maintenance of stable synaptic currents (Nishimune et al., 1998; Song et al., 1998) as well as the surface expres-Summary sion of AMPARs (Noel et al., 1999). These results raise the intriguing possibility that not only are AMPARs re-Compounds known to disrupt exocytosis or endocytodistributed in response to changes in the patterns of sis were introduced into CA1 pyramidal cells while synaptic activity, but they may also constituitively cycle monitoring excitatory postsynaptic currents (EPSCs).
into and out of the synaptic postsynaptic membrane.
Disrupting exocytosis or the interaction of GluR2 with
We have explored this possibility by applying directly NSF caused a gradual reduction in the AMPAR EPSC, into the postsynaptic cell a number of agents known to while inhibition of endocytosis caused a gradual inblock various steps in exocytosis and endocytosis. The crease in the AMPAR EPSC. These manipulations had results provide evidence for a remarkably dynamic sysno effect on the NMDAR EPSC but prevented the subtem for the control of the surface expression of synaptic sequent induction of LTD. These results suggest that AMPARs. AMPARs, but not NMDARs, cycle into and out of the synaptic membrane at a rapid rate and that certain Results forms of synaptic plasticity may utilize this dynamic process.
Inhibition of Exocytosis
We first examined the effects of loading cells with the light chains of type B botulinum toxin (Botox), which is