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Journal articles on the topic 'Synaptic transmission'

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Published: 4 June 2021
Last updated: 29 July 2024

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1

CLEMENTS, JOHN. "Quantal synaptic transmission?" Nature 353, no. 6343 (October 1991): 396. http://dx.doi.org/10.1038/353396a0.

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2

LARKMAN, ALAN, KEN STRATFORD, and JULIAN JACK. "Quantal synaptic transmission?" Nature 353, no. 6343 (October 1991): 396. http://dx.doi.org/10.1038/353396b0.

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3

Terada, Sumio, Tetsuhiro Tsujimoto, Yosuke Takei, Tomoyuki Takahashi, and Nobutaka Hirokawa. "Impairment of Inhibitory Synaptic Transmission in Mice Lacking Synapsin I." Journal of Cell Biology 145, no. 5 (May 31, 1999): 1039–48. http://dx.doi.org/10.1083/jcb.145.5.1039.

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Deletion of the synapsin I genes, encoding one of the major groups of proteins on synaptic vesicles, in mice causes late onset epileptic seizures and enhanced experimental temporal lobe epilepsy. However, mice lacking synapsin I maintain normal excitatory synaptic transmission and modulation but for an enhancement of paired-pulse facilitation. To elucidate the cellular basis for epilepsy in mutants, we examined whether the inhibitory synapses in the hippocampus from mutant mice are intact by electrophysiological and morphological means. In the cultured hippocampal synapses from mutant mice, repeated application of a hypertonic solution significantly suppressed the subsequent transmitter release, associated with an accelerated vesicle replenishing time at the inhibitory synapses, compared with the excitatory synapses. In the mutants, morphologically identifiable synaptic vesicles failed to accumulate after application of a hypertonic solution at the inhibitory preterminals but not at the excitatory preterminals. In the CA3 pyramidal cells in hippocampal slices from mutant mice, inhibitory postsynaptic currents evoked by direct electrical stimulation of the interneuron in the striatum oriens were characterized by reduced quantal content compared with those in wild type. We conclude that synapsin I contributes to the anchoring of synaptic vesicles, thereby minimizing transmitter depletion at the inhibitory synapses. This may explain, at least in part, the epileptic seizures occurring in the synapsin I mutant mice.
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4

Betz, William J., and Ling-Gang Wu. "Synaptic Transmission: Kinetics of synaptic-vesicle recycling." Current Biology 5, no. 10 (October 1995): 1098–101. http://dx.doi.org/10.1016/s0960-9822(95)00220-x.

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5

Jang, Seil, Hyejin Lee, and Eunjoon Kim. "​Synaptic adhesion molecules and excitatory synaptic transmission." Current Opinion in Neurobiology 45 (August 2017): 45–50. http://dx.doi.org/10.1016/j.conb.2017.03.005.

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6

Terada, Sumio, Tetsuhiro Tsujimoto, Yosuke Takei, Tomoyuki Takahashi, and Nobutaka Hirokawa. "Inhibitory synaptic transmission in mice lacking synapsin I." Neuroscience Research 31 (January 1998): S104. http://dx.doi.org/10.1016/s0168-0102(98)81944-5.

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7

Miesenbock, G. "Synapto-pHluorins: Genetically Encoded Reporters of Synaptic Transmission." Cold Spring Harbor Protocols 2012, no. 2 (February 1, 2012): pdb.ip067827. http://dx.doi.org/10.1101/pdb.ip067827.

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8

A. Matta, Jose, and Gerard P. Ahern. "TRPV1 and Synaptic Transmission." Current Pharmaceutical Biotechnology 12, no. 1 (January 1, 2011): 95–101. http://dx.doi.org/10.2174/138920111793937925.

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9

Spitzer, Nicholas C. "Synaptic transmission makes history." Nature Neuroscience 8, no. 11 (November 2005): 1415. http://dx.doi.org/10.1038/nn1105-1415.

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10

Ferrarelli, L. K. "Synaptic Transmission on Speed." Science Signaling 7, no. 336 (July 29, 2014): ec200-ec200. http://dx.doi.org/10.1126/scisignal.2005738.

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11

Schwartz, E. A. "Synaptic transmission without calcium." Neuroscience Research Supplements 4 (January 1986): S121—S132. http://dx.doi.org/10.1016/s0921-8696(86)80013-5.

