The combined effects of developmental lead and ethanol exposure on hippocampus dependent spatial learning and memory in rats: Role of oxidative stress

Soleimani, Elham; Goudarzi, Iran; Abrari, Kataneh; Lashkarbolouki, Taghi

doi:10.1016/j.fct.2016.07.009

Cited by 33 publications

(15 citation statements)

References 69 publications

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“…These data verified the harmful impact of maternal HSD on offspring brain functions, which could persist into adulthood, was similar to adverse environments and psychological stress during pregnancy 33 . It also confirmed by the studies that showed the alteration of gene expression, oxidative level, or neurotransmitter contents in the hippocampus after diet treatment contributed to the cognitive deficits in adult offspring 33,35 …”

Section: Discussionsupporting

confidence: 75%

“…33 It also confirmed by the studies that showed the alteration of gene expression, oxidative level, or neurotransmitter contents in the hippocampus after diet treatment contributed to the cognitive deficits in adult offspring. 33,35 Synaptic dysfunction, such as abnormal synaptic transmission and/or plasticity in hippocampus, 36 leads to cognitive deficits. In the current study, we used I-O curves to evaluate the basic transmission level of projections from CA3 to CA1 and revealed a significant attenuation in the HSD group.…”

Section: Discussionmentioning

confidence: 99%

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Maternal high‐salt diet during pregnancy impairs synaptic plasticity and memory in offspring

et al. 2021

The FASEB Journal

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Sodium chloride is a major source of salt in human nutrition. It is well-known that long-term high-salt diet (HSD) was associated with the development of hypertension and cardiovascular disease, especially when sodium intake exceeds 5 g/day. 1 There is an emerging evidence that the consumptions of dietary sodium are usually excess of requirements in the form of salt in many countries among adults and childrens, and then, leading to the excess weight gain. 2 Strikingly, both experimental data from animal and epidemiological data from clinical investigations in human being demonstrated that long-term HSD may cause cognitive dysfunction and brain tissue damage in adult individuals. 3,4 Data from rodents reported that HSD impaired cognitive function without changing blood pressure. 5,6 Furthermore, HSD disturbed the short-and long-term memory of mouse with corresponding increases in hippocampal oxidative stress and deregulation of synaptic protein/neurotrophin. 6 The importance of adequate maternal nutrition during the development for offspring's long-term physical health has

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Section: Discussionsupporting

confidence: 75%

Section: Discussionmentioning

confidence: 99%

Maternal high‐salt diet during pregnancy impairs synaptic plasticity and memory in offspring

et al. 2021

The FASEB Journal

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“…Another important aspect of teratogens is their ability to act synergistically with other compound at lower doses. One example is the case of alcohol and lead exposure during pregnancy, which can cause an exacerbated effect on spatial learning and memory in newborn rats (Soleimani, Goudarzi, Abrari, Lashkarbolouki, & Toxicology, ).…”

Section: Chemical Agentsmentioning

confidence: 99%

The role of teratogens in neural crest development

Cerrizuela

Vega-Lopez

Aybar

2020

Birth Defects Research

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The neural crest (NC), discovered by Wilhelm His 150 years ago, gives rise to a multipotent migratory embryonic cell population that generates a remarkably diverse and important array of cell types during the development of the vertebrate embryo. These cells originate in the neural plate border (NPB), which is the ectoderm between the neural plate and the epidermis. They give rise to the neurons and glia of the peripheral nervous system, melanocytes, chondrocytes, smooth muscle cells, odontoblasts and neuroendocrine cells, among others. Neurocristopathies are a class of congenital diseases resulting from the abnormal induction, specification, migration, differentiation or death of NC cells (NCCs) during embryonic development and have an important medical and societal impact. In general, congenital defects affect an appreciable percentage of newborns worldwide. Some of these defects are caused by teratogens, which are agents that negatively impact the formation of tissues and organs during development. In this review, we will discuss the teratogens linked to the development of many birth defects, with a strong focus on those that specifically affect the development of the NC, thereby producing neurocristopathies.Although increasing attention is being paid to the effect of teratogens on embryonic development in general, there is a strong need to critically evaluate the specific role of these agents in NC development. Therefore, increased understanding of the role of these factors in NC development will contribute to the planning of strategies aimed at the prevention and treatment of human neurocristopathies, whose etiology was previously not considered.

