Deletion of the lifespan determinant p66Shc improves performance in a spatial memory task, decreases levels of oxidative stress markers in the hippocampus and increases levels of the neurotrophin BDNF in adult mice

A. Berry, A. Greco, M. Giorgio, P. G. Pelicci, R. de Kloet, E. Alleva, L. Minghetti, F. Cirulli

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

Deletion of the p66Shc gene in mice results in reduced levels of oxidative stress and longer lifespan. Reactive oxygen species (ROS) can lead to tissue damage, particularly in the brain. In this study we extended previous findings on the behavioral phenotype of the p66Shc-/- mice. Cognitive performance of adult and old p66Shc-/- and p66Shc+/+ mice was tested in a Morris water maze (MWM) task while general reactivity and pain sensitivity were assayed at adulthood, respectively, in an open field and by means of a tail flick test. Levels of brain-derived neurotrophic factor (BDNF), a neurotrophin involved in several aspects of synaptic plasticity, emotionality and pain sensitivity, were assessed in selected brain areas. P66Shc-/- adult subjects, compared to WT, overall showed a better performance in the MWM, lower emotionality and a higher pain threshold, in addition to increased basal levels of BDNF in the hippocampus, as well as decreased levels of oxidative stress markers in the same brain area. Although all aged subjects failed to learn the cognitive task, aged p66Shc-/- mice were characterized by a better physical performance. These results suggest an interaction between the p66Shc gene and specific signaling pathways involved in behavioral adaptation to stress and aging.

Original languageEnglish
Pages (from-to)200-208
Number of pages9
JournalExperimental Gerontology
Volume43
Issue number3
DOIs
Publication statusPublished - Mar 2008

Fingerprint

Oxidative stress
Brain-Derived Neurotrophic Factor
Nerve Growth Factors
Hippocampus
Brain
Oxidative Stress
Data storage equipment
Genes
Water
Pain
Neuronal Plasticity
Pain Threshold
Plasticity
Reactive Oxygen Species
Gene Deletion
Aging of materials
Tissue
Tail
Phenotype
Spatial Memory

Keywords

  • Aging
  • Anxiety
  • BDNF
  • Mice
  • Morris water maze
  • Neurodegeneration
  • Open field
  • Oxidative stress
  • p66
  • Pain sensitivity

ASJC Scopus subject areas

  • Ageing
  • Medicine(all)

Cite this

@article{172caa06197d48c89bff75a1088ce1c6,
title = "Deletion of the lifespan determinant p66Shc improves performance in a spatial memory task, decreases levels of oxidative stress markers in the hippocampus and increases levels of the neurotrophin BDNF in adult mice",
abstract = "Deletion of the p66Shc gene in mice results in reduced levels of oxidative stress and longer lifespan. Reactive oxygen species (ROS) can lead to tissue damage, particularly in the brain. In this study we extended previous findings on the behavioral phenotype of the p66Shc-/- mice. Cognitive performance of adult and old p66Shc-/- and p66Shc+/+ mice was tested in a Morris water maze (MWM) task while general reactivity and pain sensitivity were assayed at adulthood, respectively, in an open field and by means of a tail flick test. Levels of brain-derived neurotrophic factor (BDNF), a neurotrophin involved in several aspects of synaptic plasticity, emotionality and pain sensitivity, were assessed in selected brain areas. P66Shc-/- adult subjects, compared to WT, overall showed a better performance in the MWM, lower emotionality and a higher pain threshold, in addition to increased basal levels of BDNF in the hippocampus, as well as decreased levels of oxidative stress markers in the same brain area. Although all aged subjects failed to learn the cognitive task, aged p66Shc-/- mice were characterized by a better physical performance. These results suggest an interaction between the p66Shc gene and specific signaling pathways involved in behavioral adaptation to stress and aging.",
keywords = "Aging, Anxiety, BDNF, Mice, Morris water maze, Neurodegeneration, Open field, Oxidative stress, p66, Pain sensitivity",
author = "A. Berry and A. Greco and M. Giorgio and Pelicci, {P. G.} and {de Kloet}, R. and E. Alleva and L. Minghetti and F. Cirulli",
year = "2008",
month = "3",
doi = "10.1016/j.exger.2007.10.016",
language = "English",
volume = "43",
pages = "200--208",
journal = "Experimental Gerontology",
issn = "0531-5565",
publisher = "Elsevier Inc.",
number = "3",

