Sayin et al. Neuroscience Journal-2015-Febrile-Seizures-Development


a Department of Neurology, University of Wisconsin, UW
Medical Foundation Centennial Building,1685 Highland
Avenue, Madison, WI 53705, USA
b Department of Medical Physics, University of Wisconsin,
Wisconsin Institutes Medical Research, 1111 Highland
Avenue, Madison, WI 53705, USA
c Department of Biomedical Engineering, University of
Wisconsin, Room 2130, Engineering Centers Building, 1550
Engineering Drive, Madison, WI 53706-1609, USA

Abstract—Neural activity promotes circuit formation in
developing systems and during critical periods permanently
modifies circuit organization and functional properties.
These observations suggest that excessive neural activity,
as occurs during seizures, might influence developing neural
circuitry with long-term outcomes that depend on age at
the time of seizures. We systematically examined long-term
structural and functional consequences of seizures induced
in rats by kainic acid, pentylenetetrazol, and hyperthermia
across postnatal ages from birth through postnatal day 90
in adulthood (P90). Magnetic resonance imaging (MRI), diffusion
tensor imaging (DTI), and electrophysiological methods
at PP95 following seizures induced from P1 to P90
demonstrated consistent patterns of gross atrophy, microstructural
abnormalities in the corpus callosum (CC) and
hippocampus, and functional alterations in hippocampal circuitry
at PP95 that were independent of the method of seizure
induction and varied systematically as a function of
age at the time of seizures. Three distinct epochs were
observed in which seizures resulted in distinct long-term
structural and functional outcomes at PP95. Seizures prior
to P20 resulted in DTI abnormalities in CC and hippocampus
in the absence of gross cerebral atrophy, and increased
paired-pulse inhibition (PPI) in the dentate gyrus (DG) at
PP95. Seizures after P30 induced a different pattern of DTI
abnormalities in the fimbria and hippocampus accompanied
by gross cerebral atrophy with increases in lateral ventricular
volume, as well as increased PPI in the DG at PP95. In
contrast, seizures between P20 and P30 did not result
in cerebral atrophy or significant imaging abnormalities in
the hippocampus or white matter, but irreversibly decreased
PPI in the DG compared to normal adult controls. These
age-specific long-term structural and functional outcomes
identify P20–30 as a potential critical period in hippocampal
development defined by distinctive long-term structural and
functional properties in adult hippocampal circuitry,
including loss of capacity for seizure-induced plasticity in
adulthood that could influence epileptogenesis and
other hippocampal-dependent behaviors and functional
properties.  2014 IBRO. Published by Elsevier Ltd. All
rights reserved.

Key words: epilepsy, hippocampus, dentate gyrus, in vivo
imaging, developmental plasticity, critical periods.


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