Age-related alterations in energy metabolism contribute to the increased vulnerability of the aging brain to anoxic damage

Eugene L. Roberts; Ching Ping Chih

doi:10.1016/0006-8993(95)00168-P

Age-related alterations in energy metabolism contribute to the increased vulnerability of the aging brain to anoxic damage

Eugene L. Roberts, Ching Ping Chih

Neurology

Research output: Contribution to journal › Article › peer-review

30 Scopus citations

Abstract

Aging increases the vulnerability of brain tissue to anoxia and ischemia. We investigated whether age-related alterations in energy metabolism underlie this increased vulnerability. Energy metabolism was manipulated in hippocampal slices from Fischer 344 rats of ages 6-9 (young adult), 16-19 (middle-aged adult), and 26-29 (aged adult) months by altering glucose concentrations or by using lactate instead of glucose as the metabolic substrate. Extracellular K⁺ activity (K_o⁺) and synaptic excitability were monitored in stratum pyramidale of hippocampal subfield CA1. Aging diminished how well increasing concentrations of glucose delayed onset of anoxic depolarization and improved postanoxic recovery of K_o⁺ homeostasis and synaptic transmission. Hippocampal slices from all age groups responded to anoxia similarly when lactate was present instead of glucose. Also, no age-related differences were seen in normoxic ATP and phosphocreatine levels. These results suggest that an age-related decline in the glycolytic capacity of brain cells contributes to earlier onset of anoxic depolarization and poorer recovery of ion homeostasis and synaptic transmission in aging brain tissue.

Original language	English (US)
Pages (from-to)	83-90
Number of pages	8
Journal	Brain research
Volume	678
Issue number	1-2
DOIs	https://doi.org/10.1016/0006-8993(95)00168-P
State	Published - Apr 24 1995

Keywords

Anoxia
Brain slice
Glucose
Hippocampus
Hypoxia
Ion transport
Lactate
Synaptic transmission

ASJC Scopus subject areas

Developmental Biology
Molecular Biology
Clinical Neurology
Neuroscience(all)

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@article{b1a6346dcf404182a4b0b7d923f5b810,

title = "Age-related alterations in energy metabolism contribute to the increased vulnerability of the aging brain to anoxic damage",

abstract = "Aging increases the vulnerability of brain tissue to anoxia and ischemia. We investigated whether age-related alterations in energy metabolism underlie this increased vulnerability. Energy metabolism was manipulated in hippocampal slices from Fischer 344 rats of ages 6-9 (young adult), 16-19 (middle-aged adult), and 26-29 (aged adult) months by altering glucose concentrations or by using lactate instead of glucose as the metabolic substrate. Extracellular K+ activity (Ko+) and synaptic excitability were monitored in stratum pyramidale of hippocampal subfield CA1. Aging diminished how well increasing concentrations of glucose delayed onset of anoxic depolarization and improved postanoxic recovery of Ko+ homeostasis and synaptic transmission. Hippocampal slices from all age groups responded to anoxia similarly when lactate was present instead of glucose. Also, no age-related differences were seen in normoxic ATP and phosphocreatine levels. These results suggest that an age-related decline in the glycolytic capacity of brain cells contributes to earlier onset of anoxic depolarization and poorer recovery of ion homeostasis and synaptic transmission in aging brain tissue.",

keywords = "Anoxia, Brain slice, Glucose, Hippocampus, Hypoxia, Ion transport, Lactate, Synaptic transmission",

author = "Roberts, {Eugene L.} and Chih, {Ching Ping}",

note = "Funding Information: This work was supportebdy PHS Grant AG08710, and by a grant from the AmericanF ederationfo r Aging Research(A FAR). We thankD r. Zi-Cai Feng (Dept. of Neurology)fo r his technicaal ssistancien completinsgo mep rotocolso f this study.W e are also gratefutlo Dr. RobertD uncan( Dept.o f Epidemiology andP ublicH ealth)a ndD r. StephenR athbun(D ept.o f StatisticsU, niversityo f Georgiaf)o r theirh elpw iththe statisticus sedi n this study.I n additionw, e thankM r. SolomonP ikarsky( Dept.of Neurologyf)o r his devel-opmento f the computehr ardwarea nd softwareu sed for data collection.F inally, we thank Drs. Myron Rosenthaaln dT homasJ. Sick (Dept.o f Neurologyf)o r theirm anyh elpfulc ommentrse gardintgh ispaper.",

year = "1995",

month = apr,

day = "24",

doi = "10.1016/0006-8993(95)00168-P",

language = "English (US)",

volume = "678",

pages = "83--90",

journal = "Brain Research",

issn = "0006-8993",

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T1 - Age-related alterations in energy metabolism contribute to the increased vulnerability of the aging brain to anoxic damage

AU - Roberts, Eugene L.

