Effects of Homocysteine and its Derivatives on Spontaneous Network Activity in the Hippocampus of Neonatal Rat Pups

Kurmashova, E.; Gataulina, E.; Зефиров, А. Л.; Ситдикова, Г. Ф.; Yakovlev, A. V.

doi:10.1007/s11055-020-00984-1

Cited by 5 publications

(1 citation statement)

References 41 publications

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“…Severe HCY can lead to abnormal neural tube formation and fetal death [6]. Mild HCY causes many physiological abnormalities in the offspring, including impaired synaptic activity due to an imbalance of excitation and inhibition in neural network [7,8] and cognitive impairment [9,10]. HCY may lead to neuronal death and neuroinflammation in the cortical areas and hippocampus [11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Maternal Hyperhomocysteinemia Produces Memory Deficits Associated with Impairment of Long-Term Synaptic Plasticity in Young Rats

Postnikova

Amakhin

Trofimova

et al. 2022

Cells

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Maternal hyperhomocysteinemia (HCY) is a common pregnancy complication caused by high levels of the homocysteine in maternal and fetal blood, which leads to the alterations of the cognitive functions, including learning and memory. In the present study, we investigated the mechanisms of these alterations in a rat model of maternal HCY. The behavioral tests confirmed the memory impairments in young and adult rats following the prenatal HCY exposure. Field potential recordings in hippocampal slices demonstrated that the long-term potentiation (LTP) was significantly reduced in HCY rats. The whole-cell patch-clamp recordings in hippocampal slices demonstrated that the magnitude of NMDA receptor-mediated currents did not change while their desensitization decreased in HCY rats. No significant alterations of glutamate receptor subunit expression except GluN1 were detected in the hippocampus of HCY rats using the quantitative real-time PCR and Western blot methods. The immunofluorescence microscopy revealed that the number of synaptopodin-positive spines is reduced, while the analysis of the ultrastructure of hippocampus using the electron microscopy revealed the indications of delayed hippocampal maturation in young HCY rats. Thus, the obtained results suggest that maternal HCY disturbs the maturation of hippocampus during the first month of life, which disrupts LTP formation and causes memory impairments.

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