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Human neoteny revisited: The case of synaptic plasticity

Authors

  • Enric Bufill,

    Corresponding author
    1. Servei de Neurología, Consorci Hospitalari de Vic, Francesc Plà, 1, E-08500 Vic, Spain
    2. Institut de Paleoecologia Humana i Evolució Social, Universitat Rovira i Virgili, Plaça Imperial Tarraco 1, E-43005 Tarragona, Spain
    • Servei de Neurología, Consorci Hospitalari de Vic, Francesc Plà, 1, E-08500 Vic, Spain
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  • Jordi Agustí,

    1. ICREA, Institut de Paleoecologia Humana i Evolució Social, Universitat Rovira i Virgili, Plaça Imperial Tarraco 1, E-43005 Tarragona, Spain
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  • Rafael Blesa

    1. Servei de Neurologia, Hospital de la Santa Creu i Sant Pau, Sant Antoni Maria Claret, 167, E-08025 Barcelona, Spain
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Abstract

The process of learning requires morphological changes in the neuronal connections and the formation of new synapses. Due to the importance of memory and learning in our species, it has been suggested that the synaptic plasticity in a number of association areas is higher in the human brain than in other primates. Cortical neurons in mammals are characterized by higher metabolism, activity, and synaptic plasticity during development and the juvenile stage than in the adult. In Homo sapiens, brain development is retarded compared with other primates, especially in some association areas. These areas are characterized by the presence of neurons, which remain structurally immature throughout their lifespans and show an increase in the expression of the genes, which deal with metabolism and the activity and synaptic plasticity in adulthood. The retention of juvenile features in some adult neurons in our species has occurred in areas, which are related to episodic memory, planning, and social navigation. The increase of the aerobic metabolism in these neurons may lead, however, to higher levels of oxidative stress, therefore, favoring the development of neurodegenerative diseases which are exclusive, or almost exclusive, to humans, such as Alzheimer's disease. Am. J. Hum. Biol. 2011. © 2011 Wiley-Liss, Inc.

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