International Journal of Molecular Sciences

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Dr. Stéphanie Moriceau

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Guest Editor

Institut Imagine and SFR Necker, 75015 Paris, France
Interests: neuroscience; cognition; brain; learning; memory; metabolism; development; neurologic disease and disorders

Special Issue Information

Dear Colleagues,

After birth, the brain undergoes a period of development that leads to the maturation of the brain, establishing social and emotional development and cognitive functions, such as attention and learning, which are largely under genetic and environmental control. This period is a tightly controlled sequence of events and creates a window of opportunity in which the brain is particularly sensitive to experience and the acquisition of new information that could lead to long-term deleterious effects, ranging from mild cognitive impairment to severe neurological and psychiatric conditions. The recent advances in research in infant neurodevelopment highlight the crucial nature of experience in shaping the brain, the role of nutrition for health development and the importance of stimulating learning.

This Special Issue aims to promote a multi-level approach to uncover and update the neural mechanisms of brain development and cognitive behavior. As such, this Special Issue welcomes submissions of original research and review articles related to any aspect of the brain–behavior relationship and its development, from molecular biology and genetics, to biochemical, neurochemical, neurophysiological, neuroendocrine, pharmacological, neurocomputation and neuroimaging studies.

Dr. Stéphanie Moriceau
Guest Editor

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Keywords

neurodevelopment
cognition
animal models
brain mecanisms
disorders

Published Papers (2 papers)

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19 pages, 1903 KiB

Open AccessReview

Evolution of Glutamate Metabolism via GLUD2 Enhances Lactate-Dependent Synaptic Plasticity and Complex Cognition

by Andreas Plaitakis, Kyriaki Sidiropoulou, Dimitra Kotzamani, Ionela Litso, Ioannis Zaganas and Cleanthe Spanaki

Int. J. Mol. Sci. 2024, 25(10), 5297; https://doi.org/10.3390/ijms25105297 - 13 May 2024

Viewed by 318

Abstract

Human evolution is characterized by rapid brain enlargement and the emergence of unique cognitive abilities. Besides its distinctive cytoarchitectural organization and extensive inter-neuronal connectivity, the human brain is also defined by high rates of synaptic, mainly glutamatergic, transmission, and energy utilization. While these adaptations’ origins remain elusive, evolutionary changes occurred in synaptic glutamate metabolism in the common ancestor of humans and apes via the emergence of GLUD2, a gene encoding the human glutamate dehydrogenase 2 (hGDH2) isoenzyme. Driven by positive selection, hGDH2 became adapted to function upon intense excitatory firing, a process central to the long-term strengthening of synaptic connections. It also gained expression in brain astrocytes and cortical pyramidal neurons, including the CA1-CA3 hippocampal cells, neurons crucial to cognition. In mice transgenic for GLUD2, theta-burst-evoked long-term potentiation (LTP) is markedly enhanced in hippocampal CA3-CA1 synapses, with patch-clamp recordings from CA1 pyramidal neurons revealing increased sNMDA receptor currents. D-lactate blocked LTP enhancement, implying that glutamate metabolism via hGDH2 potentiates L-lactate-dependent glia–neuron interaction, a process essential to memory consolidation. The transgenic (Tg) mice exhibited increased dendritic spine density/synaptogenesis in the hippocampus and improved complex cognitive functions. Hence, enhancement of neuron–glia communication, via GLUD2 evolution, likely contributed to human cognitive advancement by potentiating synaptic plasticity and inter-neuronal connectivity. Full article

(This article belongs to the Special Issue The Molecular Research in Brain Development and Cognitive Functions)

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27 pages, 7022 KiB

Open AccessArticle

Prenatal Alcohol Exposure Impairs the Placenta–Cortex Transcriptomic Signature, Leading to Dysregulation of Angiogenic Pathways

by Camille Sautreuil, Maryline Lecointre, Céline Derambure, Carole Brasse-Lagnel, Philippe Leroux, Annie Laquerrière, Gaël Nicolas, Sophie Gil, Daniel D. Savage, Stéphane Marret, Florent Marguet, Anthony Falluel-Morel and Bruno J. Gonzalez

Int. J. Mol. Sci. 2023, 24(17), 13484; https://doi.org/10.3390/ijms241713484 - 30 Aug 2023

Cited by 1 | Viewed by 1742

Abstract

Although alcohol consumption during pregnancy is a major cause of behavioral and learning disabilities, most FASD infants are late- or even misdiagnosed due to clinician’s difficulties achieving early detection of alcohol-induced neurodevelopmental impairments. Neuroplacentology has emerged as a new field of research focusing on the role of the placenta in fetal brain development. Several studies have reported that prenatal alcohol exposure (PAE) dysregulates a functional placenta–cortex axis, which is involved in the control of angiogenesis and leads to neurovascular-related defects. However, these studies were focused on PlGF, a pro-angiogenic factor. The aim of the present study is to provide the first transcriptomic “placenta–cortex” signature of the effects of PAE on fetal angiogenesis. Whole mouse genome microarrays of paired placentas and cortices were performed to establish the transcriptomic inter-organ “placenta–cortex” signature in control and PAE groups at gestational day 20. Genespring comparison of the control and PAE signatures revealed that 895 and 1501 genes were only detected in one of two placenta–cortex expression profiles, respectively. Gene ontology analysis indicated that 107 of these genes were associated with vascular development, and String protein–protein interaction analysis showed that they were associated with three functional clusters. PANTHER functional classification analysis indicated that “intercellular communication” was a significantly enriched biological process, and 27 genes were encoded for neuroactive ligand/receptors interactors. Protein validation experiments involving Western blot for one ligand–receptor couple (Agt/AGTR1/2) confirmed the transcriptomic data, and Pearson statistical analysis of paired placentas and fetal cortices revealed a negative correlation between placental Atg and cortical AGTR1, which was significantly impacted by PAE. In humans, a comparison of a 38WG control placenta with a 36WG alcohol-exposed placenta revealed low Agt immunolabeling in the syncytiotrophoblast layer of the alcohol case. In conclusion, this study establishes the first transcriptomic placenta–cortex signature of a developing mouse. The data show that PAE markedly unbalances this inter-organ signature; in particular, several ligands and/or receptors involved in the control of angiogenesis. These data support that PAE modifies the existing communication between the two organs and opens new research avenues regarding the impact of placental dysfunction on the neurovascular development of fetuses. Such a signature would present a clinical value for early diagnosis of brain defects in FASD. Full article

(This article belongs to the Special Issue The Molecular Research in Brain Development and Cognitive Functions)

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