Lat A causes loss of AMPARs from synapses. (A) After
cultures were treated with 20 μM lat A for 20 min, dendritic spines
colocalized with GluR1 staining can still be seen (arrowheads, red for
spines, green for GluR1), but there are also spines without GluR1
staining (arrows). (Scale bar: 10 μm.) (B) The
percentage of spines with colocalized GluR1 staining decreases after
treatment with lat A, indicating that AMPARs are dissociated from their
anchorings in the postsynaptic density (n = 10 and
9 for control and lat A, respectively, from three experiments).
(C) A significant reduction in both the amplitude and
frequency of AMPAR mEPSCs is observed in cultures treated with lat A.
Sample AMPAR mEPSCs are shown in Left for untreated and
lat A-treated cultures, whereas population data from 11 cells are shown
in the Right. (D) Reduction in AMPAR
mEPSCs occurs in the absence of changes in NMDAR mEPSCs. Dual component
mEPSCs were collected, and averaged responses from the same cell are
shown in the Left. After perfusion with lat A, a
significant reduction in the peak amplitude is observed, but there is
no change in the slow component (n = 5 cells).
Pharmacological isolation of AMPAR mEPSC with APV shows that the peak
is mainly due to AMPAR activation, whereas the slow component is
exclusively mediated by NMDARs.