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MINI REVIEW article

Front. Cell. Neurosci.
Sec. Cellular Neurophysiology
Volume 18 - 2024 | doi: 10.3389/fncel.2024.1465821
This article is part of the Research Topic Cellular and Molecular Mechanisms that Govern Assembly, Plasticity, and Function of GABAergic Inhibitory Circuits in the Mammalian Brain View all 8 articles

The function of Mef2c towards the development of excitatory and inhibitory cortical neurons

Provisionally accepted
  • Albert Einstein College of Medicine, New York City, United States

The final, formatted version of the article will be published soon.

    Neurodevelopmental disorders (NDDs) are caused by abnormal brain development, leading to altered brain function and affecting cognition, learning, self-control, memory, and emotion. NDDs are often demarcated as discrete entities for diagnosis, but empirical evidence indicates that NDDs share a great deal of overlap, including genetics, core symptoms, and biomarkers. Many NDDs also share a primary sensitive period for disease, specifically the last trimester of pregnancy in humans, which corresponds to the neonatal period in mice. This period is notable for cortical circuit assembly, suggesting that deficits in the establishment of brain connectivity are likely a leading cause of brain dysfunction across different NDDs. Regulators of gene programs that underlie neurodevelopment represent a point of convergence for NDDs.Here, we review how the transcription factor MEF2C, a risk factor for various NDDs, impacts cortical development. Cortical activity requires a precise balance of various types of excitatory and inhibitory neuron types. We use MEF2C loss-of-function as a study case to illustrate how brain dysfunction and altered behavior may derive from the dysfunction of specific cortical circuits at specific developmental times.

    Keywords: Cortical development, MEF2C haploinsufficiency syndrome, Autism Spectrum Disorder, GABA, Interneurons

    Received: 16 Jul 2024; Accepted: 05 Sep 2024.

    Copyright: © 2024 Ward, Sjulson and Batista-Brito. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Renata Batista-Brito, Albert Einstein College of Medicine, New York City, United States

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.