Although numerous studies have indicated that chronic stress causes cognitive dysfunction with the impairment of synaptic structures and functions, the relationship between cognitive deficits induced by repeated restraint stress and the level of NMDA receptors in the subregion of the hippocampus has been relatively unknown until now. In this study, 3-week-old male Sprague-Dawley rats were exposed to repeated restraint stress for seven consecutive days, their cognitive functions were evaluated through behavioral tests, and then they were sacrificed for electrophysiological, morphological, and biochemical assays. Chronic repeated restraint stress led to cognitive and electrophysiological impairments, with a reduced density of dendritic spines. We also found that the protein level of NMDA receptors only increased in the hippocampal CA3 region. Nevertheless, repeated restraint stress-induced cognitive and synaptic dysfunction were effectively reversed by Ro25-6981, an inhibitor of the GluN2B receptor. These findings suggest that repeated restraint stress-induced synaptic and cognitive deficits are probably mediated through NMDA receptors.

/pdf/repeated-restraint-stress-led-to-cognitive-dysfunction-by-2bdz7m2cvh.pdf

Repeated Restraint Stress Led to Cognitive Dysfunction by NMDA Receptor-Mediated Hippocampal CA3 Dendritic Spine Impairments in Juvenile Sprague-Dawley Rats.

L-glutamate (L-Glu) is a nonessential amino acid, but an extensively utilised excitatory neurotransmitter with critical roles in normal brain function. Aberrant accumulation of L-Glu has been linked to neurotoxicity and neurodegeneration. To investigate this further, we systematically reviewed the literature to evaluate the effects of L-Glu on neuronal viability linked to the pathogenesis and/or progression of neurodegenerative diseases (NDDs). A search in PubMed, Medline, Embase, and Web of Science Core Collection was conducted to retrieve studies that investigated an association between L-Glu and pathology for five NDDs: Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), and Huntington’s disease (HD). Together, 4060 studies were identified, of which 71 met eligibility criteria. Despite several inadequacies, including small sample size, employment of supraphysiological concentrations, and a range of administration routes, it was concluded that exposure to L-Glu in vitro or in vivo has multiple pathogenic mechanisms that influence neuronal viability. These mechanisms include oxidative stress, reduced antioxidant defence, neuroinflammation, altered neurotransmitter levels, protein accumulations, excitotoxicity, mitochondrial dysfunction, intracellular calcium level changes, and effects on neuronal histology, cognitive function, and animal behaviour. This implies that clinical and epidemiological studies are required to assess the potential neuronal harm arising from excessive intake of exogenous L-Glu.

/pdf/is-l-glutamate-toxic-to-neurons-and-thereby-contributes-to-30go0ib5.pdf

Is L-Glutamate Toxic to Neurons and Thereby Contributes to Neuronal Loss and Neurodegeneration? A Systematic Review

The growing consumption of ultra-processed foods and beverages has drawn attention to the use of different food additives in these products. The use of these additives for different purposes in food products is permitted under specific legislation. The objective of the present study was to assess the distribution and patterns of occurrence of the different categories of food additives present in packaged foods and beverages sold in Brazil. A descriptive cross-sectional study was conducted based on data from lists of ingredients used in foods and beverages sold in supermarkets in Brazil, collected by photographing product labels. The number, technological purpose and proportion of food additives in 9856 items (25 groups) were assessed. Exploratory factor analysis was employed to derive the patterns of food additive categories. Linear regression models were used to assess the association between the patterns and food items analyzed. Only 20.6% of the products analyzed contained no food additives, while 24.8% contained ≥6 additives. The use of food additives was high, particularly cosmetic additives, predominantly flavoring agents, colorings and stabilizers. Five patterns of food additive categories were identified and associated with ultra-processed foods and beverages. The results revealed that food additives are highly prevalent in several types of food items sold in the Brazilian market. Also, the same additive category was common to several different food groups, as were specific food additive combinations. This exposure is potentially harmful to human health, given the known deleterious effects associated with the consumption of these substances.

/pdf/distribution-and-patterns-of-use-of-food-additives-in-foods-dpspzkn4d2.pdf

Distribution and patterns of use of food additives in foods and beverages available in Brazilian supermarkets.

Psychiatric diseases and metabolic disorders frequently cooccur, yet the mechanisms underlying this interaction remain unknown. The aim of this study was to determine the role of glucocorticoid receptor (GR) phosphorylation in the comorbidity of metabolic and psychiatric disorders. Neonatal Sprague-Dawley rats were subcutaneously injected with monosodium glutamate (MSG) every 2 days for 10 days after birth. Metabolic and behavioral tests were performed 12 weeks later. Golgi staining and transmission electron microscopy (TEM) were performed to evaluate synaptic structural plasticity. Changes in GR phosphorylation and the BDNF/TrkB pathway were evaluated by western blotting and immunofluorescence. We found that MSG-treated rats displayed significant metabolic abnormalities accompanied by anxiogenic and depressive behaviors, an altered synaptic ultrastructure and the loss of dendritic spines. The expression of phosphorylated GR was reduced in the brain. Furthermore, a specific agonist of BDNF/TrkB significantly reversed the reduction in GR phosphorylation, as well as the metabolic and behavioral outcomes. These findings indicate that a decrease in BDNF/TrkB pathway–dependent GR phosphorylation is a long-term effect of MSG treatment that may contribute to metabolic and behavioral disturbances.

Role of glucocorticoid receptor phosphorylation-mediated synaptic plasticity in anxiogenic and depressive behaviors induced by monosodium glutamate

Although monosodium glutamate (MSG)-induced neurotoxicity has been recognized for decades, the potential similarities of the MSG model to Alzheimer’s disease (AD)-type neuropathology have only recently been investigated. MSG-treated mice were examined behaviourally and histologically in relation to some features of AD. Four-week old mice received 5 subcutaneous MSG (2 g/kg) injections on alternate days, or saline. At age 10–12 weeks, they were given a battery of behavioural tests for species-typical behaviours and working memory. The mice were killed at 12 weeks and the brains excised. Accumulation of hyperphosphorylated tau protein was assessed in cortical and hippocampal neurons by immunohistochemistry, and in cerebral cortical homogenates. A 78% increase in cortical concentrations of phosphorylated tau protein was observed in the MSG mice. Intracellular hyperphosphorylated tau immunostaining was observed diffusely in the cortex and hippocampus, together with cortical atrophic neurons, extensive vacuolation and dysmorphic neuropil suggestive of spongiform neurodegeneration. Nest-building was significantly impaired, and spontaneous T-maze alternation was reduced, suggesting defective short-term working memory. Subcutaneous MSG treatment also induced a 56% reduction in exploratory head dips in a holeboard (P = 0.009), and a non-significant tendency for decreased burrowing behaviour (P = 0.085). These effects occurred in the absence of MSG-induced obesity or gross locomotor deficits. The findings point to subcutaneous MSG administration in early life as a cause of tau pathology and compromised species-typical behaviour in rodents. Determining whether MSG can be useful in modelling AD requires further studies of longer duration and full behavioural characterization.

/pdf/cortical-tau-burden-and-behavioural-dysfunctions-in-mice-2st4xkzk5g.pdf

Cortical tau burden and behavioural dysfunctions in mice exposed to monosodium glutamate in early life

Monosodium glutamate exposure during the neonatal period leads to cognitive deficits in adult Sprague-Dawley rats

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Monosodium glutamate exposure during the neonatal period leads to cognitive deficits in adult Sprague-Dawley rats