegmental area.

Aversive memory extinction comprises a novel learning that blocks retrieving a previously formed traumatic memory. In this sense, aversive memory extinction is an excellent tool for decreasing fear responses. However, this tool it's not effective in the long term because of original memory spontaneous recovery. Thus, searching for alternative strategies that strengthen extinction learning is essential. In the current study, we evaluated the effects of a novel context (i.e., novelty) exposure on aversive memory extinction enhancement over days and the dopaminergic system requirement. Given the purpose, experiments were conducted using 3-month-old male Wistar rats. Animals were trained in inhibitory avoidance (IA). Twenty-four hours later, rats were submitted to a weak extinction protocol. Still, 30 min before the first extinction session, animals were submitted to an exploration of a novel context for 5 min. After, memory retention and persistence were evaluated 24 h, 3, 7, 14, and 21 days later. The exposition of a novel context caused a decrease in aversive responses in all days analyzed and an increase in dopamine levels in the hippocampus. The intrahippocampal infusion of dopamine in the CA1 area or the stimulation of the ventral tegmental area (VTA) by a glutamatergic agonist (NMDA) showed similar effects of novelty. In contrast, VTA inhibition by a gabaergic agonist (muscimol) impaired the persistence of extinction learning induced by novelty exposition and caused a decrease in hippocampal dopamine levels. In summary, we show that novel context exposure promotes persistent aversive memory extinction, revealing the significant role of the dopaminergic system.

Starting maternal exercise, unlike reducing the intensity of exercise during pregnancy, prevents memory deficits in female offspring subject to maternal deprivation.

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.

Neuroprotective effects of strength training in a neuroinflammatory animal model.

BACKGROUND: The preventive role of muscular strength on diminishing neuroinflammation is yet unknown. In this study, the role of the prophylactic muscular strength exercise was investigated in order to verify whether it would diminish cognitive alterations and modify the antioxidant intracellular scenery in an animal neuroinflammatory model in of the CA1 region of the hippocampus. METHODS: The animals received muscular strength training (SE) three times a week for eight weeks. Subsequently, the stereotaxic surgery was performed with an intra-hippocampal infusion of either saline solution (SAL) or lipopolysaccharide (LPS). Next, we performed the behavioral tests: object recognition and social recognition. Then, the animals were euthanized, and their hippocampus and prefrontal cortex were collected. In another moment, we performed the dosage of the antioxidant activity and histological analysis. RESULTS: The results showed that the muscular strength exercises could show a beneficial prophylactic effect in the cognitive deficiencies caused by acute neuroinflammation. Regarding oxidative stress, there was an increase in catalase enzyme activity (CAT) in the group (SE + LPS) compared to the control groups (p < 0.05). As for the cognitive alterations, there were found in the (SE + LPS) group, diminishing the mnemonic hazard of the discriminative and social memories compared to the control groups (p < 0.05). CONCLUSION: We concluded, therefore, that the exercise performed prophylactically presents a protective effect capable of minimizing such mnemonic deficits and increasing catalase enzyme activity in rats that suffered a local neuroinflammatory process in the hippocampus.

Concurrent exercise does not prevent recognition memory deficits induced by beta-amyloid in rats.

Alzheimer's disease affects thousands of people worldwide. Alternatives aiming to prevent the disease or reduce its symptoms include different physical exercise configurations. Here we investigate the potential of concurrent exercise to prevent recognition memory deficits in an Alzheimer's disease-like model induced by the hippocampal beta-amyloid (Aß) injection in Wistar rats. We demonstrate that the concurrent exercise, which included running and strength exercises performed in the same exercise session, is ineffective in preventing recognition memory deficits in the Aß rats. Besides, higher levels of reactive oxygen species were found in the concurrent exercise group's hippocampus. The running exercise administrated alone prevented recognition memory impairments.

Novelty promotes recognition memory persistence by D1 dopamine receptor and protein kinase A signalling in rat hippocampus.

