Reelin deficiency causes granule cell dispersion in epilepsy.
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Reelin deficiency causes granule cell dispersion in epilepsy. / Haas, Carola A; Frotscher, Michael.
in: EXP BRAIN RES, Jahrgang 200, Nr. 2, 2, 2010, S. 141-149.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Reelin deficiency causes granule cell dispersion in epilepsy.
AU - Haas, Carola A
AU - Frotscher, Michael
PY - 2010
Y1 - 2010
N2 - Cortical migration defects are often associated with epilepsy. In mesial temporal lobe epilepsy (MTLE), granule cell dispersion (GCD), a migration defect of dentate granule cells, is frequently observed. Little is known how GCD develops and to which extent it contributes to the development of seizure activity. Since the reelin-deficient reeler mouse mutant shows a similar migration defect of dentate cells, we performed a series of studies investigating whether reelin deficiency is involved in GCD development. We show that in MTLE patients and in a mouse model of MTLE, the development of GCD correlates with a loss of the extracellular matrix protein reelin. In addition, we present evidence that GCD occurs in the absence of neurogenesis, thus representing a displacement of mature neurons due to a reelin deficiency. Accordingly, antibody blockade of reelin function in naïve, adult mice induced GCD. Finally, we show that GCD formation can be prevented by infusion of exogenous reelin. In summary, these studies show that in epilepsy reelin dysfunction causes GCD development and that reelin is important for the maintenance of layered structures in the adult brain.
AB - Cortical migration defects are often associated with epilepsy. In mesial temporal lobe epilepsy (MTLE), granule cell dispersion (GCD), a migration defect of dentate granule cells, is frequently observed. Little is known how GCD develops and to which extent it contributes to the development of seizure activity. Since the reelin-deficient reeler mouse mutant shows a similar migration defect of dentate cells, we performed a series of studies investigating whether reelin deficiency is involved in GCD development. We show that in MTLE patients and in a mouse model of MTLE, the development of GCD correlates with a loss of the extracellular matrix protein reelin. In addition, we present evidence that GCD occurs in the absence of neurogenesis, thus representing a displacement of mature neurons due to a reelin deficiency. Accordingly, antibody blockade of reelin function in naïve, adult mice induced GCD. Finally, we show that GCD formation can be prevented by infusion of exogenous reelin. In summary, these studies show that in epilepsy reelin dysfunction causes GCD development and that reelin is important for the maintenance of layered structures in the adult brain.
KW - Animals
KW - Humans
KW - Mice
KW - Mice, Mutant Strains
KW - Brain pathology
KW - Cell Adhesion Molecules, Neuronal deficiency
KW - Cell Movement physiology
KW - Epilepsy pathology
KW - Extracellular Matrix Proteins deficiency
KW - Nerve Tissue Proteins deficiency
KW - Neurons physiology
KW - Serine Endopeptidases deficiency
KW - Animals
KW - Humans
KW - Mice
KW - Mice, Mutant Strains
KW - Brain pathology
KW - Cell Adhesion Molecules, Neuronal deficiency
KW - Cell Movement physiology
KW - Epilepsy pathology
KW - Extracellular Matrix Proteins deficiency
KW - Nerve Tissue Proteins deficiency
KW - Neurons physiology
KW - Serine Endopeptidases deficiency
M3 - SCORING: Zeitschriftenaufsatz
VL - 200
SP - 141
EP - 149
JO - EXP BRAIN RES
JF - EXP BRAIN RES
SN - 0014-4819
IS - 2
M1 - 2
ER -
