Geiger Julia, Weber Yvonne G, Landwehrmeyer Bernhard, Sommer Clemens, Lerche Holger
Department of Neurology, University of Ulm, Germany.
Neurosci Lett. 2006 May 29;400(1-2):101-4. doi: 10.1016/j.neulet.2006.02.017. Epub 2006 Mar 2.
KCNQ-type potassium channels generate the so-called M-current regulating excitability in many neurons. Mutations in KCNQ2/KCNQ3 channels can cause benign familial neonatal convulsions (BFNC). We describe the immunohistochemical staining of adult and developing mouse brain using an antibody directed against the N-terminus of KCNQ3 channels (KCNQ3N). A widespread KCNQ3N immunoreactivity predominantly of neuropil but also of somata was detected in different regions of the adult mouse brain, in particular in the hippocampus, cortex, thalamus and cerebellum. This staining pattern appeared gradually and became more intense during development. In the pyramidal cell layer of the hippocampus, the immunoreactivity changed from a more somatic to a neuropil staining during development. These changes during maturation might be related to the age-dependent phenotype of BFNC.
KCNQ型钾通道在许多神经元中产生所谓的M电流,调节兴奋性。KCNQ2/KCNQ3通道的突变可导致良性家族性新生儿惊厥(BFNC)。我们描述了使用针对KCNQ3通道N端的抗体(KCNQ3N)对成年和发育中小鼠脑进行免疫组织化学染色的情况。在成年小鼠脑的不同区域,特别是海马体、皮质、丘脑和小脑中,检测到广泛的KCNQ3N免疫反应性,主要在神经纤维网中,但也在体细胞中。这种染色模式在发育过程中逐渐出现并变得更加明显。在海马体的锥体细胞层,免疫反应性在发育过程中从更多的体细胞染色转变为神经纤维网染色。成熟过程中的这些变化可能与BFNC的年龄依赖性表型有关。