Skip to main content
. Author manuscript; available in PMC: 2009 Oct 1.
Published in final edited form as: Neurobiol Dis. 2008 Jul 3;32(1):26–36. doi: 10.1016/j.nbd.2008.06.013

Figure 5. HCN1 subunits are mislocalized in CA1 28 d after status epilepticus.

Figure 5

A–B, Sagittal sections of control brain [A and B (a-b)] and brain fixed 28 d after SE (28 d SE) [A and B (c–d)] were immunolabeled with gp α-HCN1 or gp α-HCN2 and ms α-PSD95 and visualized with α-gp-alexa488 (left panels, green) and α-ms-cy3 (right panels, red), respectively, for fluorescence staining. HCN1 (A–a, arrow), and HCN2 (B–a, arrow) are both enriched in distal dendritic arborizations within the SLM. The distal dendritic enrichment of HCN1 is lost (A–c, asterisk), whereas high HCN1 immunoreactivity appears in the stratum pyramidale (SP) layer (A–c, arrowheads) of area CA1 of the 28 d SE brains. HCN2 remains enriched in SLM of area CA1 of 28 d SE brain (B–c, arrow), but novel somatic staining is observed (B–c, arrowheads). Note that the distribution pattern of PSD95 is unaltered (A–b, A–d, B–b, B–d), consistent with minimal neuronal damage. Insets (A–b, A–d) are 100x (with 2x digital zoom) images of SLM dendritic fields showing a punctate staining pattern of PSD95, that is similar in 28 d SE and control dendrites of hippocampal area CA1. C–E, The relative intensity of HCN1 (C), HCN2 (D), and PSD95 (E) immunoreactivity from stratum oriens (SO) to SLM layer was quantified and graphed. Note the increased HCN1 and HCN2 intensity in soma and decreased HCN1 but not HCN2 intensity in SLM layer 28 d after SE (**p< 0.05, ***p<0.001). Distribution of PSD95 immunoreactivity at 28 d after SE was not significantly different from control. Data points are mean ±SEM of 5 different animals (control) and 10 different animals (28 d SE). Scale bars: 100µm (5µm inset). See materials and methods section for detailed description of the analysis method.