Enhancement of transmitter release accompanying with long-term potentiation in synapses between mossy fibers and CA3 neurons in hippocampus

1991 ◽  
Vol 123 (1) ◽  
pp. 73-76 ◽  
Author(s):  
Kazunari Hirata ◽  
Satsuki Sawada ◽  
Chosaburo Yamamoto
Keyword(s):  
Transmitter Release ◽  
Mossy Fibers ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Ca3 Neurons

Effect of tolbutamide on tetraethylammonium-induced postsynaptic zinc signals at hippocampal mossy fiber-CA3 synapses

2017 ◽  
Vol 95 (9) ◽  
pp. 1058-1063 ◽  
Author(s):  
Fatima C. Bastos ◽  
Vanessa N. Corceiro ◽  
Sandra A. Lopes ◽  
José G. de Almeida ◽  
Carlos M. Matias ◽  
...  
Keyword(s):  
Mossy Fiber ◽  
Mossy Fibers ◽  
Pyramidal Cells ◽  
Long Term Potentiation ◽  
Chemical Stimulation ◽  
Term Potentiation ◽  
Voltage Dependent ◽  
Zinc Release ◽  
Ca3 Pyramidal Cells

The application of tetraethylammonium (TEA), a blocker of voltage-dependent potassium channels, can induce long-term potentiation (LTP) in the synaptic systems CA3–CA1 and mossy fiber-CA3 pyramidal cells of the hippocampus. In the mossy fibers, the depolarization evoked by extracellular TEA induces a large amount of glutamate and also of zinc release. It is considered that zinc has a neuromodulatory role at the mossy fiber synapses, which can, at least in part, be due to the activation of presynaptic ATP-dependent potassium (KATP) channels. The aim of this work was to study properties of TEA-induced zinc signals, detected at the mossy fiber region, using the permeant form of the zinc indicator Newport Green. The application of TEA caused a depression of those signals that was partially blocked by the KATP channel inhibitor tolbutamide. After the removal of TEA, the signals usually increased to a level above baseline. These results are in agreement with the idea that intense zinc release during strong synaptic events triggers a negative feedback action. The zinc depression, caused by the LTP-evoking chemical stimulation, turns into potentiation after TEA washout, suggesting the existence of a correspondence between the observed zinc potentiation and TEA-evoked mossy fiber LTP.

ADAPTIVE CEREBELLAR SPIKING MODEL EMBEDDED IN THE CONTROL LOOP: CONTEXT SWITCHING AND ROBUSTNESS AGAINST NOISE

2011 ◽  
Vol 21 (05) ◽  
pp. 385-401 ◽  
Author(s):  
N. R. LUQUE ◽  
J. A. GARRIDO ◽  
R. R. CARRILLO ◽  
S. TOLU ◽  
E. ROS
Keyword(s):  
Degrees Of Freedom ◽  
Mossy Fibers ◽  
Long Term Potentiation ◽  
Biologically Inspired ◽  
Context Switching ◽  
Term Potentiation ◽  
Spiking Network ◽  
Three Degrees Of Freedom ◽  
Spiking Model

This work evaluates the capability of a spiking cerebellar model embedded in different loop architectures (recurrent, forward, and forward&recurrent) to control a robotic arm (three degrees of freedom) using a biologically-inspired approach. The implemented spiking network relies on synaptic plasticity (long-term potentiation and long-term depression) to adapt and cope with perturbations in the manipulation scenario: changes in dynamics and kinematics of the simulated robot. Furthermore, the effect of several degrees of noise in the cerebellar input pathway (mossy fibers) was assessed depending on the employed control architecture. The implemented cerebellar model managed to adapt in the three control architectures to different dynamics and kinematics providing corrective actions for more accurate movements. According to the obtained results, coupling both control architectures (forward&recurrent) provides benefits of the two of them and leads to a higher robustness against noise.

Rapid Translocation of Zn2+ From Presynaptic Terminals Into Postsynaptic Hippocampal Neurons After Physiological Stimulation

2001 ◽  
Vol 86 (5) ◽  
pp. 2597-2604 ◽  
Author(s):  
Yang Li ◽  
Christopher J. Hough ◽  
Sang Won Suh ◽  
John M. Sarvey ◽  
Christopher J. Frederickson
Keyword(s):  
Hippocampal Neurons ◽  
Hippocampal Slices ◽  
Mossy Fibers ◽  
Synaptic Cleft ◽  
Immediate Release ◽  
Long Term Potentiation ◽  
Anatomical Location ◽  
Term Potentiation ◽  
Presynaptic Boutons

Zn2+ is found in glutamatergic nerve terminals throughout the mammalian forebrain and has diverse extracellular and intracellular actions. The anatomical location and possible synaptic signaling role for this cation have led to the hypothesis that Zn2+ is released from presynaptic boutons, traverses the synaptic cleft, and enters postsynaptic neurons. However, these events have not been directly observed or characterized. Here we show, using microfluorescence imaging in rat hippocampal slices, that brief trains of electrical stimulation of mossy fibers caused immediate release of Zn2+ from synaptic terminals into the extracellular microenvironment. Release was induced across a broad range of stimulus intensities and frequencies, including those likely to induce long-term potentiation. The amount of Zn2+ release was dependent on stimulation frequency (1–200 Hz) and intensity. Release of Zn2+ required sodium-dependent action potentials and was dependent on extracellular Ca2+. Once released, Zn2+ crosses the synaptic cleft and enters postsynaptic neurons, producing increases in intracellular Zn2+ concentration. These results indicate that, like a neurotransmitter, Zn2+ is stored in synaptic vesicles and is released into the synaptic cleft. However, unlike conventional transmitters, it also enters postsynaptic neurons, where it may have manifold physiological functions as an intracellular second messenger.

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.

Voltage-clamp analysis of synaptic inhibition during long-term potentiation in hippocampus

1986 ◽  
Vol 55 (4) ◽  
pp. 767-775 ◽  
Author(s):  
W. H. Griffith ◽  
T. H. Brown ◽  
D. Johnston
Keyword(s):  
Voltage Clamp ◽  
Mossy Fiber ◽  
Long Term Potentiation ◽  
Synaptic Efficacy ◽  
Synaptic Response ◽  
Inhibitory Component ◽  
Mixed Response ◽  
Term Potentiation ◽  
Ca3 Neurons

The excitatory synaptic response evoked by stimulating the mossy fiber synaptic input to hippocampal CA3 neurons in normally accompanied by concomitant feedforward or recurrent inhibition. The purpose of the present study was to determine whether a decrease in the inhibitory conductance of this mixed synaptic response contributes to the enhanced synaptic efficacy observed during long-term potentiation (LTP). Intracellular recordings were made from CA3 neurons of rat hippocampal brain slices. Current- and voltage-clamp measurements of the mixed excitatory/inhibitory evoked synaptic response were made, using a single-electrode clamp system. Outward and inward rectification were reduced, respectively, by intracellular injection and bath application of Cs+. Biophysical analysis of the evoked synaptic conductance sequence was performed before and 15 min to 1 h after inducing LTP. As expected, measurements made in the early part of the conductance sequence, which represents primarily the monosynaptic excitatory input, demonstrated an increase in the slope conductance during LTP. Measurements made later in the conductance sequence, when the excitatory component appeared to have declined to a negligible value, revealed no decrease in the slope conductance of the inhibitory component of the mixed response. We conclude that a decrease in the conductance associated with the inhibitory component of the mixed synaptic response plays little or no role in the increase in synaptic efficacy observed during LTP of this synaptic system.

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