Effect of folic acid on oxidative stress and behavioral changes in the animal model of schizophrenia induced by ketamine

Zugno, Alexandra I.; Canever, Lara; Heylmann, Alexandra S.; Wessler, Patricia Gomes; Steckert, Amanda V.; Mastella, Gustavo Antunes; Oliveira, Mariana B.; Damázio, Louyse Sulzbach; Pacheco, Felipe Damázio; Calixto, Octacílio P.; Pereira, Flávio P.; Macan, Tamires Pavei; Pedro, Thayara H.; Schuck, Patrícia Fernanda; Quevedo, João; Budni, Josiane

doi:10.1016/j.jpsychires.2016.06.013

Cited by 28 publications

(15 citation statements)

References 68 publications

(60 reference statements)

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“…A standard paradigm was used to identify impaired social interaction in rats at P30-P32 (Schneider and Przewlocki 2005, Foley et al 2014, Zugno et al 2016). Briefly, one hour prior to testing, each rat was isolated in a clean cage.…”

Section: Methodsmentioning

confidence: 99%

Neonatal erythropoietin mitigates impaired gait, social interaction and diffusion tensor imaging abnormalities in a rat model of prenatal brain injury

Robinson

Corbett

Winer

et al. 2018

Experimental Neurology

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Children who are born preterm are at risk for encephalopathy of prematurity, a leading cause of cerebral palsy, cognitive delay and behavioral disorders. Current interventions are limited and none have been shown to reverse cognitive and behavioral impairments, a primary determinant of poor quality of life for these children. Moreover, the mechanisms of perinatal brain injury that result in functional deficits and imaging abnormalities in the mature brain are poorly defined, limiting the potential to target interventions to those who may benefit most. To determine whether impairments are reversible after a prenatal insult, we investigated a spectrum of functional deficits and diffusion tensor imaging (DTI) abnormalities in young adult animals. We hypothesized that prenatal transient systemic hypoxia-ischemia (TSHI) would induce multiple functional deficits concomitant with reduced microstructural white and gray matter integrity, and tested whether these abnormalities could be ameliorated using postnatal erythropoietin (EPO), an emerging neurorestorative intervention. On embryonic day 18 uterine arteries were transiently occluded for 60min via laparotomy. Shams underwent anesthesia and laparotomy for 60min. Pups were born and TSHI pups were randomized to receive EPO or vehicle via intraperitoneal injection on postnatal days 1 to 5. Gait, social interaction, olfaction and open field testing was performed from postnatal day 25-35 before brains underwent ex vivo DTI to measure fractional anisotropy, axial diffusivity and radial diffusivity. Prenatal TSHI injury causes hyperactivity, impaired gait and poor social interaction in young adult rats that mimic the spectrum of deficits observed in children born preterm. Collectively, these data show for the first time in a model of encephalopathy of prematurity that postnatal EPO treatment mitigates impairments in social interaction, in addition to gait deficits. EPO also normalizes TSHI-induced microstructural abnormalities in fractional anisotropy and radial diffusivity in multiple regions, consistent with improved structural integrity and recovery of myelination. Taken together, these results show behavioral and memory deficits from perinatal brain injury are reversible. Furthermore, resolution of DTI abnormalities may predict responsiveness to emerging interventions, and serve as a biomarker of CNS injury and recovery.

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Section: Methodsmentioning

confidence: 99%

Neonatal erythropoietin mitigates impaired gait, social interaction and diffusion tensor imaging abnormalities in a rat model of prenatal brain injury

Robinson

Corbett

Winer

et al. 2018

Experimental Neurology

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“…Long-lasting social interaction deficits were also described by Qiao et al [65] in mice during withdrawal from chronic PCP treatment (for a review see [66]). Similar to MK-801 and PCP, ketamine was shown to decrease social interaction following both acute [67,68,69,70] and sub-chronic [71,72,73] administration in rats and mice.…”

Section: Role Of the Nmda Receptors In Social Interactionmentioning

confidence: 99%

The Role of the N-Methyl-D-Aspartate Receptors in Social Behavior in Rodents

Zoicas

Kornhuber

2019

IJMS

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The appropriate display of social behaviors is essential for the well-being, reproductive success and survival of an individual. Deficits in social behavior are associated with impaired N-methyl-D-aspartate (NMDA) receptor-mediated neurotransmission. In this review, we describe recent studies using genetically modified mice and pharmacological approaches which link the impaired functioning of the NMDA receptors, especially of the receptor subunits GluN1, GluN2A and GluN2B, to abnormal social behavior. This abnormal social behavior is expressed as impaired social interaction and communication, deficits in social memory, deficits in sexual and maternal behavior, as well as abnormal or heightened aggression. We also describe the positive effects of pharmacological stimulation of the NMDA receptors on these social deficits. Indeed, pharmacological stimulation of the glycine-binding site either by direct stimulation or by elevating the synaptic glycine levels represents a promising strategy for the normalization of genetically-induced, pharmacologically-induced or innate deficits in social behavior. We emphasize on the importance of future studies investigating the role of subunit-selective NMDA receptor ligands on different types of social behavior to provide a better understanding of the underlying mechanisms, which might support the development of selective tools for the optimized treatment of disorders associated with social deficits.

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“…Schizophrenia is a severe mental disorder characterized by frequent relapses, cognitive impairment [ 30 , 31 , 32 ], and emotional and functional disability [ 33 , 34 , 35 ]. Compared to healthy controls, patients with schizophrenia have lower total brain, gray matter, and white matter volumes and densities; on the other hand, schizophrenia patients have significantly higher third and lateral ventricle volumes [ 36 , 37 ].…”

Section: Schizophreniamentioning

confidence: 99%

Regulation of Reactive Oxygen Species-Mediated Damage in the Pathogenesis of Schizophrenia

Madireddy

2020

Brain Sciences

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The biochemical integrity of the brain is paramount to the function of the central nervous system, and oxidative stress is a key contributor to cerebral biochemical impairment. Oxidative stress, which occurs when an imbalance arises between the production of reactive oxygen species (ROS) and the efficacy of the antioxidant defense mechanism, is believed to play a role in the pathophysiology of various brain disorders. One such disorder, schizophrenia, not only causes lifelong disability but also induces severe emotional distress; however, because of its onset in early adolescence or adulthood and its progressive development, consuming natural antioxidant products may help regulate the pathogenesis of schizophrenia. Therefore, elucidating the functions of ROS and dietary antioxidants in the pathogenesis of schizophrenia could help formulate improved therapeutic strategies for its prevention and treatment. This review focuses specifically on the roles of ROS and oxidative damage in the pathophysiology of schizophrenia, as well as the effects of nutrition, antipsychotic use, cognitive therapies, and quality of life on patients with schizophrenia. By improving our understanding of the effects of various nutrients on schizophrenia, it may become possible to develop nutritional strategies and supplements to treat the disorder, alleviate its symptoms, and facilitate long-term recovery.

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Effect of folic acid on oxidative stress and behavioral changes in the animal model of schizophrenia induced by ketamine

Cited by 28 publications

References 68 publications

Neonatal erythropoietin mitigates impaired gait, social interaction and diffusion tensor imaging abnormalities in a rat model of prenatal brain injury

Neonatal erythropoietin mitigates impaired gait, social interaction and diffusion tensor imaging abnormalities in a rat model of prenatal brain injury

The Role of the N-Methyl-D-Aspartate Receptors in Social Behavior in Rodents

Regulation of Reactive Oxygen Species-Mediated Damage in the Pathogenesis of Schizophrenia

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