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@article{1817031,
author = {Bencúrová, Petra and Laakso, Hanne and Salo, Raimo A. and Paasonen, Ekaterina and Manninen, Eppu and Paasonen, Jaakko and Michaeli, Shalom and Mangia, Silvia and Bareš, Martin and Brázdil, Milan and Kubová, Hana and Grohn, Olli},
article_location = {SAN DIEGO},
article_number = {January 2022},
doi = {http://dx.doi.org/10.1016/j.nbd.2021.105566},
keywords = {Animal model; Status Epilepticus; Temporal Lobe Epilepsy; Myelin development; White matter integrity; MRI; Histology; Thalamocortical connectivity},
language = {eng},
issn = {0969-9961},
journal = {NEUROBIOLOGY OF DISEASE},
title = {Infantile status epilepticus disrupts myelin development},
url = {https://www.sciencedirect.com/science/article/pii/S0969996121003156?via%3Dihub},
volume = {162},
year = {2022}
}
TY - JOUR
ID - 1817031
AU - Bencúrová, Petra - Laakso, Hanne - Salo, Raimo A. - Paasonen, Ekaterina - Manninen, Eppu - Paasonen, Jaakko - Michaeli, Shalom - Mangia, Silvia - Bareš, Martin - Brázdil, Milan - Kubová, Hana - Grohn, Olli
PY - 2022
TI - Infantile status epilepticus disrupts myelin development
JF - NEUROBIOLOGY OF DISEASE
VL - 162
IS - January 2022
SP - 1-13
EP - 1-13
PB - ACADEMIC PRESS INC ELSEVIER SCIENCE
SN - 09699961
KW - Animal model
KW - Status Epilepticus
KW - Temporal Lobe Epilepsy
KW - Myelin development
KW - White matter integrity
KW - MRI
KW - Histology
KW - Thalamocortical connectivity
UR - https://www.sciencedirect.com/science/article/pii/S0969996121003156?via%3Dihub
N2 - Temporal lobe epilepsy (TLE) is the most prevalent type of epilepsy in adults; it often starts in infancy or early childhood. Although TLE is primarily considered to be a grey matter pathology, a growing body of evidence links this disease with white matter abnormalities. In this study, we explore the impact of TLE onset and progression in the immature brain on white matter integrity and development utilising the rat model of Li-pilocarpine-induced TLE at the 12th postnatal day (P). Diffusion tensor imaging (DTI) and Black-Gold II histology uncovered disruptions in major white matter tracks (corpus callosum, internal and external capsules, and deep cerebral white matter) spreading through the whole brain at P28. These abnormalities were mostly not present any longer at three months after TLE induction, with only limited abnormalities detectable in the external capsule and deep cerebral white matter. Relaxation Along a Fictitious Field in the rotating frame of rank 4 indicated that white matter changes observed at both timepoints, P28 and P72, are consistent with decreased myelin content. The animals affected by TLE-induced white matter abnormalities exhibited increased functional connectivity between the thalamus and medial prefrontal and somatosensory cortex in adulthood. Furthermore, histological analyses of additional animal groups at P15 and P18 showed only mild changes in white matter integrity, suggesting a gradual age-dependent impact of TLE progression. Taken together, TLE progression in the immature brain distorts white matter development with a peak around postnatal day 28, followed by substantial recovery in adulthood. This developmental delay might give rise to cognitive and behavioural comorbidities typical for earlyonset TLE.
ER -
BENCÚROVÁ, Petra, Hanne LAAKSO, Raimo A. SALO, Ekaterina PAASONEN, Eppu MANNINEN, Jaakko PAASONEN, Shalom MICHAELI, Silvia MANGIA, Martin BAREŠ, Milan BRÁZDIL, Hana KUBOVÁ and Olli GROHN. Infantile status epilepticus disrupts myelin development. \textit{NEUROBIOLOGY OF DISEASE}. SAN DIEGO: ACADEMIC PRESS INC ELSEVIER SCIENCE, 2022, vol.~162, January 2022, p.~1-13. ISSN~0969-9961. Available from: https://dx.doi.org/10.1016/j.nbd.2021.105566.
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