Strategies for improving memory are increasingly studied, and exposure to a novel experience can be an efficient neuromodulator. Novelty effects on memory depend on D1-family dopamine receptors (D1Rs) activation. Here, we evaluated the novelty effect on memory persistence of Wistar rats and investigated the contribution of D1Rs and their signalling pathways by protein kinase A (PKA) and C (PKC). Animals with infusion cannulae inserted into the CA1 hippocampus area were trained on the novel object recognition (NOR) task, which involved exploring two different objects. After training, some rats received intrahippocampal infusions of vehicle or D1Rs agonist; others explored a novel environment for 5 min and were infused with a variety of drugs targeting D1Rs and their signalling pathways. We demonstrated that pharmacological stimulation of D1Rs or novelty exposure promoted NOR memory persistence for 14 days and that the novelty effect depended on D1Rs activation. To determine if the D1 and D5 receptor subtypes were necessary for the impact of novelty exposure on memory, we blocked or stimulated PKA or PKC-protein kinases activated mainly by D1 and D5, respectively. Only PKA inhibition impaired the effect of novelty on memory persistence. After novelty and D1Rs blocking, PKA but not PKC stimulation maintained the memory persistence effect. Thus, we concluded that novelty promoted memory persistence by a mechanism-dependent on activating hippocampal D1Rs and PKA pathway.

Report on the online course "Basic Concepts in Neurophysiology": a course promoted during the COVID-19 pandemic quarantine.

"Basic Concepts in Neurophysiology" was a 3-wk online course developed during six synchronous meetings combined with asynchronous activities. We proposed an active learning course that used free online platforms to teach physiology during a period in which undergraduates were not in classrooms or taking online classes due to the COVID-19 pandemic. Herein, we report the course organization and the students' involvement in, acceptance of, and evaluation of the course. To address the students' perceptions about these points, we sent a questionnaire to 49 participants who finished the course. We found that although most students (52.5%) had never taken a course with similar methods before, almost all of them (95%) liked the flipped class model. Additionally, a majority of the students (92.5%) said that the method increased their study frequency during the social distancing period, which is an important aspect to consider during this challenging time for both students and professors.

Infralimbic and prelimbic prefrontal cortex activation is necessary to the enhancement of aversive memory extinction promoted by reactivation.

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.

Multicomponent Training Prevents Memory Deficit Related to Amyloid-ß Protein-Induced Neurotoxicity.

BACKGROUND: Alzheimer's disease (AD) is characterized by the accumulation of the amyloid-ß peptide in the brain, leading to early oxidative stress and neurotoxicity. It has been suggested that physical exercise could be beneficial in preventing AD, but studies with multicomponent training are scanty. OBJECTIVE: Verify the effects of multicomponent exercise training to prevent deficits in recognition memory related to Aß neurotoxicity. METHODS: We subjected Wistar rats to multicomponent training (including aerobic and anaerobic physical exercise and cognitive exercise) and then infused amyloid-ß peptide into their hippocampus. RESULTS: We show that long-term multicomponent training prevents the amyloid-ß-associated neurotoxicity in the hippocampus. It reduces hippocampal lipid peroxidation, restores antioxidant capacity, and increases glutathione levels, finally preventing recognition memory deficits. CONCLUSION: Multicomponent training avoids memory deficits related to amyloid-ß neurotoxicity on an animal model.

Student assessment of online tools to foster engagement during the COVID-19 quarantine.

As a result of the installation of the COVID-19 (coronavirus disease 19) pandemic, online education has become an important teaching alternative, and new challenges about how to teach were found. Here we report our experience in offering an online course to review Human Physiology. We proposed synchronous and asynchronous activities using different online tools to address topics considered key to understanding the different systems of human physiology. The students considered important the use of this type of methodology, which uses different online tools to help understand the Human Physiology contents. The students highlighted the use of the Lt platform, Zoom, Mentimeter, and YouTube as the preferred online tools to use in physiology learning.

Noradrenergic and dopaminergic involvement in novelty modulation of aversive memory generalization of adult rats.

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, 300-400 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) antagonist + 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.