AU - Chih, Ching Ping

N1 - Funding Information: This work was supportebdy PHS Grant AG08710, and by a grant from the AmericanF ederationfo r Aging Research(A FAR). We thankD r. Zi-Cai Feng (Dept. of Neurology)fo r his technicaal ssistancien completinsgo mep rotocolso f this study.W e are also gratefutlo Dr. RobertD uncan( Dept.o f Epidemiology andP ublicH ealth)a ndD r. StephenR athbun(D ept.o f StatisticsU, niversityo f Georgiaf)o r theirh elpw iththe statisticus sedi n this study.I n additionw, e thankM r. SolomonP ikarsky( Dept.of Neurologyf)o r his devel-opmento f the computehr ardwarea nd softwareu sed for data collection.F inally, we thank Drs. Myron Rosenthaaln dT homasJ. Sick (Dept.o f Neurologyf)o r theirm anyh elpfulc ommentrse gardintgh ispaper.

PY - 1995/4/24

Y1 - 1995/4/24

N2 - Aging increases the vulnerability of brain tissue to anoxia and ischemia. We investigated whether age-related alterations in energy metabolism underlie this increased vulnerability. Energy metabolism was manipulated in hippocampal slices from Fischer 344 rats of ages 6-9 (young adult), 16-19 (middle-aged adult), and 26-29 (aged adult) months by altering glucose concentrations or by using lactate instead of glucose as the metabolic substrate. Extracellular K+ activity (Ko+) and synaptic excitability were monitored in stratum pyramidale of hippocampal subfield CA1. Aging diminished how well increasing concentrations of glucose delayed onset of anoxic depolarization and improved postanoxic recovery of Ko+ homeostasis and synaptic transmission. Hippocampal slices from all age groups responded to anoxia similarly when lactate was present instead of glucose. Also, no age-related differences were seen in normoxic ATP and phosphocreatine levels. These results suggest that an age-related decline in the glycolytic capacity of brain cells contributes to earlier onset of anoxic depolarization and poorer recovery of ion homeostasis and synaptic transmission in aging brain tissue.

AB - Aging increases the vulnerability of brain tissue to anoxia and ischemia. We investigated whether age-related alterations in energy metabolism underlie this increased vulnerability. Energy metabolism was manipulated in hippocampal slices from Fischer 344 rats of ages 6-9 (young adult), 16-19 (middle-aged adult), and 26-29 (aged adult) months by altering glucose concentrations or by using lactate instead of glucose as the metabolic substrate. Extracellular K+ activity (Ko+) and synaptic excitability were monitored in stratum pyramidale of hippocampal subfield CA1. Aging diminished how well increasing concentrations of glucose delayed onset of anoxic depolarization and improved postanoxic recovery of Ko+ homeostasis and synaptic transmission. Hippocampal slices from all age groups responded to anoxia similarly when lactate was present instead of glucose. Also, no age-related differences were seen in normoxic ATP and phosphocreatine levels. These results suggest that an age-related decline in the glycolytic capacity of brain cells contributes to earlier onset of anoxic depolarization and poorer recovery of ion homeostasis and synaptic transmission in aging brain tissue.

KW - Anoxia

KW - Brain slice

KW - Glucose

KW - Hippocampus

KW - Hypoxia

KW - Ion transport

KW - Lactate

KW - Synaptic transmission

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U2 - 10.1016/0006-8993(95)00168-P

DO - 10.1016/0006-8993(95)00168-P

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C2 - 7620902

AN - SCOPUS:0028958796

VL - 678

SP - 83

EP - 90

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 1-2

ER -

Age-related alterations in energy metabolism contribute to the increased vulnerability of the aging brain to anoxic damage

Abstract

Keywords

ASJC Scopus subject areas

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