Distinct acute stressors produce different intensity of anxiety-like behavior and differential glutamate release in zebrafish brain.

Anxiety disorder is one of the most well-characterized behavioral disorders in individuals subjected to acute or chronic stress. However, few studies have demonstrated how different types of stressors can modulate the neurochemical alterations involved in the generation of anxiety. In this study, we hypothesize that subjects exposed to different aversive stimuli (mechanical, chemical, and spatial restriction) present varied intensities of anxiety-like responses associated with distinct patterns of gamma-aminobutyric acid (GABA) and glutamate release in the brain.

Putative Activation of Cannabinoid Receptor Type 1 Prevents Brain Oxidative Stress and Inhibits Aggressive-Like Behavior in Zebrafish.

Aggression is a set of complex behaviors commonly described in different neurological disorders, such as schizophrenia, autistim spectrum disorder, and anxiety. Previous studies have described that some changes in the redox status of the brain are closely associated with aggressive behavior in different species. In addition, the endocannabinoid system acts as a neuromodulator of the central nervous system, however, its participation in aggressive behavior needs to be elucidated.

High performance liquid chromatography-based method to analyze activity of GABA transporters in central nervous system.

The GATs are the membrane proteins responsible for the uptake of GABA in the central nervous system. Alterations in GAT activity are implicated in several neurological diseases, including retinopathies. The present study describes an alternative method to determine GAT activity in tissue preparations of the central nervous system, using high performance liquid chromatography (HPLC) with fluorescence detection.

Euterpe oleracea fruit (Açai)-enriched diet suppresses the development of experimental cerebral malaria induced by Plasmodium berghei (ANKA) infection.

Background: Cerebral malaria is one of the most severe complications attributed to protozoal infection by Plasmodium falciparum, gaining prominence in children mortality rates in endemic areas. This condition has a complex pathogenesis associated with behavioral, cognitive and motor sequels in humans and current antimalarial therapies have shown little effect in those aspects. Natural products with antioxidant and anti-inflammatory properties have become a valuable alternative therapeutic option in the treatment of distinct conditions.

Lead-Induced Motor Dysfunction Is Associated with Oxidative Stress, Proteome Modulation, and Neurodegeneration in Motor Cortex of Rats.

Lead (Pb) is a toxic metal with great neurotoxic potential. The aim of this study was to investigate the effects of a long-term Pb intoxication on the global proteomic profile, oxidative biochemistry and neuronal density in motor cortex of adult rats, and the possible outcomes related to motor functions. For this, Wistar rats received for 55 days a dose of 50 mg/Kg of Pb acetate by intragastric gavage.

Putative Activation of the CB1 Cannabinoid Receptors Prevents Anxiety-Like Behavior, Oxidative Stress, and GABA Decrease in the Brain of Zebrafish Submitted to Acute Restraint Stress.

Anxiety disorder is a well-recognized condition observed in subjects submitted to acute stress. Although the brain mechanisms underlying this disorder remain unclear, the available evidence indicates that oxidative stress and GABAergic dysfunction mediate the generation of stress-induced anxiety. Cannabinoids are known to be efficient modulators of behavior, given that the activation of the cannabinoid receptors type-1 (CB1 receptors) induces anxiolytic-like effects in animal models.

Effects of lead exposure on salivary glands of rats: insights into the oxidative biochemistry and glandular morphology.

This study aimed to investigate the effects of lead (Pb) exposure on parotid and submandibular glands through morphological aspects as well as the systemic and salivary gland redox state. Male Wistar rats were exposed to 50 mg/kg/day of Pb-acetate or distilled water by intragastric gavage for 55 days (n = 40). Blood samples were used for lipid peroxidation (LPO), glutathione (GSH), and trolox equivalent antioxidant capacity (TEAC) assays.

Long-Term Lead Exposure Since Adolescence Causes Proteomic and Morphological Alterations in the Cerebellum Associated with Motor Deficits in Adult Rats.

Lead (Pb) is an environmental contaminant that presents a high risk for human health. We aimed to investigate the possible alterations triggered by the exposure to Pb acetate for a long period in motor performance and the possible relationship with biochemical, proteomic and morphological alterations in the cerebellum of rats. Male Wistar rats were exposed for 55 days, at 50 mg/Kg of Pb acetate, and the control animals received distilled water.

Long-term exposure to lead reduces antioxidant capacity and triggers motor neurons degeneration and demyelination in spinal cord of adult rats.

Lead is a toxic metal found in environment with great neurotoxic potential. The main effect is associated with impairments in hippocampus and cerebellum, driving to cognitive and motor dysfunctions, however, there is a lack of evidences about the effects over the spinal cord. In this way, we aimed to investigate in vivo the effects of long-term exposure to lead acetate in oxidative biochemistry and morphology of rats' spinal cord.

Neurochemical dysfunction in motor cortex and hippocampus impairs the behavioral performance of rats chronically exposed to inorganic mercury.

Chronic exposure to mercury chloride (HgCl) has been shown to promote oxidative stress and cell death in the central nervous system of adult rats displaying motor and cognitive impairments. However, there are no investigations about neurochemical function after this type of exposure in rodents that may be associated with those behavioral changes already reported. Thus, the aim of this study was to analyze glutamatergic and GABAergic dysfunctions in the motor cortex and hippocampus of adult rats, in a model of chronic exposure to HgCl in.

Association between methylmercury environmental exposure and neurological disorders: A systematic review.

The mercury-related central nervous system disorders have been extensively studied on animal models and human beings. However, clinical evidences of which neurological changes are in fact associated with mercury exposure remains controversial. This systematic review (Prospero registration under the number CRD42016041760) aimed to elucidate the association of methylmercury (MeHg) exposure with neurological alteration in populations living in MeHg-endemic risk area.

Proteomic approach underlying the hippocampal neurodegeneration caused by low doses of methylmercury after long-term exposure in adult rats.

Methylmercury (MeHg) is an important toxicant that causes cognitive dysfunctions in humans. This study aimed to investigate the proteomic and biochemical alterations of the hippocampus associated with behavioural consequences of low doses of MeHg in a long-term exposure model, and to realistically mimic in vivo the result of human exposure to this toxicant. Adult Wistar male rats were exposed to a dose of MeHg at 0.

Chronic ethanol forced administration from adolescence to adulthood reduces cell density in the rat spinal cord.

Ethanol (EtOH) consumption is a risk factor for central nervous system damage, especially during adolescence. This study aimed to investigate the possible effects of chronic EtOH forced administration on gray and white matter of the spinal cord, from adolescence to adulthood. For this, male Wistar rats were administered EtOH by gavage (6.

Possible role of serotoninergic system in the neurobehavioral impairment induced by acute methylmercury exposure in zebrafish (Danio rerio).

Adult zebrafish were treated acutely with methylmercury (1.0 or 5.0 μg g(-1), i.