The Journal of Neuroscience, October 11, 2006, ():
Oligomerization of KCC2 Correlates with Development of Inhibitory Neurotransmission
J. Neurosci. Blaesse et al.
26: 10407
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Supplementary Figure S2. Co-localization analysis of KCC2 with compartment-specific proteins. A-H: Double-labeling of KCC2 (green, anti-nKCC2) and various marker proteins (red) in LSO neurons at P4 (A,C,E,G) and P12 (B,D,F,H). A,B: Double-labeling of KCC2 and the dendritic marker microtubule-associated protein MAP2. At both ages, KCC2-ir was restricted to the surface of somata (arrows) and dendrites (arrowheads), as identified by MAP2-ir. Co-localization of KCC2 and MAP2 was only sparse (asterisks). C,D: No co-localization of KCC2 and the endoplasmic reticulum marker PDI was observed at P4 and P12. E,F: Double-labeling of KCC2 and the Golgi marker GM130 revealed no co-localization at P4 and P12. G,H: A weak co-localization of KCC2 and the vesicle marker VAMP2 was detectable in the neuropil at P4 and P12 (asterisks). Scale bar in A, 10 µm (A-H).
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Supplementary Fig. S3. Analysis of the KCC2 gene SLC12A5 for developmentally regulated splice variants. The open reading frame of SLC12A5 was amplified in 9 overlapping fragments using brainstem cDNA derived from P3 and P12 rats. Fragments were separated on a high-resolution 5% polyacrylamide gel and stained with silver nitrate. Numbers above the lanes indicate the primers used for amplification. The fragment amplified from P3 cDNA is always shown to the left and that from P12 cDNA to the right. No difference in size was observed for any of the fragments, thus excluding the existence of SLC12A5 splice variants in the developing rat brainstem.
