Immunhistochemische Analyse der spannungsgesteuerten Kalium-Kanäle KCNQ2 und KCNQ3 in Hirnschnitten von Mäusen in verschiedenen Entwicklungsstadien
Auch gedruckt in der BibliothekZ: J-H 11.478 ; W: W-H 9.595
Ressourcen- / MedientypDissertation, Text
Datum der Freischaltung2007-05-23
Benign familial neonatal convulsions (BFNC) are an autosomal dominant epileptic syndrome characterized by seizures starting within the first days of life and disappearing within weeks to months. BFNC are caused by loss-of-function mutations in the potassium channels KCNQ2 and KCNQ3 which can well explain the resulting neuronal hyperexcitability. The question remains as to why seizures predominantly occur in the neonatal period. A possible 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 predominant axonal staining pattern was found, best observed in the caudoputamen, the alveus and the mossy fiber pathway of the hippocampus. The hippocampal staining pattern in adult mice was not observed before P8 and gradually developed between P11 and P21. Differences in the neuronal distribution of KCNQ2 channels between the neonatal period and adult stages might contribute to the increased seizure susceptibility in BFNC in humans.
LizenzStandard (Fassung vom 03.05.2003)
MeSHEpilepsy, benign neonatal
Kcnq2 protein, mouse