scholarly journals Determinants of synaptic strength vary across an axon arbor

2012 ◽  
Vol 107 (9) ◽  
pp. 2430-2441 ◽  
Author(s):  
Xiaoyu Peng ◽  
Thomas D. Parsons ◽  
Rita J. Balice-Gordon
Keyword(s):  
Synaptic Vesicles ◽  
Hippocampal Neurons ◽  
Synaptic Strength ◽  
Pool Size ◽  
Spatial Modulation ◽  
Readily Releasable Pool ◽  
Single Axon ◽  
Individual Vesicle ◽  
Highly Correlated ◽  
Vesicle Pool

We used synaptophysin-pHluorin expressed in hippocampal neurons to address how functional properties of terminals, namely, evoked release, total vesicle pool size, and release fraction, vary spatially across individual axon arbors. Consistent with previous reports, over short arbor distances (∼100 μm), evoked release was spatially heterogeneous when terminals contacted different postsynaptic dendrites or neurons. Regardless of the postsynaptic configuration, the evoked release and total vesicle pool size spatially covaried, suggesting that the fraction of synaptic vesicles available for release (release fraction) was similar over short distances. Evoked release and total vesicle pool size were highly correlated with the amount of NMDA receptors and PSD-95 in postsynaptic specialization. However, when individual axons were followed over longer distances (several hundred micrometers), a significant increase in evoked release was observed distally that was associated with an increased release fraction in distal terminals. The increase in distal release fraction can be accounted for by changes in individual vesicle release probability as well as readily releasable pool size. Our results suggest that for a single axon arbor, presynaptic strength indicated by evoked release over short distances is correlated with heterogeneity in total vesicle pool size, whereas over longer distances presynaptic strength is correlated with the spatial modulation of release fraction. Thus the mechanisms that determine synaptic strength differ depending on spatial scale.

A Simple Depletion Model of the Readily Releasable Pool of Synaptic Vesicles Cannot Account for Paired-Pulse Depression

2007 ◽  
Vol 97 (1) ◽  
pp. 948-950 ◽  
Author(s):  
Jane M. Sullivan
Keyword(s):  
Synaptic Vesicles ◽  
Hippocampal Neurons ◽  
Synaptic Activity ◽  
Excitatory Synapses ◽  
Short Term ◽  
Paired Pulse ◽  
Short Term Plasticity ◽  
Releasable Pool ◽  
Readily Releasable Pool ◽  
Paired Pulse Depression

Paired-pulse depression (PPD) is a form of short-term plasticity that plays a central role in processing of synaptic activity and is manifest as a decrease in the size of the response to the second of two closely timed stimuli. Despite mounting evidence to the contrary, PPD is still commonly thought to reflect depletion of the pool of synaptic vesicles available for release in response to the second stimulus. Here it is shown that PPD cannot be accounted for by depletion at excitatory synapses made by hippocampal neurons because PPD is unaffected by changes in the fraction of the readily releasable pool (RRP) released by the first of a pair of pulses.

scholarly journals Endogenous Rho-Kinase Signaling Maintains Synaptic Strength by Stabilizing the Size of the Readily Releasable Pool of Synaptic Vesicles

2012 ◽  
Vol 32 (1) ◽  
pp. 68-84 ◽  
Author(s):  
D. Gonzalez-Forero ◽  
F. Montero ◽  
V. Garcia-Morales ◽  
G. Dominguez ◽  
L. Gomez-Perez ◽  
...  
Keyword(s):  
Synaptic Vesicles ◽  
Rho Kinase ◽  
Synaptic Strength ◽  
Kinase Signaling ◽  
Releasable Pool ◽  
Readily Releasable Pool

scholarly journals RNA editing of CAPS1 regulates synaptic vesicle organization, release and retrieval

2017 ◽  
Author(s):  
Randi J. Ulbricht ◽  
Sarah J. Sun ◽  
Claire E. DelBove ◽  
Kristina E. Kitko ◽  
Saad C. Rehman ◽  
...  
Keyword(s):  
Rna Editing ◽  
Neurotransmitter Release ◽  
Synaptic Vesicles ◽  
Hippocampal Neurons ◽  
Protein Isoforms ◽  
Editing Event ◽  
Calcium Dependent ◽  
Presynaptic Vesicle ◽  
Vesicle Pool ◽  
Fine Tune

