[Abstract Title]. - Society for Neuroscience

translocation. In neurons clamped at -40 mV, episodes of presynaptic activity resulted in EPSCs
associated with HPCA translocation mainly to dendritic spines while no translocation was
observed at -70 mV . At the same time HPCA-YFP translocation to spines at -70 mV was present
in Mg 2+ -free extracellular solution. NMDA receptor blocker, APV, partially blocked EPSCs and
completely blocked the translocation. Thus, Ca 2+ influx via synaptic NMDARs in which Mg 2+
block is relieved by APs is a main reason for HPCA-YFP translocation. Different types of
voltage activated Ca 2+ channels also contributed to the observed translocation. FRET
(fluorescence resonance energy transfer) between HPCA tagged by Yellow and Cyan
Fluorescent Proteins was increased in spines where the translocation was observed. It indicates
that the translocation was due to HPCA-FPs insertion in patches of spine membrane resulting in
decrease of protein concentration in the cytosol of spines and diffusion of new HPCA-FP
molecules from the dendritic trunk. As shown above this processes required association of
presynaptic glutamate release and AP generation in the postsynaptic neuron. Based on
estimations of HPCA-YFP concentration in the plasma membrane we have shown that
membranous HPCA concentration in spines is increased several times during synaptic NMDARdependent
translocation. Thus, we have shown that hippocalcin may decode [Ca 2+ ]i changes in
dendrites of hippocampal neurons, induced by simultaneous pre- and postsynaptic activity, into
its translocation to spines via diffusion from the neighboring parts of dendritic tree and robust
insertion in spine membranes.
Disclosures: V. Cherkas, None; P.V. Belan , None; A. Dovgan, None; D. Fitzgerald, None; A.
Tepikin, None; R.D. Burgoyne, None.
Poster
237. Synaptic Integration II
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 237.4/D29
Topic: B.07.c. Synaptic integration
Support: MH71401
MH7005
Title: Excitation necessary to reach threshold varies with input strength through a mechanism
involving feed forward inhibition
Authors: *A. MARIN-BURGIN 1 , F. R. POUILLE 2 , M. SCANZIANI 2 ;
1 Biol. -0634, UCSD, La Jolla, CA; 2 Biol., Univ. of California San Diego, La Jolla, CA