Prenatal hypoxia produces memory deficits associated with impairment of long-term synaptic plasticity in young rats

Журавин, И. А.; Dubrovskaya, N. М.; Vasilev, D. S.; Postnikova, Tatyana Y.; Zaitsev, Aleksey V.

doi:10.1016/j.nlm.2019.107066

Cited by 35 publications

(23 citation statements)

References 63 publications

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“…Impairments in learning ability, 60 memory consolidation, [61][62][63] and problem-solving behavior 64,65 have been reported previously in juvenile and adult rodent offspring of hypoxic pregnancy. Conversely, fewer studies have determined the long-term impact of developmental hypoxia on cerebral structure in adult offspring.…”

Section: Discussionsupporting

confidence: 54%

Maternal antioxidant treatment protects adult offspring against memory loss and hippocampal atrophy in a rodent model of developmental hypoxia

et al. 2021

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Section: Discussionsupporting

confidence: 54%

Maternal antioxidant treatment protects adult offspring against memory loss and hippocampal atrophy in a rodent model of developmental hypoxia

et al. 2021

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“…Oxidative tissue damage and inflammation in brain tissues play a significant role in homocysteine-induced neurotoxicity [ 76 , 77 ]. Indeed, oxidative stress during the prenatal period markedly reduces spatial learning and memory retention due to disturbed basal transmission in CA3–CA1 synapses and a decrease in hippocampal long-term synaptic potentiation [ 48 , 78 ]. Moreover, homocysteine accumulation during the prenatal period in different brain region including cerebellum, hippocampus, striatum induces excitotoxicity followed by apoptosis [ 31 , 79 , 80 ] and may impair neuronal network maturation during a critical period of development.…”

Section: Discussionmentioning

confidence: 99%

Hydrogen Sulfide Alleviates Anxiety, Motor, and Cognitive Dysfunctions in Rats with Maternal Hyperhomocysteinemia via Mitigation of Oxidative Stress

et al. 2020

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Hydrogen sulfide (H2S) is endogenously produced from sulfur containing amino acids, including homocysteine and exerts neuroprotective effects. An increase of homocysteine during pregnancy impairs fetal growth and development of the offspring due to severe oxidative stress. We analyzed the effects of the H2S donor—sodium hydrosulfide (NaHS) administered to female rats with hyperhomocysteinemia (hHcy) on behavioral impairments and levels of oxidative stress of their offspring. Rats born from females fed with control or high methionine diet, with or without H2S donor injections were investigated. Rats with maternal hHcy exhibit increased levels of total locomotor activity and anxiety, decreased muscle endurance and motor coordination, abnormalities of fine motor control, as well as reduced spatial memory and learning. Oxidative stress in brain tissues measured by activity of glutathione peroxidases and the level of malondialdehyde was higher in rats with maternal hHcy. Concentrations of H2S and the activity and expression of the H2S generating enzyme—cystathionine-beta synthase—were lower compared to the control group. Administration of the H2S donor to females with hHcy during pregnancy prevented behavioral alterations and oxidative stress of their offspring. The acquisition of behavioral together with biochemical studies will add to our knowledge about homocysteine neurotoxicity and proposes H2S as a potential agent for therapy of hHcy associated disorders.

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“…Previous work in vertebrates as well as in invertebrates has shown that developmental hypoxia causes axonal pathfinding errors in telencephalic neurons, through activation of the hypoxia-inducible factor (hif1) pathway (Stevenson et al, 2012;Xing et al, 2015). Hypoxia has also been noted to affect synapse development (Curristin et al, 2002;Segura et al, 2016;Zhuravin et al, 2019), but in this work we identified that hypoxia could act on dopaminergic signaling to affect synapse development, including effects on synaptic circuitry, and short-and long-term behavioral effects. However, we cannot exclude that hypoxia might have multifactorial impacts on behavior and locomotor development, for example, that hypoxia could be affecting myelin development or function; or of other aspects of circuitry, for example, motor neuron to muscle synapses.…”

Section: Discussionmentioning

confidence: 68%

Dopaminergic Co-Regulation of Locomotor Development and Motor Neuron Synaptogenesis is Uncoupled by Hypoxia in Zebrafish

Son

Stevenson

Bowles

et al. 2020

eNeuro

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Hypoxic injury to the developing human brain is a complication of premature birth and is associated with longterm impairments of motor function. Disruptions of axon and synaptic connectivity have been linked to developmental hypoxia, but the fundamental mechanisms impacting motor function from altered connectivity are poorly understood. We investigated the effects of hypoxia on locomotor development in zebrafish. We found that developmental hypoxia resulted in decreased spontaneous swimming behavior in larva, and that this motor impairment persisted into adulthood. In evaluation of the diencephalic dopaminergic neurons, which regulate early development of locomotion and constitute an evolutionarily conserved component of the vertebrate dopaminergic system, hypoxia caused a decrease in the number of synapses from the descending dopaminergic diencephalospinal tract (DDT) to spinal cord motor neurons. Moreover, dopamine signaling from the DDT was coupled jointly to motor neuron synaptogenesis and to locomotor development. Together, these results demonstrate the developmental processes regulating early locomotor development and a requirement for dopaminergic projections and motor neuron synaptogenesis. Our findings suggest new insights for understanding the mechanisms leading to motor disability from hypoxic injury of prematurity.

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Prenatal hypoxia produces memory deficits associated with impairment of long-term synaptic plasticity in young rats

Cited by 35 publications

References 63 publications

Maternal antioxidant treatment protects adult offspring against memory loss and hippocampal atrophy in a rodent model of developmental hypoxia

Maternal antioxidant treatment protects adult offspring against memory loss and hippocampal atrophy in a rodent model of developmental hypoxia

Hydrogen Sulfide Alleviates Anxiety, Motor, and Cognitive Dysfunctions in Rats with Maternal Hyperhomocysteinemia via Mitigation of Oxidative Stress

Dopaminergic Co-Regulation of Locomotor Development and Motor Neuron Synaptogenesis is Uncoupled by Hypoxia in Zebrafish

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