Relevant bibliographies by topics / Synaptic transmission

Academic literature on the topic 'Synaptic transmission'

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Published: 4 June 2021
Last updated: 29 July 2024

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Journal articles on the topic "Synaptic transmission"

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

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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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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "Synaptic transmission"

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Warren, Darren A. (Darren Allen). "Mechanisms of Synaptic Transmission." Thesis, The University of Sydney, 1996. https://hdl.handle.net/2123/27620.

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In this work we have presented the results of studies into the mechanisms of synaptic transmission in the sympathetic nervous sytem. This work has involved calcium imaging on chick ciliary ganglion cells, intracellular recording from rat main pelvic ganglion cells and extracellular recordings from visualised boutons in the rat main pelvic ganglion. Using digital imaging techniques, we studied the changes in cell calcium concentration in the avian ciliary ganglion following tetanic stimulation. The results showed a 3 fold increase for a short tetanus or a 4 fold increase for a long tetanus in the calcium concentration of both the calyx and soma. After a long tetanus the calcium concentration then declined along a double exponential with a time course similar to that of post-tetanic potentiation and long term potentiation in the ganglia. A new technique has been developed for recording the electrical signs of transmission at single boutons in the sympathetic nervous system. This technique allows recording and comparison of the relative amplitude of the presynaptic action potential, electrical signs of transmitter release and postsynaptic action potential from single or small groups of boutons. The preparation used for this work was the rat main pelvic ganglion. Extracellular electrodes placed over visualized boutons revealed evoked excitatory postsynaptic potentials (extracellular EPSP's) with amplitude histograms that were best described by single gamma distributions in most cases inlow [Ca2+]o (less than 0.5 mM). However, in some cases the gamma distribution had a very large variance which may have been due to the synchronous release of transmitter from closely apposed boutons which were observed under a confocal microscope. Intracellular electrodes used on the same preparation revealed spontaneous excitatory postsynaptic potentials (EPSP’S) with amplitude histograms which were in general well fitted by a Poisson mixtures of gamma distributions over a wide range of calcium concentrations. Using the technique of extracellular recording from single boutons or small numbers of boutons we were able to conclude that K-opioid receptors are located on the boutons of the hypogastric nerve. When activated by K—opioid receptor agonists they reduce quantal secretion without affecting the propagation of the nerve impulse along the hypogastric nerve.
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Mackenzie, Paul James. "Mechanisms regulating the reliability of synaptic transmission." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0020/NQ46382.pdf.

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Yang, Yuanjing. "ATP modulatory actions on hippocampal synaptic transmission." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ59415.pdf.

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Wahl, Linda Marie. "Sources of quantal variance in synaptic transmission." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318451.

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Nishimune, Atsushi. "NSF binding to GluR2 regulates synaptic transmission." Kyoto University, 2000. http://hdl.handle.net/2433/180867.

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Jeffry, Joseph August. "Modulation of synaptic transmission by TRP channels." OpenSIUC, 2010. https://opensiuc.lib.siu.edu/dissertations/121.

