'Silent synapses' show responses from high-affinity NMDA receptors (NMDARs)
but not low-affinity AMPA receptors (AMPARs), but gain AMPAR responses upo
n long-term potentiation (LTP). Using the rapidly reversible NMDAR antagoni
st L-AP5 to assess cleft glutamate concentration ([glu](cleft)), we found t
hat it peaked at <<170 mu M at silent neonatal synapses, but greatly increa
sed after potentiation. Cyclothiazide (CTZ), a potentiator of AMPAR, reveal
ed slowly rising AMPA EPSCs at silent synapses; LTP shortened their rise ti
mes. Thus, LTP at silent synapses increased rate-of-rise and peak amplitude
of [glu](cleft). Release probability reported by NMDARs remained unchanged
during LTP, implying that [glu](cleft) increases arose from immediately pr
esynaptic terminals. Our data suggest that changes in the dynamics of fusio
n-pore opening contribute to LTP.