Effects of vitamin E on lead-induced impairments in hippocampal synaptic plasticity

Salehi, Iraj; Karamian, Ruhollah; Komaki‬, Alireza; Tahmasebi, Lida; Taheri, Masoumeh; Nazari, Masoumeh; Shahidi, Siamak; Sarihi, Abdolrahman

doi:10.1016/j.brainres.2015.10.007

Cited by 39 publications

(10 citation statements)

References 121 publications

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“…These findings agreed with those of previous investigations [ 7 , 35 ]. However, other reports have found that lead exposure has no effect on body weight [ 36 , 37 ]. These discrepancies may be attributed to variations in lead exposure level and duration.…”

Section: Discussionmentioning

confidence: 99%

Alhagi maurorum Ethanolic Extract Rescues Hepato-Neurotoxicity and Neurobehavioral Alterations Induced by Lead in Rats via Abrogating Oxidative Stress and the Caspase-3-Dependent Apoptotic Pathway

et al. 2022

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This work investigated the probable protective effect of an Alhagi maurorum ethanolic extract on the hepatotoxicity and neurotoxicity accompanied by neurobehavioral deficits caused by lead in rats. Rats in four groups were orally administered distilled water, ethanolic extract of A. maurorum (300 mg/kg BW daily), lead (100 mg/kg BW daily for 3 months), and lead + A. maurorum extract. The results demonstrated that lead exposure resulted in elevated locomotor activities and sensorimotor deficits associated with a decrease in brain dopamine levels. Moreover, lead exposure significantly increased liver function markers. In addition, the lead-treated rats exhibited extensive liver and brain histological changes and apoptosis. The lead treatment also triggered oxidative stress, as demonstrated by the increase in malondialdehyde (MDA) concentrations with a remarkable reduction in the activities of antioxidant enzymes, reduced glutathione (GSH) levels, and transcriptional mRNA levels of antioxidant genes in the liver and brain. Nevertheless, co-treatment with the A. maurorum extract significantly ameliorated the lead-induced toxic effects. These findings indicate that the A. maurorum extract has the ability to protect hepatic and brain tissues against lead exposure in rats through the attenuation of apoptosis and oxidative stress.

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Section: Discussionmentioning

confidence: 99%

Alhagi maurorum Ethanolic Extract Rescues Hepato-Neurotoxicity and Neurobehavioral Alterations Induced by Lead in Rats via Abrogating Oxidative Stress and the Caspase-3-Dependent Apoptotic Pathway

et al. 2022

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“…Two small holes were drilled in the skull and the bipolar stimulation and recording electrodes were positioned in the perforant pathway and the dentate gyrus (DG) based on the Paxinos and Watson Atlas [47]. After a steady state was achieved, the stimulation intensity was regulated to evoke approximately 80% of the maximal EPSP response and the slope of the PS amplitude, using high frequency stimuli (HFS) protocols of 400 Hz (10 bursts of 20 stimuli, 0.2 ms stimulus duration, 10 s interburst interval) for 5, 30, and 60 min after HFS [48]. Data were analyzed using Biochart software.…”

Section: Electrophysiologymentioning

confidence: 99%

Different doses of methamphetamine alter long-term potentiation, level of BDNF and neuronal apoptosis in the hippocampus of reinstated rats

et al. 2019

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Methamphetamine (METH) is a psychostimulant. The precise mechanisms of its effects remain unknown and current relapse treatments have low efficacy. However, brain-derived neurotrophic factor (BDNF) and neuronal plasticity are essential contributors, despite paradoxical reports and a lack of comprehensive studies. Therefore, we investigated the effects of different doses of METH on long-term potentiation (LTP), BDNF expression and neuronal apoptosis in the hippocampus of reinstated rats. Rats were injected intraperitoneally with METH (1, 5, or 10 mg/kg) or saline, and trained in a conditioned place preference paradigm. Following implementation of the reinstatement model, electrophysiology, western blotting and TUNEL assay were performed to assess behavior, LTP components, BDNF expression, and neuronal apoptosis, respectively. The results demonstrated that the preference scores, population spike amplitude and BDNF expression markedly decreased in the METH (10 mg/kg) group compared with the other groups. In contrast, METH (5 mg/kg) significantly increased these factors more than the control group. There was no change in variables between METH (1 mg/kg) and the control group. Also, apoptosis of the hippocampus was increased in the METH (10 mg/kg) group compared with the METH (5 mg/kg) group. These results suggest that alterations in synaptic plasticity, expression of BDNF and neuronal apoptosis in the hippocampus has a vital role in the context-induced reinstatement of METH seeking.

