[Abstract Title]. - Society for Neuroscience

30 min of stimulus interruption the remaining depression (LTD) was 20 - 25 % and not
significantly different. When using AP5 and LY 341495 separately significantly more depression
was observed when NMDAR activation was allowed than when mGluR activation was allowed.
When mGluR activation was allowed 1 Hz stimulation produced significantly more depression
than did 0.2 Hz stimulation. Nevertheless, this depression was no more than that obtained when
both NMDARs and mGluRs were blocked. In conclusion, in the developing rat prolonged
stimulation at sub-LFS, as well as LFS, frequencies produce LTD that does not need
NMDA/mGluR activation for its induction. It is proposed that LTD in the developing CA3 -
CA1 synapse mainly reflects AMPA silencing facilitated by but not requiring NMDAR
activation and counteracted (specifically at sub-LFS frequencies) by mGluR activation.
Disclosures: J. Strandberg, None; B. Gustafsson, None.
Poster
238. LTD: Hippocampus and Cortex
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 238.22/D67
Topic: B.08.f. Long-term depression ( LTD )
Support: NIH-NINDS Grant RO1NS049661
Title: Redistribution of CaMKII to inhibitory synapses following NMDA receptor activation
Authors: *K. C. MARSDEN 1 , K. U. BAYER 2 , R. C. CARROLL 1 ;
1 Dominick P. Purpura Dept Neurosci, Albert Einstein Coll Med., Bronx, NY; 2 Univ. of Colorado
Denver Hlth. Sci. Program, Denver, CO
Abstract: Maintaining a balance between excitatory and inhibitory synaptic inputs is critical for
normal brain function, as disruptions in excitability can lead to diseases such as epilepsy, anxiety
and even autism. This balance can be regulated through the strengthening or weakening of
synapses, which in turn can happen through the insertion or removal of receptors from the
postsynaptic membrane. We have previously demonstrated that activation of NMDA receptors, a
model for long-term depression of excitatory synapses, simultaneously decreases surface AMPA
receptor (AMPAR) expression and increases that of GABAA receptors in hippocampal neurons.
This process potentiates inhibitory synaptic transmission and requires CaMKII for its expression.
CaMKII is well known for its role in excitatory LTP and AMPAR trafficking, and it has been
shown to translocate to excitatory synapses following LTP-like stimuli. Although it has
previously been implicated in GABAAR trafficking and the potentiation of inhibitory synapses,
CaMKII expression at inhibitory synaptic locations has not been examined. Here we provide data