Developmental changes in Notch1 and NLE1 expression in a genetic model of absence epilepsy
作者： Fariba Karimzadeh , Sayed Mostafa Modarres Mousavi , Fatemeh Alipour , Hassan Hosseini Ravandi , Stjepana Kovac
DOI: 10.1007/S00429-017-1371-9
关键词: Notch 1 、 Somatosensory system 、 Biology 、 Spike-and-wave 、 Genetic model 、 Epileptogenesis 、 Epilepsy 、 Childhood absence epilepsy 、 Neuroscience 、 Notch signaling pathway
摘要: Childhood absence epilepsy (CAE) is an syndrome with seizures occurring in the early childhood, highlighting that susceptibility CAE dependent on brain development. The Notch 1 signalling pathway important development, yet role of Notch1 remains elusive. We here explored and its modulator notchless homologue (NLE1) expression WAG/Rij control rats using immunohistochemistry. Functional effects were assessed vivo. lack developmental increase cortical NLE mRNA seen controls, NLE1 protein lower somatosensory cortices when compared to controls. This coincided overall decreased GFAP development rats. These region-specific as they not observed thalamic tissues. Neuron-to-glia ratio a marker impact differentiation was higher layer 4 cortex Acute application agonist Jagged suppressed, whereas DAPT, antagonist, facilitated spike wave discharges (SWDs) findings point which likely shapes architectural organization cortex, region critically involved epileptogenesis CAE. More immediate are vivo SWDs CAE, pointing possible treatment target
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