Postfusional regulation of cleft glutamate concentration during LTP at 'silent synapses'

Citation
S. Choi et al., Postfusional regulation of cleft glutamate concentration during LTP at 'silent synapses', NAT NEUROSC, 3(4), 2000, pp. 330-336
Citations number
43
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NATURE NEUROSCIENCE
ISSN journal
10976256 → ACNP
Volume
3
Issue
4
Year of publication
2000
Pages
330 - 336
Database
ISI
SICI code
1097-6256(200004)3:4<330:PROCGC>2.0.ZU;2-7
Abstract
'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.