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How Perinatal Stress Affects Brain Plasticity in Ontogenesis
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How Perinatal Stress Affects Brain Plasticity in Ontogenesis

A topical collection in Cells (ISSN 2073-4409). This collection belongs to the section "Cells of the Nervous System".

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Editors

Prof. Dr. Alexander V. Arutjunyan

E-Mail Website
Collection Editor
1. Chief Researcher of the Department of Immunology and Intercellular Interactions, D.O. Ott Institute of Obstetrics, Gynecology and Reproductology, Saint-Petersburg, Russia
2. Head of the Laboratory of Biochemistry, Saint-Petersburg Institute of Bioregulation and Gerontology, Saint-Petersburg, Russia
Interests: nervous and immune systems; neurons and glial cells; neuroinflammation; neurodegeneration; reproduction; placenta; fetus; neurotrophins; hyperhomocysteinemia; brain development and plasticity
Prof. Dr. Natalia V. Gulyaeva

E-Mail Website
Collection Editor
Russian Academy of Sciences, Department of Functional Biochemistry of the Nervous System, Moscow, Russia
Interests: adaptation; alzheimer animal models; apoptosis; cellular models; cerebral ischemia; dementia; depression; epilepsy; excitotoxicity; neuroinflammation; hippocampus; traumatic brain injury; epileptogenesis
Special Issues, Collections and Topics in MDPI journals

Topical Collection Information

Dear Colleagues, 

Neuroplasticity (brain plasticity or neural plasticity) is the remarkable capacity of the brain to alter and adapt to changing environments. This dynamic process allowing one to adapt to different experiences and learn is also a factor in recovery from brain injuries, since rehabilitation is aimed at rebuilding connections between neurons or the “rewiring” of the brain. Neuroplasticity can be observed on multiple scales, with adaptive behavior, learning, and memory being at the top of the neuroplasticity hierarchy. The base of this pyramid is formed of molecules and their interactions, which underlie subcellular/synaptic, cellular, and neuronal circuits as well as different network levels. Long-term plasticity occurs as a result of changes in gene expression that are triggered by signaling cascades during altered neuronal activity. Cerebral pathologies are often associated with limitations of the adaptive capacity of neuroplasticity or aberrant excessive neuroplasticity.

Early life stress (due to different forms of abuse and neglect as well as the effects of pathological factors experienced by the developing child) is associated with the disturbed development of the brain. Recent advances strongly support the essential role of perinatal stress in delayed psychological, psychiatric, and neurological sequelae during ontogenesis, specifically in adolescence and adulthood. A number of animal models of perinatal stress have been developed and used to study the mechanisms of its detrimental effects on the brain, with these studies having major translational significance. The brain plays a key role in the development, well-being, and survival of organisms; therefore, various stress factors during prenatal and early postnatal periods (fetal or maternal hypoxia, hyperhomocysteinemia, etc.) that affect the development of neuroplasticity mechanisms are of critical importance. The perinatal period of brain development is extremely important, since it involves the formation of the main brain structures associated with neurogenesis and gliogenesis, the maturation of synapses, as well as other essential events regulated by endocrine and immune systems and potentially vulnerable to early-life stress. Stress-induced changes involve all levels of neuroplasticity, including synaptic plasticity. This Topical Collection is aimed at the accumulation of new data regarding the effects of perinatal stress on the development of brain plasticity mechanisms at all levels of brain organization. The goal of this collection is to highlight the translational potential of these data to elucidate connections between perinatal stress and negative health outcomes.

Prof. Dr. Alexander V. Arutjunyan
Prof. Dr. Natalia V. Gulyaeva
Collection Editors

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Keywords

  • neuroplasticity
  • synaptic plasticity
  • maladaptive plasticity
  • prenatal stress
  • perinatal stress
  • early life stress
  • development
  • ontogenesis
  • neuropsychiatric disorders
  • neurogenesis

Published Papers (3 papers)

