Pubmed-entry ::= {
pmid 21899605,
medent {
em std {
year 2011,
month 10,
day 4
},
cit {
title {
name "Change in the balance of excitatory and inhibitory midline fiber
crossing as an explanation for the hopping phenotype in EphA4 knockout mice."
},
authors {
names ml {
"Restrepo CE",
"Margaryan G",
"Borgius L",
"Lundfald L",
"Sargsyan D",
"Kiehn O"
},
affil str "Mammalian Locomotor Laboratory, Department of Neuroscience,
Karolinska Institutet, Retzius vag 8, Stockholm, Sweden."
},
from journal {
title {
iso-jta "Eur. J. Neurosci.",
ml-jta "Eur J Neurosci",
issn "1460-9568",
name "The European journal of neuroscience"
},
imp {
date std {
year 2011,
month 10
},
volume "34",
issue "7",
pages "1102-1112",
language "eng",
pubstatus ppublish,
history {
{
pubstatus aheadofprint,
date std {
year 2011,
month 9,
day 7
}
},
{
pubstatus other,
date std {
year 2011,
month 9,
day 9,
hour 6,
minute 0
}
},
{
pubstatus pubmed,
date std {
year 2011,
month 9,
day 9,
hour 6,
minute 0
}
},
{
pubstatus medline,
date std {
year 2012,
month 2,
day 11,
hour 6,
minute 0
}
}
}
}
},
ids {
doi "10.1111/j.1460-9568.2011.07838.x",
pubmed 21899605,
other {
db "ELocationID doi",
tag str "10.1111/j.1460-9568.2011.07838.x"
}
}
},
abstract "Neuronal networks in the spinal cord termed central pattern
generators (CPGs) are responsible for the generation of rhythmic movements,
such as walking. The axon guidance molecule EphA4 has been suggested to play
a role in the configuration of spinal CPG networks in mammals. In EphA4
knockout (EphA4-KO) mice, the normal alternating walking pattern is replaced
by a rabbit-like hopping gait, which can be reproduced when locomotor-like
activity is induced in the isolated spinal cord. This hopping phenotype has
been explained by an abnormal midline crossing of ipsilateral axons. Here, we
investigated the nature of this overcrossing in heterozygous EphA4
(EphA4(lacZ/+) ) mice that showed normal alternating gait and homozygous
EphA4 (EphA4(lacZ/lacZ) ) mice with hopping gait. Localized lesions showed
that the hopping phenotype is maintained by fibers crossing in the ventral
commissure. Using transgenic mouse lines in which glutamatergic, GABAergic
and glycinergic neurons are intrinsically labeled, we showed a significant
increase in the number of crossing excitatory beta-galactosidase-positive
neurons and a decrease in the number of inhibitory neurons crossing the
midline in EphA4(lacZ/lacZ) mice compared with EphA4(lacZ/+) mice. These
results show that the hopping phenotype is the result of a change in the
balance between excitatory and inhibitory signals across the midline and that
EphA4-positive neurons play an essential role in the mammalian CPG.",
mesh {
{
term "Animals"
},
{
term "Axons",
qual {
{
mp TRUE,
subh "physiology"
}
}
},
{
term "Cell Count"
},
{
term "Electrophysiology"
},
{
term "Gait",
qual {
{
subh "genetics"
},
{
mp TRUE,
subh "physiology"
}
}
},
{
term "Glutamic Acid",
qual {
{
subh "metabolism"
}
}
},
{
term "Glycine",
qual {
{
subh "metabolism"
}
}
},
{
term "Mice"
},
{
term "Mice, Knockout"
},
{
term "Motor Activity",
qual {
{
subh "genetics"
},
{
mp TRUE,
subh "physiology"
}
}
},
{
term "Neurons",
qual {
{
mp TRUE,
subh "physiology"
}
}
},
{
term "Phenotype"
},
{
term "Receptor, EphA4",
qual {
{
mp TRUE,
subh "genetics"
}
}
},
{
term "Spinal Cord",
qual {
{
subh "physiology"
}
}
},
{
term "gamma-Aminobutyric Acid",
qual {
{
subh "metabolism"
}
}
}
},
substance {
{
type cas,
cit "56-12-2",
name "gamma-Aminobutyric Acid"
},
{
type cas,
cit "56-40-6",
name "Glycine"
},
{
type cas,
cit "56-86-0",
name "Glutamic Acid"
},
{
type ec,
cit "2.7.10.1",
name "Receptor, EphA4"
}
},
idnum {
"5R01NS40795-09/NS/NINDS NIH HHS"
},
pmid 21899605,
pub-type {
"Journal Article",
"Research Support, N.I.H., Extramural",
"Research Support, Non-U.S. Gov't"
},
status medline
}
}
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