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The first sensory synapse is the site where sensory afferent fibers make synaptic connections with second order neurons. Somatic and craniofacial afferents terminate in spinal cord dorsal horn (SDH) and caudal spinal trigeminal nucleus (CSTN). Neurotransmitter release from first order nerve terminals regulates ascending sensory transmission. Several lines of evidence indicate that plasticity in the spinal cord dorsal horn underlies secondary hyperalgesia. The sensory receptors, Transient Receptor Potential (TRP) channels, are expressed not only at peripheral terminals, but also at the central terminals of sensory neurons. While the role of these channels at the periphery is detecting environmental stimuli, their function at central terminals is not fully understood. Furthermore, TRP channel expression has been shown in CNS nuclei like hippocampus that are not tightly linked to somatosensation. In this study, I first determined the functionality of TRP channels at the first sensory synapse and hippocampus using pharmacological activators. I then determined if putatively endogenous TRP channel activators modulate synaptic transmission at the first sensory synapse. Lastly, I determined if recordings that respond to capsaicin demonstrate synaptic plasticity in either hippocampus or spinal cord, in an attempt to attribute synaptic plasticity mechanisms to TRPV1 activity at glutamatergic terminals. I have used slice patch-clamp technique to record miniature, spontaneous and evoked currents in lamina II neurons of spinal cord dorsal horn, CSTN and hippocampus. In lamina II neurons of SDH and CSTN, capsaicin, a TRPV1 agonist, robustly increased the frequency of mEPSCs and sEPSCs in a dose dependant manner. Although capsaicin increased m/sEPSC frequency, eEPSC amplitude, which reflects synchronous action potential propagation at glutamatergic terminals, was markedly depressed by capsaicin. Our studies indicate capsaicin inhibits action potential dependant transmission at central terminals. Resiniferatoxin (RTX) is a TRPV1 agonist that displays higher potency (>100 fold) compared to capsaicin, and deactivation with this agonist is minimal. RTX also depressed eEPSC amplitude in lamina II neurons of SDH and CSTN; unexpectedly, RTX increased m/sEPSC frequency to lesser extent compared to capsaicin. The TRPA1 agonist, N-methyl maleimide (NMM), increased s/mEPSC frequency in lamina II neurons; however, NMM did not depress eEPSC amplitude like capsaicin and RTX. It is possible that inhibition of nerve terminal firing is a unique property of TRPV1 agonists compared to other noxious chemicals. To justify a physiological relevance for nociceptive TRP channel expression at the first sensory synapse, I studied the effect of endogenous TRP channel agonists on synaptic transmission at the first sensory synapse. Anandamide (AEA) is an agonist of CB1/CB2 and TRPV1 receptors; it is less potent at TRPV1 receptors than capsaicin. AEA increased sEPSC frequency in 70% of neurons, whereas the remainder of neurons showed a decrease in sEPSC frequency. Unlike capsaicin and RTX, anandamide did not dramatically depress eEPSC amplitude. Methyl glyoxal (MG) is a putative TRPA1 agonist produced during conditions of hyperglycemia. MG increased the frequency of sEPSCs in SDH lamina II neurons. I next used high frequency synaptic stimulation (HFS-100 Hz, 1s) to model synaptic activity during pain transmission. HFS induced a modest increase in sEPSC frequency and minimally changed eEPSC amplitude; patches that showed HFS modulation also responded to capsaicin. In studying the role of TRP channels in modulating synaptic transmission at central synapses, I finally performed experiments in hippocampus with 2 objectives; 1) to determine extent of capsaicin responsiveness as an indicator of TRPV1 functionality, and 2) to evaluate synaptic plasticity in response to HFS. Capsaicin effect on sEPSC frequency in CA1 and CA3 neurons was minimal in comparison to its effect in dorsal horn neurons. HFS at schaffer collateral region caused LTP in CA1 neurons that was more pronounced than for spinal cord. In conclusion, TRP channels are expressed at central terminals of nociceptors where they modulate glutamatergic transmission. Studying their role at the first sensory synapse enhances our understanding of nociceptive transmission, and this study suggests this receptor for a target for intervening in pathological pain transmission at the level of spinal cord.
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Rizvi, Nisha. "NOVEL DOPAMINERGIC SIGNALING MODULATING HIPPOCAMPAL SYNAPTIC TRANSMISSION." OpenSIUC, 2015. https://opensiuc.lib.siu.edu/dissertations/1082.

