Regulation of hippocampal transmitter release during development and long-term potentiation

Science ◽  
1995 ◽  
Vol 269 (5231) ◽  
pp. 1730-1734 ◽  
Author(s):  
V. Bolshakov ◽  
S. Siegelbaum
Keyword(s):  
Transmitter Release ◽  
Long Term Potentiation ◽  
Term Potentiation

Presynaptic transmitter release is specified by postsynaptic neurons of Aplysia buccal ganglia

1991 ◽  
Vol 66 (6) ◽  
pp. 2150-2154 ◽  
Author(s):  
D. Gardner
Keyword(s):  
Transmitter Release ◽  
Long Term Potentiation ◽  
Variation Method ◽  
Postsynaptic Neuron ◽  
Synaptic Current ◽  
Quantal Release ◽  
Buccal Ganglia ◽  
Term Potentiation ◽  
Quantal Analysis

1. In Aplysia buccal ganglia, in which dual presynaptic neurons innervate multiple postsynaptic cells, strengths of the same identified synapses differ from animal to animal, consistent with developmental or plastic modulation. Synaptic strengths are specified by the postsynaptic neuron, so that synaptic current amplitudes are similar for inputs from different presynaptic cells converging on a postsynaptic cell but different for branches of the same neuron diverging onto different targets. 2. The coefficient of variation method of quantal analysis reveals that differences in synaptic strength, although specified postsynaptically, result partially from differences in the number of quanta released by presynaptic terminals. 3. This quantization is consistent with classical presynaptic models and suggests retrograde modulation of quantal release as postulated for hippocampal long-term potentiation.

scholarly journals Mechanism of long-term potentiation of transmitter release induced by adrenaline in bullfrog sympathetic ganglia.

1986 ◽  
Vol 87 (5) ◽  
pp. 775-793 ◽  
Author(s):  
E Kumamoto ◽  
K Kuba
Keyword(s):  
Transmitter Release ◽  
Long Term Potentiation ◽  
Sympathetic Ganglia ◽  
Presynaptic Terminal ◽  
Synaptic Delay ◽  
K Channel ◽  
Term Potentiation ◽  
Relative Change ◽  
Theoretical Considerations

A mechanism of the long-term potentiation of transmitter release induced by adrenaline (ALTP) was studied by recording intracellularly the fast excitatory postsynaptic potentials (fast EPSPs). The ALTP was produced during the blockade of K+ channels at the presynaptic terminals by tetraethylammonium (TEA). The synaptic delay, possibly reflecting a relative change in the duration of an action potential at the presynaptic terminal, was not changed during the course of the ALTP. By contrast, it was significantly lengthened by TEA and other K+ channel inhibitors (4-aminopyridine and Cs+) that markedly enhanced the evoked release of transmitter. The magnitude of facilitation of the fast EPSP, induced by a conditional stimulus to the preganglionic nerve, was decreased during the generation of the ALTP, but was unchanged during the potentiation of transmitter release caused by TEA. These results, together with theoretical considerations applying the residual Ca2+ hypothesis to the facilitation, suggest that the enhancement of transmitter release during the ALTP is not caused by an increased Ca2+ influx during a presynaptic impulse owing to the blockade of K+ channel or the modulation of Ca2+ channel, but presumably is induced by a rise in the basal level of free Ca2+ in the presynaptic terminal.

Persistent enhancement of transmitter release accompanying long-term potentiation in the guinea pig hippocampus

1991 ◽  
Vol 130 (2) ◽  
pp. 259-262 ◽  
Author(s):  
Haruyuki Kamiya ◽  
Satsuki Sawada ◽  
Chosaburo Yamamoto
Keyword(s):  
Guinea Pig ◽  
Transmitter Release ◽  
Long Term Potentiation ◽  
Term Potentiation

Distinct Transmitter Release Properties Determine Differences in Short-Term Plasticity at Functional and Silent Synapses

2006 ◽  
Vol 95 (5) ◽  
pp. 3024-3034 ◽  
Author(s):  
Carolina Cabezas ◽  
Washington Buño
Keyword(s):  
Transmitter Release ◽  
Molecular Mechanisms ◽  
Long Term Potentiation ◽  
Lower Percentage ◽  
Functional Importance ◽  
Short Term ◽  
Short Term Plasticity ◽  
Silent Synapses ◽  
Term Potentiation

Recent evidence suggests that functional and silent synapses are not only postsynaptically different but also presynaptically distinct. The presynaptic differences may be of functional importance in memory formation because a proposed mechanism for long-term potentiation is the conversion of silent synapses into functional ones. However, there is little direct experimentally evidence of these differences. We have investigated the transmitter release properties of functional and silent Schaffer collateral synapses and show that on the average functional synapses displayed a lower percentage of failures and higher excitatory postsynaptic current (EPSC) amplitudes than silent synapses at +60 mV. Moreover, functional but not silent synapses show paired-pulse facilitation (PPF) at +60 mV and thus presynaptic short-term plasticity will be distinct in the two types of synapse. We examined whether intraterminal endoplasmic reticulum Ca2+ stores influenced the release properties of these synapses. Ryanodine (100 μM) and thapsigargin (1 μM) increased the percentage of failures and decreased both the EPSC amplitude and PPF in functional synapses. Caffeine (10 mM) had the opposite effects. In contrast, silent synapses were insensitive to both ryanodine and caffeine. Hence we have identified differences in the release properties of functional and silent synapses, suggesting that synaptic terminals of functional synapses express regulatory molecular mechanisms that are absent in silent synapses.

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