}

TY - JOUR

T1 - Deletion of the lifespan determinant p66Shc improves performance in a spatial memory task, decreases levels of oxidative stress markers in the hippocampus and increases levels of the neurotrophin BDNF in adult mice

AU - Berry, A.

AU - Greco, A.

AU - Giorgio, M.

AU - Pelicci, P. G.

AU - de Kloet, R.

AU - Alleva, E.

AU - Minghetti, L.

AU - Cirulli, F.

PY - 2008/3

Y1 - 2008/3

N2 - Deletion of the p66Shc gene in mice results in reduced levels of oxidative stress and longer lifespan. Reactive oxygen species (ROS) can lead to tissue damage, particularly in the brain. In this study we extended previous findings on the behavioral phenotype of the p66Shc-/- mice. Cognitive performance of adult and old p66Shc-/- and p66Shc+/+ mice was tested in a Morris water maze (MWM) task while general reactivity and pain sensitivity were assayed at adulthood, respectively, in an open field and by means of a tail flick test. Levels of brain-derived neurotrophic factor (BDNF), a neurotrophin involved in several aspects of synaptic plasticity, emotionality and pain sensitivity, were assessed in selected brain areas. P66Shc-/- adult subjects, compared to WT, overall showed a better performance in the MWM, lower emotionality and a higher pain threshold, in addition to increased basal levels of BDNF in the hippocampus, as well as decreased levels of oxidative stress markers in the same brain area. Although all aged subjects failed to learn the cognitive task, aged p66Shc-/- mice were characterized by a better physical performance. These results suggest an interaction between the p66Shc gene and specific signaling pathways involved in behavioral adaptation to stress and aging.

AB - Deletion of the p66Shc gene in mice results in reduced levels of oxidative stress and longer lifespan. Reactive oxygen species (ROS) can lead to tissue damage, particularly in the brain. In this study we extended previous findings on the behavioral phenotype of the p66Shc-/- mice. Cognitive performance of adult and old p66Shc-/- and p66Shc+/+ mice was tested in a Morris water maze (MWM) task while general reactivity and pain sensitivity were assayed at adulthood, respectively, in an open field and by means of a tail flick test. Levels of brain-derived neurotrophic factor (BDNF), a neurotrophin involved in several aspects of synaptic plasticity, emotionality and pain sensitivity, were assessed in selected brain areas. P66Shc-/- adult subjects, compared to WT, overall showed a better performance in the MWM, lower emotionality and a higher pain threshold, in addition to increased basal levels of BDNF in the hippocampus, as well as decreased levels of oxidative stress markers in the same brain area. Although all aged subjects failed to learn the cognitive task, aged p66Shc-/- mice were characterized by a better physical performance. These results suggest an interaction between the p66Shc gene and specific signaling pathways involved in behavioral adaptation to stress and aging.

KW - Aging

KW - Anxiety

KW - BDNF

KW - Mice

KW - Morris water maze

KW - Neurodegeneration

KW - Open field

KW - Oxidative stress

KW - p66

KW - Pain sensitivity

UR - http://www.scopus.com/inward/record.url?scp=39149141395&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=39149141395&partnerID=8YFLogxK

U2 - 10.1016/j.exger.2007.10.016

DO - 10.1016/j.exger.2007.10.016

M3 - Article

C2 - 18065182

AN - SCOPUS:39149141395

VL - 43

SP - 200

EP - 208

JO - Experimental Gerontology

JF - Experimental Gerontology

SN - 0531-5565

IS - 3

ER -