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Dopaminergic systems regulate many brain functions and dysfunction of dopaminergic neurotransmission is thought to underlie numerous disorders, including schizophrenia, attention deficit hyperactivity disorder (ADHD), depression and Alzheimer’s disease. In the hippocampus, a dopaminergic projection from the ventral tegmental area (VTA) is proposed to be essential for controlling entry of sensory information into long-term memory through novelty and salience detection. However, the effects of the VTA-dopamine system on hippocampal synaptic transmission are largely under-explored and the underlying mechanisms are unclear. The goal of this project was to investigate mechanisms involved in dopaminergic modulation of hippocampal neurophysiology. Specifically, I (1) examined if dopamine modulates hippocampal synaptic transmission in a region- and input-specific manner, and (2) studied the signaling mechanisms underlying such modulation. In the first aim for the study, I tested whether SKF38393, a dopamine D1-like receptor agonist, differentially affects excitatory synaptic transmission in perforant path synapses onto dentate gyrus granule cells and whether such effects differ from those at area CA1 synapses. I found that SKF38393 produced a concentration-dependent increase in field excitatory postsynaptic potential (fEPSP) in both subregions, but that higher concentrations were needed in the dentate gyrus to produce comparable effects. This synaptic enhancement was long-lasting and largely irreversible which suggests it may be a form of long term enhancement (LTP). Also, the increase in synaptic transmission at medial perforant path synapses was larger than in the lateral perforant path. Importantly, effects in the dentate gyrus, unlike those in CA1, differed substantially along the dorsoventral axis, with effects being significantly larger at the dorsal compared to the ventral pole. In the second aim, various combinations of D1 and D2-like receptor agonists and antagonists as well as inhibitors of second messenger systems, demonstrated that differential mechanisms were required for initiation and maintenance of SKF38393-mediated early and late-phase enhancement and that a novel non-canonical phospholipase-C (PLC) dependent signaling pathway may be involved. Based on recent discoveries in other brain regions, we hypothesized that multiple subcellular signaling pathways may contribute to PLC activation which may include but are not limited to D1(5)-D2 heteromers and Gβγ complex. In conclusion, this work uncovers novel dopaminergic signaling pathways regulating hippocampal physiology, which will lead to development of better (functionally selective) therapeutic agents.
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Kuczewski, Nicola. "Cholinergic modulation of synaptic transmission and plasticity." Doctoral thesis, SISSA, 2004. http://hdl.handle.net/20.500.11767/3976.

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The physiological and cognitive states of the brain are influenced by variations in the activity of the cholinergic systems. For example, changes in the levels of ACh have been associated with arousal/sleep cycle, sustained and focal attention. Moreover interfering with cholinergic transmission affects learning and cellular plasticity. Despite cholinergic system exerts its action by modifying the extracellular cortical concentration of acetylcholine (ACh) few investigations have until now tested if and how variation in ACh concentrations could influence neuronal synaptic efficacy and plasticity in acute brain preparation. In order to investigate this aspect we have used a quantitative experimental approach (variations in the levels of cholinergic activity) rather than a simply qualitative (absence or presence of cholinergic activity) on rodent visual cortex slices. We found that the extracellular ACh concentration affected in opposite way cortical synaptic efficacy, producing either an enhancement or an inhibition of evoked field potentials (FPs) respectively with low or high concentrations of exogenously applied ACh. The versus of ACh modulatory action was dependent on the activity of AChE and relayed on specific subtypes of muscarinic acetylcholine receptors (mAChRs), thus linking the action of ACh to the activation of particular receptor subtypes. The demonstration of a synaptic-pathway specificity of ACh modulatory action, suggests that cholinergic release could control, in a dynamic way, the flow of cortical information. Moreover, we showed that ACh concentration in cortical tissue contributes to modulate long term changes of synaptic efficacy, such as LTP or LTD induced by specific patterns of afferent neuronal activity. We found that: 1) in the absence of muscarinic receptors activation LTP is not inducible as shown in slices treated with atropine, 2)cholinergic action on cortical L TP depends on the activation of the even (M2, M,i) mAChRs. In addition, the sign of long term change, whether L TP or LTD, appears to be depend on the endogenous level of ACh; indeed, we reported that burst stimulation of afferent neurons, in rats with reduced cortical cholinergic innervation, induces an LTD instead of LTP. These results suggest that the degree of activation of cholinergic system could control cortical the direction of synaptic plasticity in visual cortex.
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Uteshev, Vladimir V. "A vision of synaptic transmission between central neurons." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0004/NQ27745.pdf.

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S, Mathew Seena. "Kainate receptor modulation of synaptic transmission in neocortex." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2007p/mathew.pdf.

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Books on the topic "Synaptic transmission"

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Frotscher, Michael, and Ulrich Misgeld, eds. Central Cholinergic Synaptic Transmission. Basel: Birkhäuser Basel, 1989. http://dx.doi.org/10.1007/978-3-0348-9138-7.

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1947-, Frotscher M., and Misgeld Ulrich 1943-, eds. Central cholinergic synaptic transmission. Basel: Birkhäuser Verlag, 1989.

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W, Stone T., ed. Aspects of synaptic transmission. London: Taylor & Francis, 1991.

