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Biophys J, November 1999, p. 2418-2429, Vol. 77, No. 5
Abt. Membranbiophysik, Max-Planck-Institut für biophysikalische Chemie, Am Fassberg 11, D-37077 Göttingen, Germany
We explore the properties of models of synaptic vesicle
dynamics, in which synaptic depression is attributed to depletion of a
pool of release-ready vesicles. Two alternative formulations of the
model allow for either recruitment of vesicles from an unlimited
reserve pool (vesicle state model) or for recovery of a fixed number of
release sites to a release-ready state (release-site model). It is
assumed that, following transmitter release, the recovery of the
release-ready pool of vesicles is regulated by the intracellular free
Ca++ concentration, [Ca++]i.
Considering the kinetics of [Ca++]i after
single presynaptic action potentials, we show that pool recovery can be
described by two distinct kinetic components. With such a model,
complex kinetic and steady-state properties of synaptic depression as
found in several types of synapses can be accurately described.
However, the specific assumption that enhanced recovery is proportional
to [Ca++]i, as measured with Ca++
indicator dyes, is not confirmed by experiments at the calyx of Held,
in which [Ca++]i-homeostasis was altered by
adding low concentrations of the exogenous Ca++ buffer,
fura-2, to the presynaptic terminal. We conclude that synaptic
depression at the calyx of Held is governed by localized, near membrane
[Ca++]i signals not visible to the indicator
dye, or else by an altogether different mechanism. We demonstrate that,
in models in which a Ca++-dependent process is linearly
related to [Ca++]i, the addition of buffers
has only transient but not steady-state consequences.
Biophys J, November 1999, p. 2418-2429, Vol. 77, No. 5
© 1999 by the Biophysical Society 0006-3495/99/11/2418/12 $2.00
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