A. Schiegg, W. Gerstner, R. Ritz, and J.Leo van Hemmen
Intracellular Ca2+ stores can account for the time course of LTP
induction: A model of Ca2+ dynamics in dendritic spines.
J. Neurophysiol. 74(3), 1046-1055, 1995
Summary and Conclusions
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A model of Ca2+ dynamics in spines of CA1 hippocampal neurons
is presented. In contrast to traditional models which concentrate
on the effects of Ca2+ influx, diffusion, buffering,
and extrusion, we also consider the additional effect
of intracellular Ca2+ stores.
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It is shown that traditional models without Ca2+ stores
cannot account for the time course of LTP induction as found
in recent experiments. Experimental data suggest that
the intracellular Ca2+ concentration should be elevated
for up to two seconds, whereas the Ca2+ concentration in
standard models of Ca2+ dynamics decays much faster.
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When intracellular Ca2+ stores are taken into account,
a much slower decay is found.
In particular, a model simulation with a stimulation paradigm consisting of
two bursts of four impulses at 100Hz each and variable interburst
intervals can reproduce experimental results
found for primed or theta burst stimulation.
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In our model, Ca2+ release from the store
has a nonlinear, bell-shaped dependence
upon the intracellular Ca2+ concentration,
similar to the one found for
inositoltrisphosphat and ryanodine receptors. These receptors are known
to control calcium release from intracellular stores.
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Our model suggests an important
role of intracellular calcium stores
in the induction of LTP. The stores serve as a long-term calcium source
which can sustain an intracellular Ca2+ concentration above the
resting level for 1-2s.
Raphael Ritz
Wed Sep 6 16:33:21 PDT 1995