Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2009 Jul 13;186(1):85–97. doi: 10.1083/jcb.200901084

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2009 Rex et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

PMC Copyright notice

Figure 7. — Inhibition of Rac-PAK signaling extends the period over which actin filament assembly is required for LTP. Stimulation was applied to Schaffer collateral afferents to hippocampal field CA1b. (A) Slices labeled for F-actin after 4-min local infusion of 0.2 µM Lat A. (left) Images show that Lat A blocked increases in phalloidin-labeled spines when applied 30 s but not 10 min after TBS. (middle) The plot shows F-actin–labeled spine counts (mean ± SEM) from slices treated with vehicle (veh) at 30 s after TBS or with Lat A initiated at the time points indicated (*, P < 0.05 vs. control). (right) The plot shows mean LTP magnitude (percent fEPSP slope measured 80–90 min after TBS vs. baseline) from experiments in which slices were treated locally with Lat A or vehicle for 4 min beginning at the time points indicated (**, P < 0.01 vs. respective control pathways). Measures for untreated, unstimulated (control [con]) slices are also shown. The dashed line indicates baseline level. (B) Prolonged Lat A bath infusion (open horizontal line), timed to hit slices at 10 min after TBS (arrow), did not disrupt LTP when applied alone (with vehicle) but blocked the stable maintenance of LTP in the presence of the Rac inhibitor NSC23766 (closed horizontal bar). A second control pathway (triangles) not receiving TBS was unaffected by drug manipulations. (top) Representative fEPSP traces collected at time points indicated in the plot. (C) Western blots from slices incubated with 2 µM of the Group I PAK–specific inhibitor IPA-3 for 1 h and probed for pPAK^S141 or pPAK^T423. β-Actin bands shown were generated from the stripped PAK^T423 blot. Plots show group mean (±SEM) band densities as a fraction of vehicle controls (*, P < 0.05 vs. vehicle). (D) Slices incubated for 50 min with 2 µM IPA-3 (closed horizontal bar) before TBS (arrow; TBS pathway shown as closed circles) exhibited stable LTP of typical magnitude (dashed line), but Lat A washed in at 30 min after TBS caused potentiation to decay to baseline levels within 2 h. The unstimulated control pathway (open triangles) was unaffected by drug manipulations. (top) Representative fEPSP traces from the time points indicated. (B and D) Vertical bar, 1 mV; horizontal bar, 10 ms. Bar, 5 µm.