Abstract
Objective
De novo somatic mutations in mTOR pathway genes during fetal development lead to focal malformation of cortical development (FMCD) and epilepsy. This FMCD is characterized by misplacement of enlarged pyramidal neurons displaying increased mTOR activity. Whether these neurons display enhanced excitability has remained an open question. Several lines of evidence in experimental murine FMCD suggest that FMCD neurons display a complex set of alterations, including dendrite hypertrophy associated with decreased rheobase but opposing changes in excitability due to the abnormal ...
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