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12

Schwartz, E. A. "Synaptic transmission without calcium." Neuroscience Research 4 (January 1986): S121—S132. http://dx.doi.org/10.1016/0168-0102(86)90077-5.

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13

Perea, Gertrudis, and Alfonso Araque. "GLIA modulates synaptic transmission." Brain Research Reviews 63, no. 1-2 (May 2010): 93–102. http://dx.doi.org/10.1016/j.brainresrev.2009.10.005.

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14

Thomas, Panakkezhum D., and Gregory J. Brewer. "Gangliosides and synaptic transmission." Biochimica et Biophysica Acta (BBA) - Reviews on Biomembranes 1031, no. 3 (October 1990): 277–89. http://dx.doi.org/10.1016/0304-4157(90)90013-3.

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15

Sabatini, B. L., and W. G. Regehr. "TIMING OF SYNAPTIC TRANSMISSION." Annual Review of Physiology 61, no. 1 (March 1999): 521–42. http://dx.doi.org/10.1146/annurev.physiol.61.1.521.

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16

Benfenati, F., and F. Valtorta. "Synapsins and Synaptic Transmission." Physiology 8, no. 1 (February 1, 1993): 18–23. http://dx.doi.org/10.1152/physiologyonline.1993.8.1.18.

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The synapsins are a family of nerve terminal-specific phosphoproteins associated with the cytoplasmic side of synaptic vesicles that interact with various cytoskeletal proteins in a phosporylation-dependent fashion. They are implicated in the short-term regulation of neurotransmitter release and in the maturation of developing nerve terminals during synaptogenesis.
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17

Ma, Long, Gerald Reis, Luis F. Parada, and Erin M. Schuman. "Neuronal NT-3 Is not Required For Synaptic Transmission or Long-Term Potentiation in Area CA1 of the Adult Rat Hippocampus." Learning & Memory 6, no. 3 (May 1, 1999): 267–75. http://dx.doi.org/10.1101/lm.6.3.267.

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Neurotrophic factors, including BDNF and NT-3, have been implicated in the regulation of synaptic transmission and plasticity. Previous attempts to analyze synaptic transmission and plasticity in mice lacking the NT-3 gene have been hampered by the early death of the NT-3 homozygous knockout animals. We have bypassed this problem by examining synaptic transmission in mice in which the NT-3 gene is deleted in neurons later in development, by crossing animals expressing the CRE recombinase driven by the synapsin I promoter to animals in which the NT-3 gene is floxed. We conducted blind field potential recordings at the Schaffer collateral–CA1 synapse in hippocampal slices from homozygous knockout and wild-type mice. We examined the following indices of synaptic transmission: (1) input-output relationship; (2) paired-pulse facilitation; (3) post-tetanic potentiation; and (4) long-term potentiation: induced by two different protocols: (a) two trains of 100-Hz stimulation and (b) theta burst stimulation. We found no difference between the knockout and wild-type mice in any of the above measurements. These results suggest that neuronal NT-3 does not play an essential role in normal synaptic transmission and some forms of plasticity in the mouse hippocampus.
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18

Terada, Sumio, Tetsuhiro Tsujimoto, Yosuke Takei, Tomoyuki Takahashi, and Nobutaka Hirokawa. "313 Inhibitory synaptic transmission in mice lacking synapsin I." Neuroscience Research 28 (January 1997): S57. http://dx.doi.org/10.1016/s0168-0102(97)90144-9.

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19

Chan, Betty, Jeffrey R. Cottrell, Bing Li, Kelley C. Larson, Crystle J. Ashford, Jonathan M. Levenson, Pascal Laeng, David J. Gerber, and Jianping Song. "Development of a High-Throughput AlphaScreen Assay for Modulators of Synapsin I Phosphorylation in Primary Neurons." Journal of Biomolecular Screening 19, no. 2 (October 2, 2013): 205–14. http://dx.doi.org/10.1177/1087057113505905.