ABSTRACTCalcium-dependent activator protein for secretion 1 (CAPS1) facilitates the docking and priming of synaptic and dense core vesicles. A conserved hairpin structure in the CAPS1 pre-mRNA allows an post-transcriptional adenosine-to-inosine RNA editing event to alter a genomically-encoded glutamate to a glycine codon. Functional comparisons of CAPS1 protein isoforms in primary hippocampal neurons show that elevation of edited CAPS1 isoforms facilitates presynaptic vesicle clustering and turnover. Conversely, non-edited CAPS1 isoforms slow evoked release, increase spontaneous fusion, and loosen the clustering of synaptic vesicles. Therefore, CAPS1 editing promotes organization of the vesicle pool in a way that is beneficial for evoked release, while non-edited isoforms promote more lax vesicle organization that widens distribution, attenuates evoked release and eases the control of spontaneous fusion. Overall, RNA editing of CAPS1 is a mechanism to fine tune neurotransmitter release.IMPACT STATEMENTPost-transcriptional RNA editing of CAPS1 is a mechanism to regulate neurotransmitter release from synaptic vesicles.

scholarly journals Doc2-mediated superpriming supports synaptic augmentation

2018 ◽  
Vol 115 (24) ◽  
pp. E5605-E5613 ◽  
Author(s):  
Renhao Xue ◽  
David A. Ruhl ◽  
Joseph S. Briguglio ◽  
Alexander G. Figueroa ◽  
Robert A. Pearce ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Synaptic Vesicles ◽  
Hippocampal Neurons ◽  
Underlying Mechanism ◽  
Short Term ◽  
Short Term Plasticity ◽  
Releasable Pool ◽  
Readily Releasable Pool

Various forms of synaptic plasticity underlie aspects of learning and memory. Synaptic augmentation is a form of short-term plasticity characterized by synaptic enhancement that persists for seconds following specific patterns of stimulation. The mechanisms underlying this form of plasticity are unclear but are thought to involve residual presynaptic Ca2+. Here, we report that augmentation was reduced in cultured mouse hippocampal neurons lacking the Ca2+ sensor, Doc2; other forms of short-term enhancement were unaffected. Doc2 binds Ca2+ and munc13 and translocates to the plasma membrane to drive augmentation. The underlying mechanism was not associated with changes in readily releasable pool size or Ca2+ dynamics, but rather resulted from superpriming a subset of synaptic vesicles. Hence, Doc2 forms part of the Ca2+-sensing apparatus for synaptic augmentation via a mechanism that is molecularly distinct from other forms of short-term plasticity.

scholarly journals Presynaptically silent synapses are modulated by the density of surrounding astrocytes

2020 ◽  
Author(s):  
Kohei Oyabu ◽  
Kotomi Takeda ◽  
Hiroyuki Kawano ◽  
Kaori Kubota ◽  
Takuya Watanabe ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Synaptic Vesicles ◽  
Hippocampal Neurons ◽  
Cell Type ◽  
Countable Number ◽  
Glutamatergic Synapses ◽  
Readily Releasable Pool ◽  
Silent Synapses ◽  
Patch Clamp Electrophysiology ◽  
Lower Ratio

ABSTRACTThe astrocyte, a major glial cell type, is involved in formation and maturation of synapses, and thus contributes to sustainable synaptic transmission between neurons. Given that the animals in the higher phylogenetic tree have brains with higher density of glial cells with respect to neurons, there is a possibility that the relative astrocytic density directly influences synaptic transmission. However, the notion has not been tested thoroughly. Here we addressed it, by using a primary culture preparation where single hippocampal neurons are surrounded by a variable but countable number of cortical astrocytes in dot-patterned microislands, and recording synaptic transmission by patch-clamp electrophysiology. Neurons with a higher astrocytic density showed a higher amplitude of evoked excitatory postsynaptic current (EPSC) than that of neurons with a lower astrocytic density. The size of readily releasable pool of synaptic vesicles per neuron was significantly higher. The frequency of spontaneous synaptic transmission (miniature EPSC) was higher, but the amplitude was unchanged. The number of morphologically identified glutamatergic synapses was unchanged, but the number of functional ones was increased, indicating a lower ratio of presynaptically silent synapses. Taken together, the higher astrocytic density enhanced excitatory synaptic transmission by increasing the number of functional synapses through presynaptic un-silencing.

scholarly journals Post-tetanic increase in the fast-releasing synaptic vesicle pool at the expense of the slowly releasing pool

2010 ◽  
Vol 136 (3) ◽  
pp. 259-272 ◽  
Author(s):  
Jae Sung Lee ◽  
Won-Kyung Ho ◽  
Suk-Ho Lee
Keyword(s):  
Synaptic Vesicles ◽  
Late Phase ◽  
High Frequency Stimulation ◽  
First Line ◽  
Pipette Solution ◽  
Readily Releasable Pool ◽  
Whole Cell Patch Clamp ◽  
Frequency Stimulation ◽  
Post Tetanic Potentiation ◽  
Vesicle Pool

