Motor Enrichment and the Induction of Plasticity before or after Brain Injury

Jeffrey Kleim, Theresa A. Jones, Timothy Schallert

Research output: Contribution to journalArticle

255 Citations (Scopus)

Abstract

Voluntary exercise, treadmill activity, skills training, and forced limb use have been utilized in animal studies to promote brain plasticity and functional change. Motor enrichment may prime the brain to respond more adaptively to injury, in part by upregulating trophic factors such as GDNF, FGF-2, or BDNF. Discontinuation of exercise in advance of brain injury may cause levels of trophic factor expression to plummet below baseline, which may leave the brain more vulnerable to degeneration. Underfeeding and motor enrichment induce remarkably similar molecular and cellular changes that could underlie their beneficial effects in the aged or injured brain. Exercise begun before focal ischemic injury increases BDNF and other defenses against cell death and can maintain or expand motor representations defined by cortical microstimulation. Interfering with BDNF synthesis causes the motor representations to recede or disappear. Injury to the brain, even in sedentary rats, causes a small, gradual increase in astrocytic expression of neurotrophic factors in both local and remote brain regions. The neurotrophic factors may inoculate those areas against further damage and enable brain repair and use-dependent synaptogenesis associated with recovery of function or compensatory motor learning. Plasticity mechanisms are particularly active during time-windows early after focal cortical damage or exposure to dopamine neurotoxins. Motor and cognitive impairments may contribute to self-imposed behavioral impoverishment, leading to a reduced plasticity. For slow degenerative models, early forced forelimb use or exercise has been shown to halt cell loss, whereas delayed rehabilitation training is ineffective and disuse is prodegenerative. However, it is possible that, in the chronic stages after brain injury, a regimen of exercise would reactivate mechanisms of plasticity and thus enhance rehabilitation targeting residual functional deficits.

Original languageEnglish (US)
Pages (from-to)1757-1769
Number of pages13
JournalNeurochemical Research
Volume28
Issue number11
DOIs
StatePublished - Nov 2003
Externally publishedYes

Fingerprint

Brain Injuries
Plasticity
Brain
Brain-Derived Neurotrophic Factor
Nerve Growth Factors
Rehabilitation
Glial Cell Line-Derived Neurotrophic Factor
Patient rehabilitation
Forelimb
Recovery of Function
Wounds and Injuries
Neurotoxins
Fibroblast Growth Factor 2
Dopamine
Exercise equipment
Teaching
Cell Death
Extremities
Learning
Cell death

Keywords

  • Aging
  • BDNF
  • Degeneration
  • Enrichment
  • Exercise
  • Experience
  • FGF-2
  • GDNF
  • Neurotrophic factors
  • Parkinson's disease
  • Rehabilitation
  • Stroke

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry

Cite this

Motor Enrichment and the Induction of Plasticity before or after Brain Injury. / Kleim, Jeffrey; Jones, Theresa A.; Schallert, Timothy.

In: Neurochemical Research, Vol. 28, No. 11, 11.2003, p. 1757-1769.

Research output: Contribution to journalArticle

Kleim, Jeffrey ; Jones, Theresa A. ; Schallert, Timothy. / Motor Enrichment and the Induction of Plasticity before or after Brain Injury. In: Neurochemical Research. 2003 ; Vol. 28, No. 11. pp. 1757-1769.
@article{6443a05e4e0941e8a81979335ebb9e78,
title = "Motor Enrichment and the Induction of Plasticity before or after Brain Injury",
abstract = "Voluntary exercise, treadmill activity, skills training, and forced limb use have been utilized in animal studies to promote brain plasticity and functional change. Motor enrichment may prime the brain to respond more adaptively to injury, in part by upregulating trophic factors such as GDNF, FGF-2, or BDNF. Discontinuation of exercise in advance of brain injury may cause levels of trophic factor expression to plummet below baseline, which may leave the brain more vulnerable to degeneration. Underfeeding and motor enrichment induce remarkably similar molecular and cellular changes that could underlie their beneficial effects in the aged or injured brain. Exercise begun before focal ischemic injury increases BDNF and other defenses against cell death and can maintain or expand motor representations defined by cortical microstimulation. Interfering with BDNF synthesis causes the motor representations to recede or disappear. Injury to the brain, even in sedentary rats, causes a small, gradual increase in astrocytic expression of neurotrophic factors in both local and remote brain regions. The neurotrophic factors may inoculate those areas against further damage and enable brain repair and use-dependent synaptogenesis associated with recovery of function or compensatory motor learning. Plasticity mechanisms are particularly active during time-windows early after focal cortical damage or exposure to dopamine neurotoxins. Motor and cognitive impairments may contribute to self-imposed behavioral impoverishment, leading to a reduced plasticity. For slow degenerative models, early forced forelimb use or exercise has been shown to halt cell loss, whereas delayed rehabilitation training is ineffective and disuse is prodegenerative. However, it is possible that, in the chronic stages after brain injury, a regimen of exercise would reactivate mechanisms of plasticity and thus enhance rehabilitation targeting residual functional deficits.",
keywords = "Aging, BDNF, Degeneration, Enrichment, Exercise, Experience, FGF-2, GDNF, Neurotrophic factors, Parkinson's disease, Rehabilitation, Stroke",
author = "Jeffrey Kleim and Jones, {Theresa A.} and Timothy Schallert",
year = "2003",
month = "11",
doi = "10.1023/A:1026025408742",
language = "English (US)",
volume = "28",
pages = "1757--1769",
journal = "Neurochemical Research",
issn = "0364-3190",
publisher = "Springer New York",
number = "11",