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Alterations in synaptic transmission have been implicated in a number of psychiatric and neurological disorders. The discovery of small-molecule modulators of proteins that regulate neurotransmission represents a novel therapeutic strategy for these diseases. However, high-throughput screening (HTS) approaches in primary neurons have been limited by challenges in preparing and applying primary neuronal cultures under conditions required for generating sufficiently robust and sensitive HTS assays. Synapsin I is an abundant presynaptic protein that plays a critical role in neurotransmission through tethering synaptic vesicles to the actin cytoskeleton. It has several phosphorylation sites that regulate its modulation of synaptic vesicle trafficking and, therefore, the efficacy of synaptic transmission. Here, we describe the development of a rapid, sensitive, and homogeneous assay to detect phospho-synapsin I (pSYN1) in primary cortical neurons in 384-well plates using AlphaScreen technology. From results of a pilot screening campaign, we show that the assay can identify compounds that modulate synapsin I phosphorylation via multiple signaling pathways. The implementation of the AlphaScreen pSYN1 assay and future development of additional primary neuronal HTS assays provides an attractive approach for discovery of novel classes of therapeutic candidates for a variety of CNS disorders.
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20

Jang, Seil, Daeyoung Oh, Yeunkum Lee, Eric Hosy, Hyewon Shin, Christoph van Riesen, Daniel Whitcomb, et al. "Synaptic adhesion molecule IgSF11 regulates synaptic transmission and plasticity." Nature Neuroscience 19, no. 1 (November 23, 2015): 84–93. http://dx.doi.org/10.1038/nn.4176.

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21

Liu, Guosong, and Richard W. Tsien. "Properties of synaptic transmission at single hippocampal synaptic boutons." Nature 375, no. 6530 (June 1995): 404–8. http://dx.doi.org/10.1038/375404a0.

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22

Hirase, Hajime, Youichi Iwai, Norio Takata, Yoshiaki Shinohara, and Tsuneko Mishima. "Volume transmission signalling via astrocytes." Philosophical Transactions of the Royal Society B: Biological Sciences 369, no. 1654 (October 19, 2014): 20130604. http://dx.doi.org/10.1098/rstb.2013.0604.

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The influence of astrocytes on synaptic function has been increasingly studied, owing to the discovery of both gliotransmission and morphological ensheathment of synapses. While astrocytes exhibit at best modest membrane potential fluctuations, activation of G-protein coupled receptors (GPCRs) leads to a prominent elevation of intracellular calcium which has been reported to correlate with gliotransmission. In this review, the possible role of astrocytic GPCR activation is discussed as a trigger to promote synaptic plasticity, by affecting synaptic receptors through gliotransmitters. Moreover, we suggest that volume transmission of neuromodulators could be a biological mechanism to activate astrocytic GPCRs and thereby to switch synaptic networks to the plastic mode during states of attention in cerebral cortical structures.
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23

Gambrill, Abigail C., Granville P. Storey, and Andres Barria. "Dynamic Regulation of NMDA Receptor Transmission." Journal of Neurophysiology 105, no. 1 (January 2011): 162–71. http://dx.doi.org/10.1152/jn.00457.2010.

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N-methyl-d-aspartate receptors (NMDARs) are critical for establishing, maintaining, and modifying glutamatergic synapses in an activity-dependent manner. The subunit composition, synaptic expression, and some of the properties of NMDARs are regulated by synaptic activity, affecting processes like synaptic plasticity. NMDAR transmission is dynamic, and we were interested in studying the effect of acute low or null synaptic activity on NMDA receptors and its implications for synaptic plasticity. Periods of no stimulation or low-frequency stimulation increased NMDAR transmission. Changes became stable after periods of 20 min of low or no stimulation. These changes in transmission have a postsynaptic origin and are explained by incorporation of GluN2B-containing receptors to synapses. Importantly, periods of low or no stimulation facilitate long-term potentiation induction. Moreover, recovery after a weak preconditioning stimulus that normally blocks subsequent potentiation is facilitated by a nonstimulation period. Thus synaptic activity dynamically regulates the level of NMDAR transmission adapting constantly the threshold for plasticity.
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24

Stern, Michael, and Barry Ganetzky. "Altered Synaptic Transmission inDrosophila HyperkineticMutants." Journal of Neurogenetics 5, no. 4 (January 1989): 215–28. http://dx.doi.org/10.3109/01677068909066209.

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25

Boxall and Lancaster. "Tyrosine kinases and synaptic transmission." European Journal of Neuroscience 10, no. 1 (January 1998): 2–7. http://dx.doi.org/10.1046/j.1460-9568.1998.00009.x.

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26

Lewis, Sian. "Erratum: Synaptic transmission: Closer encounters." Nature Reviews Neuroscience 19, no. 1 (January 2018): 58. http://dx.doi.org/10.1038/nrn.2017.167.

