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The Journal of Neurophysiology Vol. 85 No. 1 January 2001, pp. 399-406
Copyright ©2001 by the American Physiological Society
Department of Neurosciences, University of New Mexico, School of Medicine, Albuquerque, New Mexico 87131
Cormier, R. J.,
A. C. Greenwood, and
J. A. Connor.
Bidirectional Synaptic Plasticity Correlated With the Magnitude
of Dendritic Calcium Transients Above a Threshold. J. Neurophysiol. 85: 399-406, 2001. The magnitude
of postsynaptic Ca2+ transients is thought to
affect activity-dependent synaptic plasticity associated with learning and memory. Large Ca2+ transients have been
implicated in the induction of long-term potentiation (LTP), while
smaller Ca2+ transients have been associated with
long-term depression (LTD). However, a direct relationship has not been
demonstrated between Ca2+ measurements and
direction of synaptic plasticity in the same cells, using one induction
protocol. Here, we used glutamate iontophoresis to induce
Ca2+ transients in hippocampal CA1 neurons
injected with the Ca2+-indicator fura-2. Test
stimulation of one or two synaptic pathways before and after
iontophoresis showed that the direction of synaptic plasticity
correlated with glutamate-induced Ca2+ levels
above a threshold, below which no plasticity occurred (~180 nM).
Relatively low Ca2+ levels (180-500 nM)
typically led to LTD of synaptic transmission and higher levels (>500
nM) often led to LTP. Failure to show plasticity correlated with
Ca2+ levels in two distinct ranges: <180 nM and
~450-600 nM, while only LTD occurred between these ranges. Our data
support a class of models in which failure of
Ca2+ transients to affect transmission may arise
either from insufficient Ca2+ to
affect Ca2+-sensitive proteins regulating
synaptic strength through opposing activities or from higher
Ca2+ levels that reset activities of such
proteins without affecting the net balance of activities. Our estimates
of the threshold Ca2+ level for LTD (~180 nM)
and for the transition from LTD to LTP (~540 nM) may assist in
constraining the molecular details of such models.
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