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Graziane, Nicholas, and Yan Dong, eds. Electrophysiological Analysis of Synaptic Transmission. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2589-7.

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Graziane, Nicholas, and Yan Dong. Electrophysiological Analysis of Synaptic Transmission. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3274-0.

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N, Andrianov I͡U︡, ed. Sensory hair cells: Synaptic transmission. Berlin: Springer-Verlag, 1993.

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Zimmermann, Herbert, ed. Cellular and Molecular Basis of Synaptic Transmission. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73172-3.

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1944-, Zimmermann Herbert, and North Atlantic Treaty Organization. Scientific Affairs Division., eds. Cellular and molecular basis of synaptic transmission. Berlin: Springer-Verlag, 1988.

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Newton, Afra Jamila. Molecular mechanisms of synaptic vesicle trafficking. Cambridge, Mass: Harvard University, 2007.

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Uteshev, Vladimir V. A vision of synaptic transmission between central neurons. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1997.

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Book chapters on the topic "Synaptic transmission"

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Beckstead, Robert M. "Synaptic Transmission." In A Survey of Medical Neuroscience, 45–59. New York, NY: Springer New York, 1996. http://dx.doi.org/10.1007/978-1-4419-8570-5_4.

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von Gersdorff, Henrique. "Synaptic Transmission." In Neuroscience in Medicine, 95–109. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-455-5_5.

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Schmidt, R. F. "Synaptic Transmission." In Fundamentals of Neurophysiology, 69–102. New York, NY: Springer New York, 1985. http://dx.doi.org/10.1007/978-1-4613-9553-9_3.

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Frotscher, M. "Synaptic Transmission." In Comprehensive Human Physiology, 321–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-60946-6_17.

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von Gersdorff, Henrique, and Court Hull. "Synaptic Transmission." In Neuroscience in Medicine, 73–87. Totowa, NJ: Humana Press, 2003. http://dx.doi.org/10.1007/978-1-59259-371-2_4.

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Szabo, Bela, and Klaus Starke. "Synaptic Transmission." In Encyclopedia of Molecular Pharmacology, 1–9. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-21573-6_139-1.

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Szabo, Bela, and Klaus Starke. "Synaptic Transmission." In Encyclopedia of Molecular Pharmacology, 1476–84. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-57401-7_139.

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Cheng, Hwee Ming, Kin Kheong Mah, and Kumar Seluakumaran. "Synaptic Transmission." In Defining Physiology: Principles, Themes, Concepts. Volume 2, 95–99. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-62285-5_23.

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Miftahof, Roustem N., and Hong Gil Nam. "The Synaptic Transmission." In Biomechanics of the Human Urinary Bladder, 117–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-36146-3_8.

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Sewell, William F. "Neurotransmitters and Synaptic Transmission." In Springer Handbook of Auditory Research, 503–33. New York, NY: Springer New York, 1996. http://dx.doi.org/10.1007/978-1-4612-0757-3_9.

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Conference papers on the topic "Synaptic transmission"

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Hutchison, Felix. "Electronic model of synaptic transmission." In 2012 38th Annual Northeast Bioengineering Conference (NEBEC). IEEE, 2012. http://dx.doi.org/10.1109/nebc.2012.6207015.

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"SYNAPTIC TRANSMISSION AND FOKKER-PLANCK EQUATION." In 1st International Conference on Operations Research and Enterprise Systems. SciTePress - Science and and Technology Publications, 2012. http://dx.doi.org/10.5220/0003757100590063.

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Veletic, Mladen, Fabio Mesiti, Pal Anders Floor, and Ilangko Balasingham. "Communication theory aspects of synaptic transmission." In 2015 IEEE International Conference on Signal Processing for Communications (ICC). IEEE, 2015. http://dx.doi.org/10.1109/icc.2015.7248472.

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Mahmoudi, Mehrak, Piroz Zamankhan, and William Polashenski. "Simulations of Synaptic Transmission Using Lattice Boltzmann Methods." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32812.