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27

Narasimhan, Kalyani. "Imaging heterogeneity in synaptic transmission." Nature Neuroscience 8, no. 9 (September 2005): 1137. http://dx.doi.org/10.1038/nn0905-1137.

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28

Huettner, James E. "Kainate receptors and synaptic transmission." Progress in Neurobiology 70, no. 5 (August 2003): 387–407. http://dx.doi.org/10.1016/s0301-0082(03)00122-9.

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29

Forsythe, Ian D., and Margaret Barnes-Davies. "Synaptic transmission: Well-placed modulators." Current Biology 7, no. 6 (June 1997): R362—R365. http://dx.doi.org/10.1016/s0960-9822(06)00175-8.

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30

Schuman, Erin M. "Neurotrophin regulation of synaptic transmission." Current Opinion in Neurobiology 9, no. 1 (February 1999): 105–9. http://dx.doi.org/10.1016/s0959-4388(99)80013-0.

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31

Nurrish, Stephen, Laurent Ségalat, and Joshua M. Kaplan. "Serotonin Inhibition of Synaptic Transmission." Neuron 24, no. 1 (September 1999): 231–42. http://dx.doi.org/10.1016/s0896-6273(00)80835-1.

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32

Raabe, W. "Synaptic transmission in ammonia intoxication." Neurochemical Pathology 6, no. 1-2 (February 1987): 145–66. http://dx.doi.org/10.1007/bf02833604.

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33

Kurachi, Yoshihisa. "Synaptic transmission and ion channels." Neuroscience Research 31 (January 1998): S25. http://dx.doi.org/10.1016/s0168-0102(98)81603-9.

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34

Karczmar, Alexander G. "A century of synaptic transmission." Trends in Pharmacological Sciences 23, no. 7 (July 2002): 346. http://dx.doi.org/10.1016/s0165-6147(02)01971-5.

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35

Whitteridge, David. "The Controversy Over Synaptic Transmission." Physiology 8, no. 3 (June 1, 1993): 135–36. http://dx.doi.org/10.1152/physiologyonline.1993.8.3.135.

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36

Vesce, Sabino, Paola Bezzi, and Andrea Volterra. "Synaptic Transmission with the Glia." Physiology 16, no. 4 (August 2001): 178–84. http://dx.doi.org/10.1152/physiologyonline.2001.16.4.178.

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For decades, scientists thought that all of the missing secrets of brain function resided in neurons. However, a wave of new findings indicates that glial cells, formerly considered mere supporters and subordinate to neurons, participate actively in synaptic integration and processing of information in the brain.
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37

Navarrete, Marta, and Alfonso Araque. "Basal Synaptic Transmission: Astrocytes Rule!" Cell 146, no. 5 (September 2011): 675–77. http://dx.doi.org/10.1016/j.cell.2011.08.006.

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38

Copenhagen, David R. "Synaptic transmission in the retina." Current Opinion in Neurobiology 1, no. 2 (August 1991): 258–62. http://dx.doi.org/10.1016/0959-4388(91)90087-n.

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39

Kaya, Cihan, Bing Liu, James R. Faeder, and Ivet Bahar. "Unified Model of Synaptic Transmission." Biophysical Journal 108, no. 2 (January 2015): 155a. http://dx.doi.org/10.1016/j.bpj.2014.11.852.

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40

Sinning, Anne, and Christian A. Hübner. "Minireview: pH and synaptic transmission." FEBS Letters 587, no. 13 (May 10, 2013): 1923–28. http://dx.doi.org/10.1016/j.febslet.2013.04.045.

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41

Lalo, Ulyana, Alexei Verkhratsky, Geoffrey Burnstock, and Yuri Pankratov. "P2X receptor-mediated synaptic transmission." Wiley Interdisciplinary Reviews: Membrane Transport and Signaling 1, no. 3 (January 11, 2012): 297–309. http://dx.doi.org/10.1002/wmts.28.

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42

Hvalby, Øivind, Vidar Jensen, Hung-Teh Kao, and S. Ivar Walaas. "Synapsin-regulated synaptic transmission from readily releasable synaptic vesicles in excitatory hippocampal synapses in mice." Journal of Physiology 571, no. 1 (February 2006): 75–82. http://dx.doi.org/10.1113/jphysiol.2005.100685.

