Definition of the Readily Releasable Pool of Vesicles at Hippocampal Synapses

A readily releasable pool of quanta, tentatively identified with docked synaptic vesicles, has been defined by analysis of the neurotransmitter release caused by application of hypertonic solutions. The goal of this work is to determine the relationship of this functionally defined readily releasable pool to the one drawn upon by action potential-evoked release. We find that hypertonic solutions do not act through changes in intracellular calcium. Since the release produced by action potentials and hypertonic solutions varies in parallel as the pool size is changed, we conclude that the same pool is shared by both mechanisms. This conclusion, taken together with other observations in the literature, means that the synaptic release probability depends on the size of the readily releasable pool.

[1]  J. T. Hackett,et al.  Ca(2+)-independent and Ca(2+)-dependent stimulation of quantal neurosecretion in avian ciliary ganglion neurons. , 1992, Journal of neurophysiology.

[2]  E. Alnaes,et al.  Is hyperosmotic neurosecretion from motor nerve endings a calcium-dependent process? , 1977, Nature.

[3]  C. Jahr,et al.  Quisqualate receptor-mediated depression of calcium currents in hippocampal neurons , 1990, Neuron.

[4]  E. Liberman,et al.  A study of the mechanism of quantal transmitter release at a chemical synapse , 1968, The Journal of physiology.

[5]  F. Sachs,et al.  Block of stretch-activated ion channels in Xenopus oocytes by gadolinium and calcium ions. , 1989, Science.

[6]  D. Faber,et al.  Quantal analysis and synaptic efficacy in the CNS , 1991, Trends in Neurosciences.

[7]  M. Turelli,et al.  The kinetics of quantal transmitter release from retinal amacrine cells. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[8]  I. Cohen,et al.  Calcium and transmitter release. , 1985, International review of neurobiology.

[9]  Robert F. Miller,et al.  Hyperosmotic activation of transmitter release from presynaptic terminals onto retinal ganglion cells , 1995, Journal of Neuroscience Methods.

[10]  C. Stevens,et al.  Facilitation and depression at single central synapses , 1995, Neuron.

[11]  J. T. Hackett,et al.  Calcium: Is It Required for Transmitter Secretion? , 1971, Science.

[12]  J. Clements,et al.  Presynaptic glutamate receptors depress excitatory monosynaptic transmission between mouse hippocampal neurones. , 1990, The Journal of physiology.

[13]  S. Redman.  Quantal analysis of synaptic potentials in neurons of the central nervous system. , 1990, Physiological reviews.

[14]  R. Tsien,et al.  Properties of synaptic transmission at single hippocampal synaptic boutons , 1995, Nature.

[15]  R. Nicoll,et al.  Presynaptic inhibition: transmitter and ionic mechanisms. , 1979, International review of neurobiology.

[16]  R. Zucker.  Changes in the statistics of transmitter release during facilitation , 1973, The Journal of physiology.

[17]  Christian Rosenmund,et al.  Synaptic NMDA receptor channels have a low open probability , 1995, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[18]  Christian Rosenmund,et al.  Nonuniform probability of glutamate release at a hippocampal synapse. , 1993, Science.

[19]  C. Stevens,et al.  Estimates for the pool size of releasable quanta at a single central synapse and for the time required to refill the pool. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[20]  C. Stevens,et al.  The kinetics of transmitter release at the frog neuromuscular junction , 1972, The Journal of physiology.

[21]  D. Tank,et al.  Presynaptic calcium and serotonin-mediated enhancement of transmitter release at crayfish neuromuscular junction , 1991, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[22]  R E Thies,et al.  NEUROMUSCULAR DEPRESSION AND THE APPARENT DEPLETION OF TRANSMITTER IN MAMMALIAN MUSCLE. , 1965, Journal of neurophysiology.

[23]  J. Hubbard,et al.  An examination of the effects of osmotic pressure changes upon transmitter release from mammalian motor nerve terminals , 1968, The Journal of physiology.

[24]  V N Morozov,et al.  Mechanical deformation enhances catalytic activity of crystalline carboxypeptidase A , 1995, Protein science : a publication of the Protein Society.

[25]  Thomas C. Südhof,et al.  The synaptic vesicle cycle: a cascade of protein–protein interactions , 1995, Nature.

[26]  C. Stevens,et al.  Excitatory and inhibitory autaptic currents in isolated hippocampal neurons maintained in cell culture. , 1991, Proceedings of the National Academy of Sciences of the United States of America.

[27]  T. Südhof,et al.  Synaptotagmin I: A major Ca2+ sensor for transmitter release at a central synapse , 1994, Cell.