Brain Research最新文献

This study evaluated the influence of maternal consumption of pequi pulp and nuts during pregnancy and lactation on reflex and somatic maturation and memory performance in rat offspring. The pups were divided into three groups: Control, treated with distilled water; a Pulp group and a Nuts group, treated with 2000 mg/kg of body weight of pequi pulp and nuts, respectively. Reflex and somatic maturation of the offspring were evaluated during lactation. Short and long-term memory consolidation in adolescent offspring were measured by evaluating habituation to the open field and object recognition. Data showed an acceleration of reflex maturation in three of the seven parameters evaluated in the Nuts group and four parameters in the Pulp group compared to the control. There was an acceleration in the appearance of somatic maturation in one parameter in the Nuts group and three in the pulp group compared to the control. The long-term object recognition rate was higher in the Nuts group compared to the control and highest in the Pulp group. Maternal levels of malonaldehyde in the brain were measured and their levels in the Pulp and Nuts groups were lower than those in the Control group. We can conclude that consumption of both pulp and pequi nuts promoted a reduction in oxidative stress in the maternal brain, promoted acceleration of reflex and somatic maturation, and improved long-term memory in the offspring, with these effects being more intense in the Pulp group.

Background: Glioma is the most common malignant tumor of the central nervous system, and is characterized by high recurrence, poor prognosis and especially complex pathogenesis. The synaptic plasticity-related protein DLGAP3 is mainly involved in the assembly and function of postsynaptic density complex. It's widely known that DLGAP3 participating in the occurrence of various neuropsychiatric diseases, but its role in glioma tumorigenesis remains largely unclear.

Methods: We ectopically expressed and knocked down DLGAP3 in glioma cells to perform a series of functional studies in vitro. Meanwhile, western blot analysis, co-immunoprecipitation, enrichment analysis and dual-luciferase reporter system assays were performed to explore the mechanism of DLGAP3 suppressing glioma tumorigenesis and progression.

Results: We found that DLGAP3 was low expressed in gliomas, and decreased DLGAP3 expression was strongly correlated with poor survival of glioma patients. Ectopic expression of DLGAP3 in glioma cell lines dramatically inhibited cell proliferation, invasion and migration. In addition, our data also showed that DLGAP3 can tightly connected with RGS12, and DLGAP3 overexpression significantly increased the expression of RGS12 and inhibited the phosphorylation levels of MEK and ERK. Furthermore, the RGS12 inhibited transcription and translation of BRAF, which further decreased the activity of MAPK/ERK signaling pathway. This suggests that DLGAP3 may act as a tumor suppressor in gliomas and inhibits glioma tumorigenesis by regulating RGS12 and the downstream MAPK/ERK signals axis.

Conclusion: Our data indicates that DLGAP3 is a potential tumor suppressor and valuable prognostic biomarker in gliomas.

High-gamma frequency flashes can enhance cognition by synchronizing neural oscillations in mammals. Early flash treatment promotes the development of improved cognitive functions in young children. However, it is unclear whether exposure to high-gamma frequency flashes in preschool-aged individuals affects cognition in preadolescents by regulating neural oscillations in the brain. Here, we aimed to investigate the effects of gamma-frequency flashes on cognitive ability. In this study, the effect of high-frequency flicker on cognitive performance was verified by behavioural experiments such as the open-field test and the water maze, but also proteomics. We found that external 40 Hz and 70 Hz frequency flashes synchronized neural oscillations at the corresponding frequencies in the primary visual cortex (V1) of rats. Rats that underwent 70 Hz flash intervention had better cognitive behavioural performance in the early stages of training. The 70 Hz flash frequency upregulated proteins associated with neuronal growth and differentiation, such as Snapin, FoxO3, Hspa12a, and Penk, and activated the MAPK signalling pathway, signalling pathway regulating stem cell pluripotency, and the neuroactive ligand-receptor interaction pathway. These proteins and pathways play important roles in cognitive functions. Our study revealed that 70 Hz flashes received by young children early in their development substantially promote the growth of cognitive capabilities in the brain. Exposure to 70 Hz flashes may be a new intervention method and a new strategy for improving cognition.

In the context of our previous analyses on the main active ingredients of Jieyudan, a classic formula targeting aphasia in stroke, we further delve into the function and mechanisms of its active ingredient, Diosmin (DM), which may exert neuroprotective effects, in ischemic stroke. Herein, bioinformatics analysis revealed targets of DM and their intersection with differentially expressed genes in ischemic stroke. Middle cerebral artery occlusion (MCAO) rats and oxygen-glucose deprivation (OGD) cells were used to construct in vivo and in vitro models of ischemic stroke. The effects of DM on MCAO rats were assessed by Zea-Longa score, Morris water maze, TTC staining, Nissl staining, immunohistochemistry, and Western blot. At the cellular level, cell counting kit-8 assay and Western blot were carried out to verify the mechanism of DM in ischemic stroke. In vivo, DM decreased neurological deficit score, cerebral infarct volume and neuronal damage, and improved cognitive function in MCAO rats. In vitro, DM increased the viability of OGD-treated cells. In addition, DM down-regulated the expressions of NLR family pyrin domain containing 3 (NLRP3) and pyroptosis-associated proteins, while up-regulating ribosomal protein S6 kinase A3 (RSK2) level and activating cyclic-AMP response element-binding protein (CREB) signaling. Conversely, RSK2 inhibitor LJH685 reduced the viability and promoted pyroptosis-associated protein levels, which also partially reversed the effects of DM in vitro. Collectively, DM plays a therapeutic role in ischemic stroke by inhibiting NLRP3 inflammasome-mediated cellular pyroptosis via the RSK2/CREB pathway.

A high number of COVID-19 patients report ongoing neurological impairments including headache, fatigue and memory impairments. Our understanding of COVID-19 disease mechanisms in the brain is limited and relies on post-mortem human tissues, in vitro studies in various cell lines (both human and animal) as well as preclinical studies in a variety of species. Notably the use of rats in the study of COVID-19 has been scarce in part due to early reports of low infectivity of the original Wuhan strain in mice and rats. Evidence has shown that subsequent strains that have mutated from the original strain and are capable of infection in rats. Here we present an immunohistological characterization of ACE2 expression in the rat brain perivascular region. We found ACE2 to be expressed in pericytes but not endothelial cells or astrocytes in the perivascular space. We further examined the uptake of Omicron variants 1.1.529 and BA.2 receptor binding domains (RBD) of the SARS-CoV2 spike protein in primary brain pericytes derived from rats. We demonstrate that rat primary brain pericytes are susceptible to SARS-CoV2 spike protein uptake and induce functional changes in pericytes associated with a reduction in tight junction protein expression. These data provide evidence that rat primary cell responses to SARS-CoV2 infection are consistent with reports of infectivity in other species (transgenic mice expressing hACE2, ferrets, hamsters) and supports the use of this model organism with a long history of use in the study of disease which should be leveraged for study of COVID-19 in the brain.