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43

Ricoy, Ulises M., and Matthew E. Frerking. "Distinct roles for Cav2.1–2.3 in activity-dependent synaptic dynamics." Journal of Neurophysiology 111, no. 12 (June 15, 2014): 2404–13. http://dx.doi.org/10.1152/jn.00335.2013.

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Synaptic transmission throughout most of the CNS is steeply dependent on presynaptic calcium influx through the voltage-gated calcium channels Cav2.1–Cav2.3. In addition to triggering exocytosis, this calcium influx also recruits short-term synaptic plasticity. During the complex patterns of presynaptic activity that occur in vivo, several forms of plasticity combine to generate a synaptic output that is dynamic, in which the size of a given excitatory postsynaptic potential (EPSP) in response to a given spike depends on the short-term history of presynaptic activity. It remains unclear whether the different Cav2 channels play distinct roles in defining these synaptic dynamics and, if so, under what conditions different Cav2 family members most effectively determine synaptic output. We examined these questions by measuring the effects of calcium channel-selective toxins on synaptic transmission at the Schaffer collateral synapse in hippocampal slices from adult mice in response to both low-frequency stimulation and complex stimulus trains derived from in vivo recordings. Blockade of Cav2.1 had a greater inhibitory effect on synaptic transmission during low-frequency components of the stimulus train than on synaptic transmission during high-frequency components of the train, indicating that Cav2.1 had a greater fractional contribution to synaptic transmission at low frequencies than at high frequencies. Relative to Cav2.1, Cav2.2 had a disproportionately reduced contribution to synaptic transmission at frequencies >20 Hz, while Cav2.3 had a disproportionately increased contribution to synaptic transmission at frequencies >1 Hz. These activity-dependent effects of different Cav2 family members shape the filtering characteristics of GABAB receptor-mediated presynaptic inhibition. Thus different Cav2 channels vary in their coupling to synaptic transmission over different frequency ranges, with consequences for the frequency tuning of both synaptic dynamics and presynaptic neuromodulation.
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44

Ramirez, Alejandra E., Eduardo J. Fernández-Pérez, Nicol Olivos, Carlos F. Burgos, Subramanian Boopathi, Lorena Armijo-Weingart, Carla R. Pacheco, Wendy González, and Luis G. Aguayo. "The Stimulatory Effects of Intracellular α-Synuclein on Synaptic Transmission Are Attenuated by 2-Octahydroisoquinolin-2(1H)-ylethanamine." International Journal of Molecular Sciences 22, no. 24 (December 9, 2021): 13253. http://dx.doi.org/10.3390/ijms222413253.

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α-Synuclein (αSyn) species can be detected in synaptic boutons, where they play a crucial role in the pathogenesis of Parkinson’s Disease (PD). However, the effects of intracellular αSyn species on synaptic transmission have not been thoroughly studied. Here, using patch-clamp recordings in hippocampal neurons, we report that αSyn oligomers (αSynO), intracellularly delivered through the patch electrode, produced a fast and potent effect on synaptic transmission, causing a substantial increase in the frequency, amplitude and transferred charge of spontaneous synaptic currents. We also found an increase in the frequency of miniature synaptic currents, suggesting an effect located at the presynaptic site of the synapsis. Furthermore, our in silico approximation using docking analysis and molecular dynamics simulations showed an interaction between a previously described small anti-amyloid beta (Aβ) molecule, termed M30 (2-octahydroisoquinolin-2(1H)-ylethanamine), with a central hydrophobic region of αSyn. In line with this finding, our empirical data aimed to obtain oligomerization states with thioflavin T (ThT) and Western blot (WB) indicated that M30 interfered with αSyn aggregation and decreased the formation of higher-molecular-weight species. Furthermore, the effect of αSynO on synaptic physiology was also antagonized by M30, resulting in a decrease in the frequency, amplitude, and charge transferred of synaptic currents. Overall, the present results show an excitatory effect of intracellular αSyn low molecular-weight species, not previously described, that are able to affect synaptic transmission, and the potential of a small neuroactive molecule to interfere with the aggregation process and the synaptic effect of αSyn, suggesting that M30 could be a potential therapeutic strategy for synucleinopathies.
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45

Goldman, Mark S. "Enhancement of Information Transmission Efficiency by Synaptic Failures." Neural Computation 16, no. 6 (June 1, 2004): 1137–62. http://dx.doi.org/10.1162/089976604773717568.

