Fructose consumption reduces hippocampal synaptic plasticity underlying cognitive performance

Pedro Cisternas, Paulina Salazar, Felipe G. Serrano, Carla Montecinos-Oliva, Sebastián B. Arredondo, Lorena Varela-Nallar, Salesa Barja, Carlos P. Vio, Fernando Gomez-Pinilla, Nibaldo C. Inestrosa

Resultado de la investigación: Article

23 Citas (Scopus)

Resumen

Metabolic syndrome (MetS) is a global epidemic, which involves a spectrum of metabolic disorders comprising diabetes and obesity. The impact of MetS on the brain is becoming to be a concern, however, the poor understanding of mechanisms involved has limited the development of therapeutic strategies. We induced a MetS-like condition by exposing mice to fructose feeding for 7. weeks. There was a dramatic deterioration in the capacity of the hippocampus to sustain synaptic plasticity in the forms of long-term potentiation (LTP) and long-term depression (LTD). Mice exposed to fructose showed a reduction in the number of contact zones and the size of postsynaptic densities (PSDs) in the hippocampus, as well as a decrease in hippocampal neurogenesis. There was an increase in lipid peroxidation likely associated with a deficiency in plasma membrane excitability. Consistent with an overall hippocampal dysfunction, there was a subsequent decrease in hippocampal dependent learning and memory performance, i.e., spatial learning and episodic memory. Most of the pathological sequel of MetS in the brain was reversed three month after discontinue fructose feeding. These results are novel to show that MetS triggers a cascade of molecular events, which disrupt hippocampal functional plasticity, and specific aspects of learning and memory function. The overall information raises concerns about the risk imposed by excessive fructose consumption on the pathology of neurological disorders.

Idioma originalEnglish
Páginas (desde-hasta)2379-2390
Número de páginas12
PublicaciónBiochimica et Biophysica Acta - Molecular Basis of Disease
Volumen1852
N.º11
DOI
EstadoPublished - 1 nov 2015

Huella dactilar

Neuronal Plasticity
Fructose
Metabolic Brain Diseases
Hippocampus
Learning
Post-Synaptic Density
Episodic Memory
Long-Term Potentiation
Neurogenesis
Nervous System Diseases
Lipid Peroxidation
Obesity
Cell Membrane
Depression
Pathology
Therapeutics

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology

Citar esto

Cisternas, Pedro ; Salazar, Paulina ; Serrano, Felipe G. ; Montecinos-Oliva, Carla ; Arredondo, Sebastián B. ; Varela-Nallar, Lorena ; Barja, Salesa ; Vio, Carlos P. ; Gomez-Pinilla, Fernando ; Inestrosa, Nibaldo C. / Fructose consumption reduces hippocampal synaptic plasticity underlying cognitive performance. En: Biochimica et Biophysica Acta - Molecular Basis of Disease. 2015 ; Vol. 1852, N.º 11. pp. 2379-2390.
@article{5bae7dad395a468eb21932e0c0b2f15b,
title = "Fructose consumption reduces hippocampal synaptic plasticity underlying cognitive performance",
abstract = "Metabolic syndrome (MetS) is a global epidemic, which involves a spectrum of metabolic disorders comprising diabetes and obesity. The impact of MetS on the brain is becoming to be a concern, however, the poor understanding of mechanisms involved has limited the development of therapeutic strategies. We induced a MetS-like condition by exposing mice to fructose feeding for 7. weeks. There was a dramatic deterioration in the capacity of the hippocampus to sustain synaptic plasticity in the forms of long-term potentiation (LTP) and long-term depression (LTD). Mice exposed to fructose showed a reduction in the number of contact zones and the size of postsynaptic densities (PSDs) in the hippocampus, as well as a decrease in hippocampal neurogenesis. There was an increase in lipid peroxidation likely associated with a deficiency in plasma membrane excitability. Consistent with an overall hippocampal dysfunction, there was a subsequent decrease in hippocampal dependent learning and memory performance, i.e., spatial learning and episodic memory. Most of the pathological sequel of MetS in the brain was reversed three month after discontinue fructose feeding. These results are novel to show that MetS triggers a cascade of molecular events, which disrupt hippocampal functional plasticity, and specific aspects of learning and memory function. The overall information raises concerns about the risk imposed by excessive fructose consumption on the pathology of neurological disorders.",
keywords = "Diabetes, Fructose, Metabolic syndrome, Neuronal dysfunction",
author = "Pedro Cisternas and Paulina Salazar and Serrano, {Felipe G.} and Carla Montecinos-Oliva and Arredondo, {Sebasti{\'a}n B.} and Lorena Varela-Nallar and Salesa Barja and Vio, {Carlos P.} and Fernando Gomez-Pinilla and Inestrosa, {Nibaldo C.}",
year = "2015",
month = "11",
day = "1",
doi = "10.1016/j.bbadis.2015.08.016",
language = "English",
volume = "1852",
pages = "2379--2390",
journal = "Biochimica et Biophysica Acta - Molecular Basis of Disease",
issn = "0925-4439",
publisher = "Elsevier",
number = "11",