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“…Maternal ethanol exposure either during prenatal and postnatal period or only during postnatal impairs cognitive function in the offspring (Lee et al, 2016;Mahdinia et al, 2019;Soleimani et al, 2016;Tipyasang et al, 2014;Tiwari & Chopra, 2011). Alcohol exposed models have indicated brain-derived neurotrophic factors (BDNF) signaling alteration in several brain regions.…”

Section: Introductionmentioning

confidence: 99%

“…It is recognized that maternal ethanol treatment induces oxidative stress as well as reducing BDNF expression in the offspring hippocampus. Also, evidence shows that oxidative stress can impair learning and memory (Mohammadi et al, 2014;Soleimani et al, 2016Soleimani et al, , 2017, and on the other hand, BDNF can influence synaptic plasticity that is underlying mechanism of cognitive function. Whether BDNF and oxidative stress can interrelate to affect learning and memory is unknown.…”

Section: Introductionmentioning

confidence: 99%

Maternal ethanol exposure induces behavioral deficits through oxidative stress and brain‐derived neurotrophic factor interrelation in rat offspring

Mahdinia

Goudarzi

Lashkarbolouki

et al. 2021

Intl J of Devlp Neuroscience

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Alcohol consumption during pregnancy damages the central nervous system of developing fetus and results in persistent physical and neurobehavioral abnormalities, including learning and memory disorders. The hippocampus which is involved in learning and memory is highly susceptible to the ethanol neurotoxic effects. Oxidative stress is one of the mechanisms in alcoholinduced disorders. Ethanol also interferes with the brain-derived neurotrophic factors (BDNF) expression. Using vitamin E as a potent antioxidant, we studied the possible interrelation between oxidative stress and BDNF on cognition.Ethanol (4 g/kg) and vitamin E (100, 200, and 400 mg/kg) were given to pregnant Wistar rats on first day of gestation (GD) until weaning (28 days).Oxidative stress marker, BDNF expression, and cyclic AMP-response bindingprotein (CREB) expression levels were measured on postnatal days (PND) 28. Object location memory (OLM) was evaluated on PND 34. Our results demonstrated that ethanol exposure significantly reduced glutathione peroxidase (GPx) activity, reduced glutathione (GSH), reduced/oxidized glutathione (GSH/GSSG) ratio, and increased superoxide dismutase (SOD) activity, malondialdehyde (MDA) levels, and carbonyl protein content in the hippocampus. Total BDNF, BDNF mRNA, and CREB expression significantly reduced in the hippocampus by ethanol exposure. Also, ethanol significantly reduced the discrimination index (DI) in the OLM test. In addition, vitamin E administration could reduce oxidative stress, increase significantly BDNF and CREB levels, and improve cognitive dysfunction induced by ethanol exposure. Collectively, results suggest that probably oxidative stress can interrelate with the BDNF system for modulating cognitive function in the ethanol-exposed rat.

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The combined effects of developmental lead and ethanol exposure on hippocampus dependent spatial learning and memory in rats: Role of oxidative stress

Cited by 33 publications

References 69 publications

Maternal high‐salt diet during pregnancy impairs synaptic plasticity and memory in offspring

Maternal high‐salt diet during pregnancy impairs synaptic plasticity and memory in offspring

The role of teratogens in neural crest development

Maternal ethanol exposure induces behavioral deficits through oxidative stress and brain‐derived neurotrophic factor interrelation in rat offspring

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