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Many synapses have a high percentage of synaptic transmission failures. I consider the hypothesis that synaptic failures can increase the efficiency of information transmission across the synapse. I use the information transmitted per vesicle release about the presynaptic spike train as a measure of synaptic transmission efficiency and show that this measure can increase with the synaptic failure probability. I analytically calculate the Shannon mutual information transmitted across two model synapses with probabilistic transmission: one with a constant probability of vesicle release and one with vesicle release probabilities governed by the dynamics of synaptic depression. For inputs generated by a non-Poisson process with positive autocorrelations, both synapses can transmit more information per vesicle release than a synapse with perfect transmission, although the information increases are greater for the depressing synapse than for a constant-probability synapse with the same average transmission probability. The enhanced performance of the depressing synapse over the constant-release-probability synapse primarily reflects a decrease in noise entropy rather than an increase in the total transmission entropy. This indicates alimitation of analysis methods, such as decorrelation, that consider only the total response entropy. My results suggest that synaptic transmission failures governed by appropriately tuned synaptic dynamics can increase the information-carrying efficiency of a synapse.
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46

Cheung, Giselle, Oana Chever, Astrid Rollenhagen, Nicole Quenech’du, Pascal Ezan, Joachim H. R. Lübke, and Nathalie Rouach. "Astroglial Connexin 43 Regulates Synaptic Vesicle Release at Hippocampal Synapses." Cells 12, no. 8 (April 11, 2023): 1133. http://dx.doi.org/10.3390/cells12081133.

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Connexin 43, an astroglial gap junction protein, is enriched in perisynaptic astroglial processes and plays major roles in synaptic transmission. We have previously found that astroglial Cx43 controls synaptic glutamate levels and allows for activity-dependent glutamine release to sustain physiological synaptic transmissions and cognitiogns. However, whether Cx43 is important for the release of synaptic vesicles, which is a critical component of synaptic efficacy, remains unanswered. Here, using transgenic mice with a glial conditional knockout of Cx43 (Cx43−/−), we investigate whether and how astrocytes regulate the release of synaptic vesicles from hippocampal synapses. We report that CA1 pyramidal neurons and their synapses develop normally in the absence of astroglial Cx43. However, a significant impairment in synaptic vesicle distribution and release dynamics were observed. In particular, the FM1-43 assays performed using two-photon live imaging and combined with multi-electrode array stimulation in acute hippocampal slices, revealed a slower rate of synaptic vesicle release in Cx43−/− mice. Furthermore, paired-pulse recordings showed that synaptic vesicle release probability was also reduced and is dependent on glutamine supply via Cx43 hemichannel (HC). Taken together, we have uncovered a role for Cx43 in regulating presynaptic functions by controlling the rate and probability of synaptic vesicle release. Our findings further highlight the significance of astroglial Cx43 in synaptic transmission and efficacy.
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47

Hilfiker, Sabine, Vincent A. Pieribone, Andrew J. Czernik, Hung-Teh Kao, George J. Augustine, and Paul Greengard. "Synapsins as regulators of neurotransmitter release." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 354, no. 1381 (February 28, 1999): 269–79. http://dx.doi.org/10.1098/rstb.1999.0378.

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One of the crucial issues in understanding neuronal transmission is to define the role(s) of the numerous proteins that are localized within presynaptic terminals and are thought to participate in the regulation of the synaptic vesicle life cycle. Synapsins are a multigene family of neuron–specific phosphoproteins and are the most abundant proteins on synaptic vesicles. Synapsins are able to interact in vitro with lipid and protein components of synaptic vesicles and with various cytoskeletal proteins, including actin. These and other studies have led to a model in which synapsins, by tethering synaptic vesicles to each other and to an actin–based cytoskeletal meshwork, maintain a reserve pool of vesicles in the vicinity of the active zone. Perturbation of synapsin function in a variety of preparations led to a selective disruption of this reserve pool and to an increase in synaptic depression, suggesting that the synapsin–dependent cluster of vesicles is required to sustain release of neurotransmitter in response to high levels of neuronal activity. In a recent study performed at the squid giant synapse, perturbation of synapsin function resulted in a selective disruption of the reserve pool of vesicles and in addition, led to an inhibition and slowing of the kinetics of neurotransmitter release, indicating a second role for synapsins downstream from vesicle docking. These data suggest that synapsins are involved in two distinct reactions which are crucial for exocytosis in presynaptic nerve terminals. This review describes our current understanding of the molecular mechanisms by which synapsins modulate synaptic transmission, while the increasingly well–documented role of the synapsins in synapse formation and stabilization lies beyond the scope of this review.
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48

Ludwar, Bjoern Ch, Colin G. Evans, Jian Jing, and Elizabeth C. Cropper. "Two Distinct Mechanisms Mediate Potentiating Effects of Depolarization on Synaptic Transmission." Journal of Neurophysiology 102, no. 3 (September 2009): 1976–83. http://dx.doi.org/10.1152/jn.00418.2009.