Post-tetanic potentiation (PTP) at the calyx of Held synapse is caused by increases not only in release probability (Pr) but also in the readily releasable pool size estimated from a cumulative plot of excitatory post-synaptic current amplitudes (RRPcum), which contribute to the augmentation phase and the late phase of PTP, respectively. The vesicle pool dynamics underlying the latter has not been investigated, because PTP is abolished by presynaptic whole-cell patch clamp. We found that supplement of recombinant calmodulin to the presynaptic pipette solution rescued the increase in the RRPcum after high-frequency stimulation (100 Hz for 4-s duration, HFS), but not the increase in Pr. Release-competent synaptic vesicles (SVs) are heterogeneous in their releasing kinetics. To investigate post-tetanic changes of fast and slowly releasing SV pool (FRP and SRP) sizes, we estimated quantal release rates before and 40 s after HFS using the deconvolution method. After HFS, the FRP size increased by 19.1% and the SRP size decreased by 25.4%, whereas the sum of FRP and SRP sizes did not increase. Similar changes in the RRP were induced by a single long depolarizing pulse (100 ms). The post-tetanic complementary changes of FRP and SRP sizes were abolished by inhibitors of myosin II or myosin light chain kinase. The post-tetanic increase in the FRP size coupled to a decrease in the SRP size provides the first line of evidence for the idea that a slowly releasing SV can be converted to a fast releasing one.

scholarly journals BDNF mobilizes synaptic vesicles and enhances synapse formation by disrupting cadherin–β-catenin interactions

2006 ◽  
Vol 174 (2) ◽  
pp. 289-299 ◽  
Author(s):  
Shernaz X. Bamji ◽  
Beatriz Rico ◽  
Nikole Kimes ◽  
Louis F. Reichardt
Keyword(s):  
Synaptic Vesicle ◽  
Synaptic Vesicles ◽  
Hippocampal Neurons ◽  
Molecular Mechanisms ◽  
Synapse Formation ◽  
Time Lapse ◽  
Synapse Density ◽  
Vesicle Mobility ◽  
Small Clusters ◽  
Vertebrate Central Nervous System

Neurons of the vertebrate central nervous system have the capacity to modify synapse number, morphology, and efficacy in response to activity. Some of these functions can be attributed to activity-induced synthesis and secretion of the neurotrophin brain-derived neurotrophic factor (BDNF); however, the molecular mechanisms by which BDNF mediates these events are still not well understood. Using time-lapse confocal analysis, we show that BDNF mobilizes synaptic vesicles at existing synapses, resulting in small clusters of synaptic vesicles “splitting” away from synaptic sites. We demonstrate that BDNF's ability to mobilize synaptic vesicle clusters depends on the dissociation of cadherin–β-catenin adhesion complexes that occurs after tyrosine phosphorylation of β-catenin. Artificially maintaining cadherin–β-catenin complexes in the presence of BDNF abolishes the BDNF-mediated enhancement of synaptic vesicle mobility, as well as the longer-term BDNF-mediated increase in synapse number. Together, this data demonstrates that the disruption of cadherin–β-catenin complexes is an important molecular event through which BDNF increases synapse density in cultured hippocampal neurons.

VARIATION IN SIZE OF THE 'READILY RELEASABLE POOL' OF LUTEINIZING HORMONE DURING THE OESTROUS CYCLE OF THE RAT

1979 ◽  
Vol 83 (1) ◽  
pp. 53-59 ◽  
Author(s):  
A. J.-M. C. PICKERING ◽  
G. FINK
Keyword(s):  
Luteinizing Hormone ◽  
Fold Increase ◽  
Pool Size ◽  
Oestrous Cycle ◽  
Apparent Increase ◽  
Storage Pool ◽  
Releasable Pool ◽  
Readily Releasable Pool ◽  
Significant Change

SUMMARY The size of the 'readily releasable pool' of luteinizing hormone at various times of the oestrous cycle has been determined by injecting a supramaximal dose of luteinizing hormone releasing factor (LH-RF) i.v. into rats anaesthetized with sodium pentobarbitone. In an attempt to block replenishment of the 'pool' during release, cycloheximide was administered 30 min before LH-RF. A 20-fold increase in pool size occurred between the morning of dioestrus and the evening of pro-oestrus in the absence of any significant change in total pituitary content of LH. This suggests that increased responsiveness may be brought about by a change in the receptor-release apparatus and/or a transfer of LH from a 'storage pool' which leads to an apparent increase in the proportion of LH available for release.

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