}

TY - JOUR

T1 - Motor Enrichment and the Induction of Plasticity before or after Brain Injury

AU - Kleim, Jeffrey

AU - Jones, Theresa A.

AU - Schallert, Timothy

PY - 2003/11

Y1 - 2003/11

N2 - Voluntary exercise, treadmill activity, skills training, and forced limb use have been utilized in animal studies to promote brain plasticity and functional change. Motor enrichment may prime the brain to respond more adaptively to injury, in part by upregulating trophic factors such as GDNF, FGF-2, or BDNF. Discontinuation of exercise in advance of brain injury may cause levels of trophic factor expression to plummet below baseline, which may leave the brain more vulnerable to degeneration. Underfeeding and motor enrichment induce remarkably similar molecular and cellular changes that could underlie their beneficial effects in the aged or injured brain. Exercise begun before focal ischemic injury increases BDNF and other defenses against cell death and can maintain or expand motor representations defined by cortical microstimulation. Interfering with BDNF synthesis causes the motor representations to recede or disappear. Injury to the brain, even in sedentary rats, causes a small, gradual increase in astrocytic expression of neurotrophic factors in both local and remote brain regions. The neurotrophic factors may inoculate those areas against further damage and enable brain repair and use-dependent synaptogenesis associated with recovery of function or compensatory motor learning. Plasticity mechanisms are particularly active during time-windows early after focal cortical damage or exposure to dopamine neurotoxins. Motor and cognitive impairments may contribute to self-imposed behavioral impoverishment, leading to a reduced plasticity. For slow degenerative models, early forced forelimb use or exercise has been shown to halt cell loss, whereas delayed rehabilitation training is ineffective and disuse is prodegenerative. However, it is possible that, in the chronic stages after brain injury, a regimen of exercise would reactivate mechanisms of plasticity and thus enhance rehabilitation targeting residual functional deficits.

AB - Voluntary exercise, treadmill activity, skills training, and forced limb use have been utilized in animal studies to promote brain plasticity and functional change. Motor enrichment may prime the brain to respond more adaptively to injury, in part by upregulating trophic factors such as GDNF, FGF-2, or BDNF. Discontinuation of exercise in advance of brain injury may cause levels of trophic factor expression to plummet below baseline, which may leave the brain more vulnerable to degeneration. Underfeeding and motor enrichment induce remarkably similar molecular and cellular changes that could underlie their beneficial effects in the aged or injured brain. Exercise begun before focal ischemic injury increases BDNF and other defenses against cell death and can maintain or expand motor representations defined by cortical microstimulation. Interfering with BDNF synthesis causes the motor representations to recede or disappear. Injury to the brain, even in sedentary rats, causes a small, gradual increase in astrocytic expression of neurotrophic factors in both local and remote brain regions. The neurotrophic factors may inoculate those areas against further damage and enable brain repair and use-dependent synaptogenesis associated with recovery of function or compensatory motor learning. Plasticity mechanisms are particularly active during time-windows early after focal cortical damage or exposure to dopamine neurotoxins. Motor and cognitive impairments may contribute to self-imposed behavioral impoverishment, leading to a reduced plasticity. For slow degenerative models, early forced forelimb use or exercise has been shown to halt cell loss, whereas delayed rehabilitation training is ineffective and disuse is prodegenerative. However, it is possible that, in the chronic stages after brain injury, a regimen of exercise would reactivate mechanisms of plasticity and thus enhance rehabilitation targeting residual functional deficits.

KW - Aging

KW - BDNF

KW - Degeneration

KW - Enrichment

KW - Exercise

KW - Experience

KW - FGF-2

KW - GDNF

KW - Neurotrophic factors

KW - Parkinson's disease

KW - Rehabilitation

KW - Stroke

UR - http://www.scopus.com/inward/record.url?scp=0142116301&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0142116301&partnerID=8YFLogxK

U2 - 10.1023/A:1026025408742

DO - 10.1023/A:1026025408742

M3 - Article

C2 - 14584829

AN - SCOPUS:0142116301

VL - 28

SP - 1757

EP - 1769

JO - Neurochemical Research

JF - Neurochemical Research

SN - 0364-3190

IS - 11

ER -