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Two distinct mechanisms mediate potentiating effects of depolarization on synaptic transmission. Recently there has been renewed interest in a type of plasticity in which a neuron's somatic membrane potential influences synaptic transmission. We study mechanisms that mediate this type of control at a synapse between a mechanoafferent, B21, and B8, a motor neuron that receives chemical synaptic input. Previously we demonstrated that the somatic membrane potential determines spike propagation within B21. Namely, B21 must be centrally depolarized if spikes are to propagate to an output process. We now demonstrate that this will occur with central depolarizations that are only a few millivolts. Depolarizations of this magnitude are not, however, sufficient to induce synaptic transmission to B8. B21-induced postsynaptic potentials (PSPs) are only observed if B21 is centrally depolarized by ≥10 mV. Larger depolarizations have a second impact on B21. They induce graded changes in the baseline intracellular calcium concentration that are virtually essential for the induction of chemical synaptic transmission. During motor programs, subthreshold depolarizations that increase calcium concentrations are observed during one of the two antagonistic phases of rhythmic activity. Chemical synaptic transmission from B21 to B8 is, therefore, likely to occur in a phase-dependent manner. Other neurons that receive mechanoafferent input are electrically coupled to B21. Differential control of spike propagation and chemical synaptic transmission may, therefore, represent a mechanism that permits selective control of afferent transmission to different types of neurons contacted by B21. Afferent transmission to neurons receiving chemical synaptic input will be phase specific, whereas transmission to electrically coupled followers will be phase independent.
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49

Duprat, Fabrice, Michael Daw, Wonil Lim, Graham Collingridge, and John Isaac. "GluR2 protein-protein interactions and the regulation of AMPA receptors during synaptic plasticity." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 358, no. 1432 (April 29, 2003): 715–20. http://dx.doi.org/10.1098/rstb.2002.1215.

Full text
Abstract:
AMPA-type glutamate receptors mediate most fast excitatory synaptic transmissions in the mammalian brain. They are critically involved in the expression of long-term potentiation and long-term depression, forms of synaptic plasticity that are thought to underlie learning and memory. A number of synaptic proteins have been identified that interact with the intracellular C-termini of AMPA receptor subunits. Here, we review recent studies and present new experimental data on the roles of these interacting proteins in regulating the AMPA receptor function during basal synaptic transmission and plasticity.
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50

Seabrooke, Sara, and Bryan A. Stewart. "Synaptic transmission and plasticity are modulated by nonmuscle myosin II at the neuromuscular junction of Drosophila." Journal of Neurophysiology 105, no. 5 (May 2011): 1966–76. http://dx.doi.org/10.1152/jn.00718.2010.

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Abstract:
The synaptic vesicle population in a nerve terminal is traditionally divided into subpopulations according to physiological criteria; the readily releasable pool (RRP), the recycling pool, and the reserve pool. It is recognized that the RRP subserves synaptic transmission evoked by low-frequency neural activity and that the recycling and reserve populations are called on to supply vesicles as neural activity increases. Here we investigated the contribution of nonmuscle myosin II (NMMII) to synaptic transmission with emphasis on the role a motor protein could play in the supply of vesicles. We used Drosophila genetics to manipulate NMMII and assessed synaptic transmission at the larval neuromuscular junction. We observed a positive correlation between synaptic strength at low-frequency stimulation and NMMII expression: reducing NMMII reduced the evoked response, while increasing NMMII increased the evoked response. Further, we found that NMMII contributed to the spontaneous release of vesicles differentially from evoked release, suggesting differential contribution to these two release mechanisms. By measuring synaptic responses under conditions of differing external calcium concentration in saline, we found that NMMII is important for normal synaptic transmission under high-frequency stimulation. This research identifies diverse functions for NMMII in synaptic transmission and suggests that this motor protein is an active contributor to the physiology of synaptic vesicle recruitment.
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