Abstract：
:The syndrome of benign familial neonatal convulsions (BFNC) is characterized by seizures starting within the first days of life and disappearing within weeks to months. BFNC is caused by loss-of-function mutations in the potassium channels KCNQ2 and KCNQ3 which can well explain the resulting neuronal hyperexcitability. However, it is not understood why seizures predominantly occur in the neonatal period. A potential explanation might be a change in the expression pattern of these channels during development. We therefore performed an immunohistochemical analysis of mouse brain slices at different stages of postnatal development using an antibody recognizing the C-terminus of the KCNQ2 channel. A widespread immunohistochemical staining was observed, particularly in the hippocampus, caudoputamen, globus pallidus, cortex, thalamus, hypothalamus and midbrain. In the adult mouse brain, a predominantly axonal staining pattern was found, most observed in the caudoputamen, the alveus and the mossy fiber pathway of the hippocampus. The hippocampal staining pattern of adult mice was not observed before P8 and gradually developed between P11 and P21. Differences in the distribution of KCNQ2 channels within neurons between the neonatal period and adult stages might contribute to the increased seizure susceptibility in BFNC in humans.
journal_name
Brain Resjournal_title
Brain researchauthors
Weber YG,Geiger J,Kämpchen K,Landwehrmeyer B,Sommer C,Lerche Hdoi
10.1016/j.brainres.2006.01.023subject
Has Abstractpub_date
2006-03-10 00:00:00pages
1-6issue
1eissn
0006-8993issn
1872-6240pii
S0006-8993(06)00074-6journal_volume
1077pub_type
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