}

Cisternas, P, Salazar, P, Serrano, FG, Montecinos-Oliva, C, Arredondo, SB, Varela-Nallar, L, Barja, S, Vio, CP, Gomez-Pinilla, F & Inestrosa, NC 2015, 'Fructose consumption reduces hippocampal synaptic plasticity underlying cognitive performance', Biochimica et Biophysica Acta - Molecular Basis of Disease, vol. 1852, n.º 11, pp. 2379-2390. https://doi.org/10.1016/j.bbadis.2015.08.016

Fructose consumption reduces hippocampal synaptic plasticity underlying cognitive performance. / Cisternas, Pedro; Salazar, Paulina; Serrano, Felipe G.; Montecinos-Oliva, Carla; Arredondo, Sebastián B.; Varela-Nallar, Lorena; Barja, Salesa; Vio, Carlos P.; Gomez-Pinilla, Fernando; Inestrosa, Nibaldo C.

En: Biochimica et Biophysica Acta - Molecular Basis of Disease, Vol. 1852, N.º 11, 01.11.2015, p. 2379-2390.

Resultado de la investigación: Article

TY - JOUR

T1 - Fructose consumption reduces hippocampal synaptic plasticity underlying cognitive performance

AU - Cisternas, Pedro

AU - Salazar, Paulina

AU - Serrano, Felipe G.

AU - Montecinos-Oliva, Carla

AU - Arredondo, Sebastián B.

AU - Varela-Nallar, Lorena

AU - Barja, Salesa

AU - Vio, Carlos P.

AU - Gomez-Pinilla, Fernando

AU - Inestrosa, Nibaldo C.

PY - 2015/11/1

Y1 - 2015/11/1

N2 - Metabolic syndrome (MetS) is a global epidemic, which involves a spectrum of metabolic disorders comprising diabetes and obesity. The impact of MetS on the brain is becoming to be a concern, however, the poor understanding of mechanisms involved has limited the development of therapeutic strategies. We induced a MetS-like condition by exposing mice to fructose feeding for 7. weeks. There was a dramatic deterioration in the capacity of the hippocampus to sustain synaptic plasticity in the forms of long-term potentiation (LTP) and long-term depression (LTD). Mice exposed to fructose showed a reduction in the number of contact zones and the size of postsynaptic densities (PSDs) in the hippocampus, as well as a decrease in hippocampal neurogenesis. There was an increase in lipid peroxidation likely associated with a deficiency in plasma membrane excitability. Consistent with an overall hippocampal dysfunction, there was a subsequent decrease in hippocampal dependent learning and memory performance, i.e., spatial learning and episodic memory. Most of the pathological sequel of MetS in the brain was reversed three month after discontinue fructose feeding. These results are novel to show that MetS triggers a cascade of molecular events, which disrupt hippocampal functional plasticity, and specific aspects of learning and memory function. The overall information raises concerns about the risk imposed by excessive fructose consumption on the pathology of neurological disorders.

AB - Metabolic syndrome (MetS) is a global epidemic, which involves a spectrum of metabolic disorders comprising diabetes and obesity. The impact of MetS on the brain is becoming to be a concern, however, the poor understanding of mechanisms involved has limited the development of therapeutic strategies. We induced a MetS-like condition by exposing mice to fructose feeding for 7. weeks. There was a dramatic deterioration in the capacity of the hippocampus to sustain synaptic plasticity in the forms of long-term potentiation (LTP) and long-term depression (LTD). Mice exposed to fructose showed a reduction in the number of contact zones and the size of postsynaptic densities (PSDs) in the hippocampus, as well as a decrease in hippocampal neurogenesis. There was an increase in lipid peroxidation likely associated with a deficiency in plasma membrane excitability. Consistent with an overall hippocampal dysfunction, there was a subsequent decrease in hippocampal dependent learning and memory performance, i.e., spatial learning and episodic memory. Most of the pathological sequel of MetS in the brain was reversed three month after discontinue fructose feeding. These results are novel to show that MetS triggers a cascade of molecular events, which disrupt hippocampal functional plasticity, and specific aspects of learning and memory function. The overall information raises concerns about the risk imposed by excessive fructose consumption on the pathology of neurological disorders.

KW - Diabetes

KW - Fructose

KW - Metabolic syndrome

KW - Neuronal dysfunction

UR - http://www.scopus.com/inward/record.url?scp=84940781575&partnerID=8YFLogxK

U2 - 10.1016/j.bbadis.2015.08.016

DO - 10.1016/j.bbadis.2015.08.016

M3 - Article

AN - SCOPUS:84940781575

VL - 1852

SP - 2379

EP - 2390

JO - Biochimica et Biophysica Acta - Molecular Basis of Disease

JF - Biochimica et Biophysica Acta - Molecular Basis of Disease

SN - 0925-4439

IS - 11

ER -