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The nervous system remains one of the least understood biological structures due in large part to the enormous complexity of this organ. A theoretical model for the transfer of nerve impulses would be valuable for the analysis of various phenomena in the nervous system, which are difficult to study by experiments. The central nervous system is composed of more than 100 billion neurons, through which information is transmitted via nerve impulses. Nerve impulses are not immediately apparent since each impulse may be blocked during transmission, changed from a single impulse into repetitive impulse, or integrated with impulses from other neurons to form highly intricate patterns. In the human central nervous system, a neuron secretes a chemical substance called a neurotransmitter at the synapse, and this transmitter in turn acts on another neuron to cause excitation, inhibition, or some other modification of its sensitivity.
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Allam, Sushmita L., Jean-Marie C. Bouteiller, Renaud Greget, Serge Bischoff, Michel Baudry, and Theodore W. Berger. "EONS Synaptic Modeling Platform: Exploration of Mechanisms Regulating Information Processing in the CNS and Application to Drug Discovery." In ASME 2008 3rd Frontiers in Biomedical Devices Conference. ASMEDC, 2008. http://dx.doi.org/10.1115/biomed2008-38095.

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EONS modeling platform is a resourceful learning and research tool to study the mechanisms underlying the non-linear dynamics of synaptic transmission with the aid of mathematical models. Mathematical modeling of information processing in CNS pathways, in particular modeling of molecular events and synaptic dynamics, have not been extensively developed owing to the complex computations involved in integrating a multitude of parameters. In this paper, we discuss the development of a strategy to adapt the EONS synaptic modeling platform to a multi-node environment using a parallel computational framework to compute data intensive long simulations in a shorter time frame. We describe how this strategy can be applied to (i) determine the optimal values of the numerous parameters required for fitting experimental data, (ii) determine the impact of all parameters on various aspects of synaptic transmission (under normal conditions or conditions mimicking pathological conditions) and (iii) study the effects of exogenous molecules on both healthy and pathological synaptic models.
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Volcho, Gleb, Marina Starostina, and Nikolay Beregovoy. "MP2 MODIFIES SYNAPTIC TRANSMISSION IN HIPPOCAMPUS OF MORPHINIZED MICE." In XVII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2021. http://dx.doi.org/10.29003/m2077.sudak.ns2021-17/100-101.

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Seeger, Raphaela. "Imaging of SNARE-Dependent Spontaneous and Evoked Synaptic Transmission." In European Microscopy Congress 2020. Royal Microscopical Society, 2021. http://dx.doi.org/10.22443/rms.emc2020.676.

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Yuniati, Anis, and Retno Dwi Astuti. "Neural Network Synchronization of the Morris-Lecar Neuron Model Coupled with Short-Term Plasticity (STP)." In The 6th International Conference on Science and Engineering. Switzerland: Trans Tech Publications Ltd, 2024. http://dx.doi.org/10.4028/p-ymnn4n.

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This study used the Morris-Lecar (ML) neuron model coupled with Short-Term Plasticity (STP) to simulate neuronal connectivity and synaptic patterns. We analyze this neural network synchronization activity, examined the post-synaptic conductance patterns in the modelled neural network, investigated the dynamics of the neural network membrane potentials in the synchronous state, and analyze the Short-Term Plasticity (STP) synaptic transmission patterns by varying the inter-neuron connection probability for both inhibitory (pi) and excitatory (pe). This computational-based study was executed using Brian2 Simulator. The results revealed that the higher the connection probability, the more connections and synapses are formed. The greater value of pe, the more synchronous the neural network activity. In contrast, the higher value of pi, the less synchronous the neural network activity. A synchronous neural network implies that the spikes occur coincidentally, where coincidental spikes lead to easily detectable membrane potentials and postsynaptic conductance. Furthermore, spikes affect the release of neurotransmitters, thereby affecting synaptic transmission patterns. We further determined the frequency of this neural network synchronization.
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Nelson, Grace, Armando Salinas, Charles Levy, and Logan Slade. "Ethanol Effects on Synaptic Transmission: Implications for Motor Learning and Memory." In ASPET 2023 Annual Meeting Abstracts. American Society for Pharmacology and Experimental Therapeutics, 2023. http://dx.doi.org/10.1124/jpet.122.184440.

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Carpenter, Gail A. "Distributed recognition codes, catastrophic forgetting, and the rules of synaptic transmission." In Photonics for Industrial Applications, edited by David P. Casasent. SPIE, 1994. http://dx.doi.org/10.1117/12.188902.

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