InChI |
InChI=1S/C49H92N18O13S/c1-26(2)38(67-45(76)31(15-8-11-22-52)63-44(75)33(19-24-81-5)64-42(73)32(16-12-23-58-49(56)57)62-41(72)29(53)13-6-9-20-50)47(78)60-28(4)39(70)61-30(14-7-10-21-51)43(74)66-35(25-37(55)69)46(77)59-27(3)40(71)65-34(48(79)80)17-18-36(54)68/h26-35,38H,6-25,50-53H2,1-5H3,(H2,54,68)(H2,55,69)(H,59,77)(H,60,78)(H,61,70)(H,62,72)(H,63,75)(H,64,73)(H,65,71)(H,66,74)(H,67,76)(H,79,80)(H4,56,57,58)/t27-,28-,29-,30-,31-,32-,33-,34-,35-,38-/m0/s1
|
Reference |
- Blockade of the NSF–GluR2 interaction by a specific peptide (pep2m) introduced into neurons prevented homosynaptic, de novo long-term depression (LTD). Moreover, saturation of LTD prevented the pep2m-induced reduction in AMPAR-mediated excitatory postsynaptic currents (EPSCs). Minimal stimulation experiments indicated that both pep2m action and LTD were due to changes in quantal size and quantal content but were not associated with changes in AMPAR single-channel conductance or EPSC kinetics.
- Hippocampal LTD Expression Involves a Pool of AMPARs Regulated by the NSF–GluR2 Interaction
- Viral expression of pep2m reduced the surface expression of α-amino-3-hydroxy-5-methyl-isoxazolepropionate (AMPA) receptors, whereas NMDA receptor surface expression in the same living cells was unchanged. In permeabilized neurons, the total amount of GluR2 immunoreactivity was unchanged, and a punctate distribution of GluR2 was observed throughout the dendritic tree.
- Surface Expression of AMPA Receptors in Hippocampal Neurons Is Regulated by an NSF-Dependent Mechanism
|