ReviewFrontiers in pediatrics2014
Alterations of neocortical pyramidal neurons: turning points in the genesis of mental retardation.
Review in Frontiers in pediatrics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- WDR5-HOTTIP Histone Modifying Complex Regulates Neural Migration and Dendrite Polarity of Pyramidal Neurons via Reelin Signaling.Molecular neurobiology · 2022Article
- Dendrites of Neocortical Pyramidal Neurons: The Key to Understand Intellectual Disability.Cellular and molecular neurobiology · 2022Article
- Dendritic spine and synapse pathology in chromatin modifier-associated autism spectrum disorders and intellectual disability.Frontiers in molecular neuroscience · 2022Review
- The Effect of Physical Activity on Cognitive Performance in an Italian Elementary School: Insights From a Pilot Study Using Structural Equation Modeling.Frontiers in physiology · 2019Article
- ANKRD11 associated with intellectual disability and autism regulates dendrite differentiation via the BDNF/TrkB signaling pathway.Neurobiology of disease · 2018Article
- Selective reduction of cerebral cortex GABA neurons in a late gestation model of fetal alcohol spectrum disorder.Alcohol (Fayetteville, N.Y.) · 2015Article
- Experimental models of early exposure to alcohol: a way to unravel the neurobiology of mental retardation.Frontiers in pediatrics · 2014Article
- I performed experiments and I have results. Wow, and now?Muscles, ligaments and tendons journalArticle
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Authors and funding
2 authors.
Funding
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Abstract
Pyramidal neurons (PNs) represent the majority of neocortical cells and their involvement in cognitive functions is decisive. Therefore, they are the most obvious target of developmental disorders characterized by mental retardation. Genetic and non-genetic forms of intellectual disability share a few basic pathogenetic signatures that result in the anomalous function of PNs. Here, we review the key mechanisms impairing these neurons and their participation in the cortical network, with special focus on experimental models of fetal exposure to alcohol. Due to the heterogeneity of PNs, some alterations affect selectively a given cell population, which may also differ depending on the considered pathology. These specific features open new possibilities for the interpretation of cognitive defects observed in mental retardation syndromes, as well as for novel therapeutic interventions.
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