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“…Beneficial effects of vitamin E on synaptic plasticity and hippocampus-dependent cognition have been confirmed in various pathological conditions associated with excessive ROS accumulation in the brain, as in rodent models of chronic exposure to neurotoxicant such as lead [135,136] and melamine [137], in rats fed an oxidative, high-fat high-carbohydrate diet [138], in rats exposed to sleep-deprivation [139], chronic stress [140] and traumatic brain injury [141], as well as in rodent models of diabetes [142,143] and Down syndrome [144]. When changes in redox markers were also assessed, vitamin E-induced amelioration in neural plasticity and cognitive abilities was consistently associated with a parallel reduction of brain and circulating markers of oxidative damage [135,138,139,141,143,144], thus suggesting that the radical scavenging properties of vitamin E may play an important role in rescuing neuroplasticity.…”

Section: α-Tocopherol Synaptic Plasticity and Cognitive Functionsmentioning

confidence: 99%

“…When changes in redox markers were also assessed, vitamin E-induced amelioration in neural plasticity and cognitive abilities was consistently associated with a parallel reduction of brain and circulating markers of oxidative damage [135,138,139,141,143,144], thus suggesting that the radical scavenging properties of vitamin E may play an important role in rescuing neuroplasticity.…”

Section: α-Tocopherol Synaptic Plasticity and Cognitive Functionsmentioning

confidence: 99%

α-Tocopherol and Hippocampal Neural Plasticity in Physiological and Pathological Conditions

Ambrogini

Betti

Galati

et al. 2016

IJMS

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Neuroplasticity is an “umbrella term” referring to the complex, multifaceted physiological processes that mediate the ongoing structural and functional modifications occurring, at various time- and size-scales, in the ever-changing immature and adult brain, and that represent the basis for fundamental neurocognitive behavioral functions; in addition, maladaptive neuroplasticity plays a role in the pathophysiology of neuropsychiatric dysfunctions. Experiential cues and several endogenous and exogenous factors can regulate neuroplasticity; among these, vitamin E, and in particular α-tocopherol (α-T), the isoform with highest bioactivity, exerts potent effects on many plasticity-related events in both the physiological and pathological brain. In this review, the role of vitamin E/α-T in regulating diverse aspects of neuroplasticity is analyzed and discussed, focusing on the hippocampus, a brain structure that remains highly plastic throughout the lifespan and is involved in cognitive functions. Vitamin E-mediated influences on hippocampal synaptic plasticity and related cognitive behavior, on post-natal development and adult hippocampal neurogenesis, as well as on cellular and molecular disruptions in kainate-induced temporal seizures are described. Besides underscoring the relevance of its antioxidant properties, non-antioxidant functions of vitamin E/α-T, mainly involving regulation of cell signaling molecules and their target proteins, have been highlighted to help interpret the possible mechanisms underlying the effects on neuroplasticity.

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Effects of vitamin E on lead-induced impairments in hippocampal synaptic plasticity

Cited by 39 publications

References 121 publications

Alhagi maurorum Ethanolic Extract Rescues Hepato-Neurotoxicity and Neurobehavioral Alterations Induced by Lead in Rats via Abrogating Oxidative Stress and the Caspase-3-Dependent Apoptotic Pathway

Alhagi maurorum Ethanolic Extract Rescues Hepato-Neurotoxicity and Neurobehavioral Alterations Induced by Lead in Rats via Abrogating Oxidative Stress and the Caspase-3-Dependent Apoptotic Pathway

Different doses of methamphetamine alter long-term potentiation, level of BDNF and neuronal apoptosis in the hippocampus of reinstated rats

α-Tocopherol and Hippocampal Neural Plasticity in Physiological and Pathological Conditions

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