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2023

24 pages, 1686 KiB  
Review
Current Understanding of the Roles of Gut–Brain Axis in the Cognitive Deficits Caused by Perinatal Stress Exposure
by Mara Roxana Rubinstein, Adriana Laura Burgueño, Sofia Quiroga, Miriam Ruth Wald and Ana María Genaro
Cells 2023, 12(13), 1735; https://doi.org/10.3390/cells12131735 - 28 Jun 2023
Cited by 3 | Viewed by 4040
Abstract
The term ‘perinatal environment’ refers to the period surrounding birth, which plays a crucial role in brain development. It has been suggested that dynamic communication between the neuro–immune system and gut microbiota is essential in maintaining adequate brain function. This interaction depends on [...] Read more.
The term ‘perinatal environment’ refers to the period surrounding birth, which plays a crucial role in brain development. It has been suggested that dynamic communication between the neuro–immune system and gut microbiota is essential in maintaining adequate brain function. This interaction depends on the mother’s status during pregnancy and/or the newborn environment. Here, we show experimental and clinical evidence that indicates that the perinatal period is a critical window in which stress-induced immune activation and altered microbiota compositions produce lasting behavioral consequences, although a clear causative relationship has not yet been established. In addition, we discuss potential early treatments for preventing the deleterious effect of perinatal stress exposure. In this sense, early environmental enrichment exposure (including exercise) and melatonin use in the perinatal period could be valuable in improving the negative consequences of early adversities. The evidence presented in this review encourages the realization of studies investigating the beneficial role of melatonin administration and environmental enrichment exposure in mitigating cognitive alteration in offspring under perinatal stress exposure. On the other hand, direct evidence of microbiota restoration as the main mechanism behind the beneficial effects of this treatment has not been fully demonstrated and should be explored in future studies. Full article
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24 pages, 8820 KiB  
Article
Cognitive Impairment Is Associated with AMPAR Glutamatergic Dysfunction in a Mouse Model of Neuronal Methionine Synthase Deficiency
by Ziad Hassan, David Coelho, Carine Bossenmeyer-Pourié, Karim Matmat, Carole Arnold, Aurélie Savladori, Jean-Marc Alberto, Rémy Umoret, Jean-Louis Guéant and Grégory Pourié
Cells 2023, 12(9), 1267; https://doi.org/10.3390/cells12091267 - 27 Apr 2023
Cited by 1 | Viewed by 1689
Abstract
Impairment of one-carbon metabolism during pregnancy, either due to nutritional deficiencies in B9 or B12 vitamins or caused by specific genetic defects, is often associated with neurological defects, including cognitive dysfunction that persists even after vitamin supplementation. Animal nutritional models do not allow [...] Read more.
Impairment of one-carbon metabolism during pregnancy, either due to nutritional deficiencies in B9 or B12 vitamins or caused by specific genetic defects, is often associated with neurological defects, including cognitive dysfunction that persists even after vitamin supplementation. Animal nutritional models do not allow for conclusions regarding the specific brain mechanisms that may be modulated by systemic compensations. Using the Cre-lox system associated to the neuronal promoter Thy1.2, a knock-out model for the methionine synthase specifically in the brain was generated. Our results on the neurobehavioral development of offspring show that the absence of methionine synthase did not lead to growth retardation, despite an effective reduction of both its expression and the methylation status in brain tissues. Behaviors were differently affected according to their functional outcome. Only temporary retardations were recorded in the acquisition of vegetative functions during the suckling period, compared to a dramatic reduction in cognitive performance after weaning. Investigation of the glutamatergic synapses in cognitive areas showed a reduction of AMPA receptors phosphorylation and clustering, indicating an epigenomic effect of the neuronal deficiency of methionine synthase on the reduction of glutamatergic synapses excitability. Altogether, our data indicate that cognitive impairment associated with methionine synthase deficiency may not only result from neurodevelopmental abnormalities, but may also be the consequence of alterations in functional plasticity of the brain. Full article
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28 pages, 4672 KiB  
Article
Maternal Hyperhomocysteinemia Disturbs the Mechanisms of Embryonic Brain Development and Its Maturation in Early Postnatal Ontogenesis
by Dmitrii S. Vasilev, Anastasiia D. Shcherbitskaia, Natalia L. Tumanova, Anastasiia V. Mikhel, Yulia P. Milyutina, Anna A. Kovalenko, Nadezhda M. Dubrovskaya, Daria B. Inozemtseva, Irina V. Zalozniaia and Alexander V. Arutjunyan
Cells 2023, 12(1), 189; https://doi.org/10.3390/cells12010189 - 3 Jan 2023
Cited by 7 | Viewed by 2191
Abstract
Maternal hyperhomocysteinemia causes the disruption of placental blood flow and can lead to serious disturbances in the formation of the offspring’s brain. In the present study, the effects of prenatal hyperhomocysteinemia (PHHC) on the neuronal migration, neural tissue maturation, and the expression of [...] Read more.
Maternal hyperhomocysteinemia causes the disruption of placental blood flow and can lead to serious disturbances in the formation of the offspring’s brain. In the present study, the effects of prenatal hyperhomocysteinemia (PHHC) on the neuronal migration, neural tissue maturation, and the expression of signaling molecules in the rat fetal brain were described. Maternal hyperhomocysteinemia was induced in female rats by per os administration of 0.15% aqueous methionine solution in the period of days 4–21 of pregnancy. Behavioral tests revealed a delay in PHHC male pups maturing. Ultrastructure of both cortical and hippocampus tissue demonstrated the features of the developmental delay. PHHC was shown to disturb both generation and radial migration of neuroblasts into the cortical plate. Elevated Bdnf expression, together with changes in proBDNF/mBDNF balance, might affect neuronal cell viability, positioning, and maturation in PHHC pups. Reduced Kdr gene expression and the content of SEMA3E might lead to impaired brain development. In the brain tissue of E20 PHHC fetuses, the content of the procaspase-8 was decreased, and the activity level of the caspase-3 was increased; this may indicate the development of apoptosis. PHHC disturbs the mechanisms of early brain development leading to a delay in brain tissue maturation and formation of the motor reaction of pups. Full article
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