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Modulation of Hippocampal Neural Plasticity by Glucose-Related Signaling

Hormones and peptides involved in glucose homeostasis are emerging as important modulators of neural plasticity. In this regard, increasing evidence shows that molecules such as insulin, insulin-like growth factor-I, glucagon-like peptide-1, and ghrelin impact on the function of the hippocampus, whi...

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Detalles Bibliográficos
Autores principales: Mainardi, Marco, Fusco, Salvatore, Grassi, Claudio
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4419237/
https://www.ncbi.nlm.nih.gov/pubmed/25977822
http://dx.doi.org/10.1155/2015/657928
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author Mainardi, Marco
Fusco, Salvatore
Grassi, Claudio
author_facet Mainardi, Marco
Fusco, Salvatore
Grassi, Claudio
author_sort Mainardi, Marco
collection PubMed
description Hormones and peptides involved in glucose homeostasis are emerging as important modulators of neural plasticity. In this regard, increasing evidence shows that molecules such as insulin, insulin-like growth factor-I, glucagon-like peptide-1, and ghrelin impact on the function of the hippocampus, which is a key area for learning and memory. Indeed, all these factors affect fundamental hippocampal properties including synaptic plasticity (i.e., synapse potentiation and depression), structural plasticity (i.e., dynamics of dendritic spines), and adult neurogenesis, thus leading to modifications in cognitive performance. Here, we review the main mechanisms underlying the effects of glucose metabolism on hippocampal physiology. In particular, we discuss the role of these signals in the modulation of cognitive functions and their potential implications in dysmetabolism-related cognitive decline.
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spelling pubmed-44192372015-05-14 Modulation of Hippocampal Neural Plasticity by Glucose-Related Signaling Mainardi, Marco Fusco, Salvatore Grassi, Claudio Neural Plast Review Article Hormones and peptides involved in glucose homeostasis are emerging as important modulators of neural plasticity. In this regard, increasing evidence shows that molecules such as insulin, insulin-like growth factor-I, glucagon-like peptide-1, and ghrelin impact on the function of the hippocampus, which is a key area for learning and memory. Indeed, all these factors affect fundamental hippocampal properties including synaptic plasticity (i.e., synapse potentiation and depression), structural plasticity (i.e., dynamics of dendritic spines), and adult neurogenesis, thus leading to modifications in cognitive performance. Here, we review the main mechanisms underlying the effects of glucose metabolism on hippocampal physiology. In particular, we discuss the role of these signals in the modulation of cognitive functions and their potential implications in dysmetabolism-related cognitive decline. Hindawi Publishing Corporation 2015 2015-04-21 /pmc/articles/PMC4419237/ /pubmed/25977822 http://dx.doi.org/10.1155/2015/657928 Text en Copyright © 2015 Marco Mainardi et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Mainardi, Marco
Fusco, Salvatore
Grassi, Claudio
Modulation of Hippocampal Neural Plasticity by Glucose-Related Signaling
title Modulation of Hippocampal Neural Plasticity by Glucose-Related Signaling
title_full Modulation of Hippocampal Neural Plasticity by Glucose-Related Signaling
title_fullStr Modulation of Hippocampal Neural Plasticity by Glucose-Related Signaling
title_full_unstemmed Modulation of Hippocampal Neural Plasticity by Glucose-Related Signaling
title_short Modulation of Hippocampal Neural Plasticity by Glucose-Related Signaling
title_sort modulation of hippocampal neural plasticity by glucose-related signaling
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4419237/
https://www.ncbi.nlm.nih.gov/pubmed/25977822
http://dx.doi.org/10.1155/2015/657928
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