Exogenous reelin prevents granule cell dispersion in experimental epilepsy

Müller, Martin C.; Osswald, Matthias; Tinnes, Stefanie; Häussler, Ute; Jacobi, Anne; Förster, Eckart; Frotscher, Michael; Haas, Carola A.

doi:10.1016/j.expneurol.2008.12.029

Cited by 54 publications

(45 citation statements)

References 28 publications

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“…Recently, Haas and colleagues provided experimental evidence that Reelin deficiency and displacement of mature neurons underlie the granule cell dispersion in the epileptic hippocampus (Heinrich et al, 2006;Muller et al, 2009). Moreover, the group of Bluemcke showed that this phenomenon was associated with increased reelin promoter methylation in the epileptic brain (Kobow et al, 2009) however, most individuals continue to experience cognitive deficits throughout their life.…”

Section: Implications Of Altered Reelin Signaling For Neurological Anmentioning

confidence: 99%

Reelin-mediated signaling in neuropsychiatric and neurodegenerative diseases

Knuesel

2010

Progress in Neurobiology

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Section: Implications Of Altered Reelin Signaling For Neurological Anmentioning

confidence: 99%

Reelin-mediated signaling in neuropsychiatric and neurodegenerative diseases

Knuesel

2010

Progress in Neurobiology

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“…Two major functions seem to be associated with the reelin pathway. First, recent studies indicate reelin as an important factor to preserve hippocampal lamination, i.e., application of recombinant reelin in a kainate model of epilepsy inhibits seizure-associated granule cell dispersion of the dentate gyrus (Müller et al 2009). Vice versa, inhibition of reelin by hippocampal injection of the CR-50 antibody results in massive granule cell dispersion (Heinrich et al 2006).…”

Section: Reelin In Synaptic Transmission and Plasticitymentioning

confidence: 99%

“…Reelin signaling influences granule cell dispersion in the dentate gyrus during experimental epilepsy, implying a role in the maintenance of cortical lamination (Heinrich et al 2006;Müller et al 2009). Furthermore, an increasing body of evidence suggests a function of reelin in synaptic transmission and plasticity.…”

Section: Introductionmentioning

confidence: 99%

Laminar distribution of neurotransmitter receptors in different reeler mouse brain regions

et al. 2011

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Mapping of multiple receptors of neurotransmitters provides insight into the spatial distribution of neurotransmission-relevant molecules in the cerebral cortex. During development, lack of reelin leads to impaired migration, disturbed lamination of the hippocampus and inverted neocortical layering. In the adult, reelin may regulate synaptic plasticity by modulating neurotransmitter receptor function. Using quantitative in vitro receptor autoradiography, different receptors, in particular, the binding site densities and laminar distribution of various glutamate, GABA, muscarinic and nicotinic acetylcholine, serotonin, dopamine and adenosine receptors, were analyzed in cortical and subcortical structures of reeler and wild-type brains. Differential changes in the laminar distribution, maximum binding capacity (B (max)) and regional density of neurotransmitter receptors were found in the reeler brain. A decrease of whole brain B (max) was found for adenosine A(1) and GABA(A) receptors. In the forebrain, several binding sites were differentially up- or down-regulated (kainate, A(1), benzodiazepine, 5-HT(1), M(2), α(1) and α(2)). In the hippocampus, a significant decrease of GABA(B), 5-HT(1) and A'₁ receptors were observed. The density of M(2) receptors increased, while other receptors remained unchanged. In the neocortex, some receptors demonstrated an obviously inverted laminar distribution (AMPA, kainate, NMDA, GABA(B), 5-HT(1), M(1), M(3), nAch), while the distribution of others (A(1), GABA(A), benzodiazepine, 5-HT(2), muscarinic M(2), adrenergic α(1), α(2)) seemed to be less affected. Thus, the laminar receptor distribution is modulated by the developmental impairment and suggests and reflects partially the laminar inversion in reeler mice.

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“…The most recent classification allowed correlations between clinical histories, post-surgical outcomes and neuropathological findings [19][20][21][22][23]. For example, an early (<3 years old) initial precipitating event is associated with a type 1a or 1b HS (i.e., classical or total HS) and a better post-surgical outcome [14,19,[24][25][26][27][28]. A recent consensus classification, validated through the neuropathology taskforce of the International League Against Epilepsy (ILAE) tried to incorporate aspects of all previous schemes [27,[29][30][31][32].…”

Section: Introductionmentioning

confidence: 99%