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Modulation of hippocampal neural plasticity by glucose-related signaling.

Mainardi M, Fusco S, Grassi C - Neural Plast. (2015)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Institute of Human Physiology, Medical School, Università Cattolica, Largo Francesco Vito 1, 00168 Rome, Italy.

ABSTRACT
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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Schematic showing the convergence of the action of key molecules in metabolic signaling on different aspects of hippocampal physiology.
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fig1: Schematic showing the convergence of the action of key molecules in metabolic signaling on different aspects of hippocampal physiology.

Mentions: Strikingly, glucose sensing in the brain appears to be also involved in the modulation of brain cell functions having no direct relationships with metabolism. Indeed, glucose-related signaling has a strong impact on neuronal activity. In particular, we will here attempt to review the increasing body of evidence indicating that messengers essential to glucose homeostasis also affect at multiple levels the activity of the hippocampus, which is a brain area critically involved in cognitive functions. We will focus on a few key molecules: insulin and insulin-response substrates (IRSs), insulin-like growth factor-I (IGF-I), glucagon-like peptide-1 (GLP-1), and ghrelin. After briefly summarizing nonmetabolic glucose-related signaling in the brain, we will try to convey the message that these molecules exert multiple actions on hippocampal physiology by affecting structural and functional neuroplasticity. This is, in turn, correlated to modifications in hippocampal-dependent learning and memory processes (Figure 1).


Modulation of hippocampal neural plasticity by glucose-related signaling.

Mainardi M, Fusco S, Grassi C - Neural Plast. (2015)

Schematic showing the convergence of the action of key molecules in metabolic signaling on different aspects of hippocampal physiology.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4419237&req=5

fig1: Schematic showing the convergence of the action of key molecules in metabolic signaling on different aspects of hippocampal physiology.
Mentions: Strikingly, glucose sensing in the brain appears to be also involved in the modulation of brain cell functions having no direct relationships with metabolism. Indeed, glucose-related signaling has a strong impact on neuronal activity. In particular, we will here attempt to review the increasing body of evidence indicating that messengers essential to glucose homeostasis also affect at multiple levels the activity of the hippocampus, which is a brain area critically involved in cognitive functions. We will focus on a few key molecules: insulin and insulin-response substrates (IRSs), insulin-like growth factor-I (IGF-I), glucagon-like peptide-1 (GLP-1), and ghrelin. After briefly summarizing nonmetabolic glucose-related signaling in the brain, we will try to convey the message that these molecules exert multiple actions on hippocampal physiology by affecting structural and functional neuroplasticity. This is, in turn, correlated to modifications in hippocampal-dependent learning and memory processes (Figure 1).

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Institute of Human Physiology, Medical School, Università Cattolica, Largo Francesco Vito 1, 00168 Rome, Italy.

ABSTRACT
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.

Show MeSH
Related in: MedlinePlus