Exposure to electromagnetic fields can affect human health, damaging tissues and cell homeostasis. Stress modulates neuronal responses and composition of brain lipids. The aim of this study was to evaluate the effects of chronic extremely low frequency electromagnetic field (ELF-EMF) exposure, restraint stress (RS) or both (RS + ELF-EMF) on lipid profile and lipid peroxidation in Wistar rat brain. Twenty-four young male Wistar rats were allocated into four groups: control, RS, ELF-EMF exposure, and RS + ELF-EMF for 21 days. After treatment, rats were euthanized, the blood was obtained for quantitate plasma corticosterone concentration and their brains were dissected in cortex, cerebellum and subcortical structures for cholesterol, triacylglycerols, total free fatty acids, and thiobarbituric acid reactive substances (TBARS) analysis. In addition, fatty acid methyl esters (FAMEs) were identified by gas chromatography. Increased values of plasma corticosterone were found in RS and ELF-EMF exposed groups (p < 0.05), this effect was higher in RS + ELF-EMF group (p < 0.05, vs. control group). Chronic ELF-EMF exposure increased total lipids in cerebellum, and total cholesterol in cortex, but decreased polar lipids in cortex. In subcortical structures, increased concentrations of non-esterified fatty acids were observed in RS + ELF-EMF group. FAMEs analysis revealed a decrease of polyunsaturated fatty acids of cerebellum and increases of subcortical structures in the ELF-EMF exposed rats. TBARS concentration in lipids was increased in all treated groups compared to control group, particularly in cortex and cerebellum regions. These findings suggest that chronic exposure to ELF-EMF is similar to physiological stress, and induce changes on brain lipid profile.

Human embryonic stem cells (hESCs) differentiate into specialized cells, including midbrain dopaminergic neurons (DANs), and Non-human primates (NHPs) injected with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine develop some alterations observed in Parkinson’s disease (PD) patients. Here, we obtained well-characterized DANs from hESCs and transplanted them into two parkinsonian monkeys to assess their behavioral and imaging changes. DANs from hESCs expressed dopaminergic markers, generated action potentials, and released dopamine (DA) in vitro. These neurons were transplanted bilaterally into the putamen of parkinsonian NHPs, and using magnetic resonance imaging techniques, we calculated the fractional anisotropy (FA) and mean diffusivity (MD), both employed for the first time for these purposes, to detect in vivo axonal and cellular density changes in the brain. Likewise, positron-emission tomography scans were performed to evaluate grafted DANs. Histological analyses identified grafted DANs, which were quantified stereologically. After grafting, animals showed signs of partially improved motor behavior in some of the HALLWAY motor tasks. Improvement in motor evaluations was inversely correlated with increases in bilateral FA. MD did not correlate with behavior but presented a negative correlation with FA. We also found higher 11C-DTBZ binding in positron-emission tomography scans associated with grafts. Higher DA levels measured by microdialysis after stimulation with a high-potassium solution or amphetamine were present in grafted animals after ten months, which has not been previously reported. Postmortem analysis of NHP brains showed that transplanted DANs survived in the putamen long-term, without developing tumors, in immunosuppressed animals. Although these results need to be confirmed with larger groups of NHPs, our molecular, behavioral, biochemical, and imaging findings support the integration and survival of human DANs in this pre-clinical PD model.

Background: There has been an increasing interest in researching on the effects of extremely low-frequency magnetic fields on living systems. The mechanism of action of extremely low-frequency magnetic fields on organisms has not been established. One of the hypotheses is related to induce changes in oxidative balance. In this study, we measured the effects of chronic unpredictable mild stress induced-oxidative balance of rat’s brain exposed to extremely low-frequency magnetic fields. Methods: A first experiment was conducted to find out if 14 days of chronic unpredictable mild stress caused oxidative unbalance in male Wistar rat’s brain. Catalase activity, reduced glutathione concentration, and lipoperoxidation were measured in cerebrum and cerebellum. In the second experiment, we investigate the effects of 7 days extremely low-frequency magnetic fields exposure on animals stressed and unstressed. Results: The main results obtained were a significant increase in the catalase activity and reduced glutathione concentration on the cerebrum of animals where the chronic unpredictable mild stress were suspended at day 14 and then exposed 7 days to extremely low-frequency magnetic fields. Interestingly, the same treatment decreases the lipoperoxidation in the cerebrum. The stressed animals that received concomitant extremely low frequency magnetic fields exposure showed an oxidative status like stressed animals by 21 days. Thus, no changes were observed on the chronic unpredictable mild stress induced-oxidative damage in the rat’s cerebrum by the extremely low-frequency magnetic field exposure together with chronic unpredictable mild stress. Conclusions: The extremely low-frequency electromagnetic field exposure can partially restore the cerebrum antioxidant system of previously stressed animals.

Obesity affects one in eight individuals globally. Overeating, especially high-calorie foods, plays a significant role in obesity. Binge eating disorder (BED) is a complex condition caused by a combination of biological, psychological, and social factors. It involves excessive consumption of high-calorie foods in a short period and is often linked to anxiety and cravings. Here, we present a protocol employing continuous and intermittent access to a new highly palatable food (HPF) -- M&M's -- to develop a mouse model for investigating binge eating disorder (BED). The HPF, chosen for its high fat and sugar content, represents an optimal food source to study due to its strong palatability, which makes it particularly suited for examining compulsive eating behaviors. Using C57BL/6 mice, we provided continuous or intermittent access to M&M's while allowing unrestricted access to standard chow and water. By the 8th day, the mice in the intermittent access group exhibited pronounced binge-eating behaviors, which persisted through the 26th day. These mice also consumed significantly more calories -- predominantly from the confectionary -- than those in the continuous access and control groups. The contrast between continuous and intermittent access underscores the critical role of feeding schedules in promoting the overconsumption of palatable foods. Furthermore, behavioral assessments revealed intermittent access to the HPF-induced anxiety-like behaviors, highlighting the psychological impact of access patterns on both eating behavior and emotional states. By incorporating these two distinct feeding paradigms, this study offers valuable insights into how the availability of highly palatable foods can exacerbate binge-eating tendencies. This model provides a more realistic approach to studying binge-eating behaviors and their metabolic consequences. It highlights the importance of standardized models in biomedical research. Our findings offer insights into the physiological and neural mechanisms underlying BED, which could pave the way for developing effective therapeutic interventions for BED and obesity.

Major Depressive Disorder (MDD) is a prevalent chronic mental illness worldwide. Antidepressants are a fundamental part of their treatment, being effective in 60-70 % of patients. Alternative therapies, such as repetitive transcranial magnetic stimulation (rTMS), have also been proposed for modulating cortical neuronal activity and activating circuits associated with the stimulated area. Dopamine is one of the principal neurotransmitters in the nigrostriatal pathway. Changes in dopaminergic transmission through the mesolimbic pathway have been identified as part of the pathophysiology of depression; however, there are only a small number of studies examining the relationship between the nigrostriatal pathway and depression. This study aims to describe the effect of rTMS on the dorsal striatum and prefrontal cortex in a rat model of depression. Behaviors associated with the developed depression and anxiety were assessed through a test battery consisting of sucrose preference, forced swimming, open field, and elevated plus maze.The10 Hz rTMS was applied daily for 15 days, and behavioral tests were re-evaluated. The brains were obtained and analyzed through immunofluorescence labeling of tyrosine hydroxylase and dopamine D2 receptors. It was observed that rTMS reduces depression-like behaviors.Dopamine D2 receptor density decreased in the dorsal striatum and prefrontal cortex of rats that received treatment compared to those with sham stimulation and untreated animals. These results indicate that rTMS affects not only the stimulated region but also influences the dorsal striatum. This finding might contribute to improving the anti-depressive behavior observed in the chronic unpredictable mild stress rat model.

Autism spectrum disorder (ASD) is associated with atypical brain network organization. Functional connectivity has been extensively studied using fMRI, which often reports reduced long-range connectivity alongside local hyperconnectivity. However, BOLD-based connectivity reflects neurovascular coupling and therefore provides an indirect estimate of neuronal activity. Complementary information may be obtained from [ ¹⁸ F]FDG microPET, which quantifies regional glucose uptake—an index of synaptic energy demand integrated over minutes—although FDG-derived network organization has been scarcely examined in ASD. Here, “metabolic connectivity” refers to between-subject covariance in regional [ ¹⁸ F]FDG uptake (group-level metabolic covariance networks), not within-subject temporal coupling as in BOLD-fMRI functional connectivity. We tested whether the C58/J mouse strain—an ASD-relevant model with social deficits and repetitive behaviors—recapitulates ASD-relevant metabolic network-level alterations. Using [ ¹⁸ F]FDG microPET, we constructed ROI-wise metabolic covariance networks by correlating uptake values across animals and compared C58/J mice with C57BL/6 controls. The C58/J network exhibited higher clustering and a more locally cohesive organization than the C57BL/6 network. Nodal degree/edge density was reduced in the olfactory bulb, hippocampus, and hypothalamus. In contrast, the motor-related regions—including the striatum, brainstem, and superior and inferior colliculi—showed a higher degree/denser covariance. These findings suggest that C58/J mice display FDG-derived metabolic covariance network features qualitatively consistent with those reported in ASD FDG-PET studies, supporting this strain as a tool to investigate ASD-relevant pathophysiological mechanisms and to evaluate candidate interventions.