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Journal articles on the topic 'Transmission neuronale'

Author: Grafiati

Published: 25 June 2021

Last updated: 1 February 2022

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1

Vincent, Jean-Didier, and Pierre-Marie Lledo. "Connectivité neuronale et médiateurs chimiques impliqués dans la transmission du message olfactif." Bulletin de l'Académie Nationale de Médecine 185, no. 4 (April 2001): 689–705. http://dx.doi.org/10.1016/s0001-4079(19)34516-9.

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2

Martin-Soelch, C. "Modelle der Substanzabhängigkeit." Zeitschrift für Neuropsychologie 21, no. 3 (January 2010): 153–66. http://dx.doi.org/10.1024/1016-264x/a000015.

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Neurobiologische Modelle der Substanzabhängigkeit postulieren, dass Abhängigkeit aus einem Zusammenspiel zwischen positiver und negativer Verstärkung entsteht. Die positive Verstärkung wird über die dopaminerge Transmission im Striatum vermittelt, während die negative Verstärkung die neurobiologischen Stresssysteme involviert. Abhängigkeit geht mit lang anhaltenden Änderungen der zerebralen Motivationssysteme einher. Neuropsychologische Forschungsarbeiten weisen auf ein beeinträchtigtes Entscheidungsverhalten hin, welches mit einer Dysfunktion im ventromedialen präfrontalen Kortex zusammenhängen könnte. Sie betonen die Rolle der Insula, welche die neuronale Grundlage für die fehlende Einsicht ins problematische Suchtverhalten als auch für die Vermittlung des bewussten Drangs, die Substanz zu konsumieren, sein könnte. Neurobiologische und neuropsychologische Sichtweisen werden in einem Modell integriert, das impulsive subkortikale und dopamin-bezogene Prozesse mit einer Beeinträchtigung der kortikalen Hemmung und kognitiven Defiziten verbindet.

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3

Klaiber, Stefan, Fabian Bauer, and Peter Bretschneider. "Verbesserung der Netzverlustprognose für Energieübertragungsnetze." at - Automatisierungstechnik 68, no. 9 (September 25, 2020): 738–49. http://dx.doi.org/10.1515/auto-2020-0076.

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ZusammenfassungBei der Energieübertragung entstehen Netzverluste in den Leitungen und Betriebsmitteln des elektrischen Energiesystems. Die Höhe der Netzverluste ist sowohl von der Netzlast als auch von zahlreichen weiteren Einflussgrößen abhängig. Einen besonderen Einfluss hat dabei die fluktuierende und größtenteils verbrauchsferne Erzeugung durch erneuerbare Energien. Die Übertragungsnetzbetreiber müssen die elektrische Energie zum Ausgleich der Netzverluste im Voraus beschaffen. Um die benötigte Ausgleichsenergie möglichst kostenminimal einzukaufen, ist eine genaue Prognose der Netzverluste notwendig. Im Rahmen des vorliegenden Beitrags wird ein Verfahren vorgestellt, das für die Prognose der Netzverluste im Übertragungsnetz der 50Hertz Transmission GmbH zum Einsatz kommt. Als Modellansatz der Prognosemethode werden Künstliche Neuronale Netze verwendet. Das als Ergebnis der Arbeiten entwickelte Modell für die Netzverlustprognose steigert die Prognosegüte im Vergleich zum bisherigen Modell um sieben Prozent und befindet sich bei 50Hertz seit Juni 2019 im operativen Einsatz.

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4

SARRADIN, P., P. BERTHON, and F. LANTIER. "Le point sur l’épidémiologie et la physiopathologie des encéphalopathies spongiformes des ruminants." INRAE Productions Animales 10, no. 2 (April 7, 1997): 123–32. http://dx.doi.org/10.20870/productions-animales.1997.10.2.3988.

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L’épidémie d’encéphalopathie spongiforme bovine (ESB) résulte de la consommation par les bovins de farines de viandes et d’os contaminées. En recyclant l’agent infectieux, ces farines ont permis d’amplifier la dissémination d’une maladie dont l’origine et l’agent responsable demeurent inconnus. Les hypothèses sur la nature protéique ou/et virale de l’agent sont évoquées, ainsi que l’éventualité d’une transmission à l’homme. Une grande partie de nos connaissances des encéphalopathies spongiformes résulte des études réalisées de longue date sur la tremblante des ovins. En particulier, l’idée que l’on peut se faire de la physiopathologie de l’infection des bovins est en grande partie extrapolée à partir du résultat d’infections expérimentales réalisées chez le mouton. Toutefois, la contamination des tissus lymphoïdes périphériques, qui est la règle au cours de la phase de dissémination dans l’organisme de l’agent de la tremblante, semble absente dans le cas de la maladie bovine. Il est donc possible que ce type de tissus, considéré comme infectieux en matière de tremblante, le soit peu au cours de la phase préclinique dans le cas de l’ESB. L’atteinte du système nerveux central des bovins pourrait alors résulter d’une dissémination empruntant les voies nerveuses. Les mécanismes conduisant à la mort neuronale responsable des symptômes observés restent mal connus. La protéine PrP, protéine normale de la membrane de nombreux types cellulaires, et qui s’accumule sous sa forme pathologique PrPSC au niveau des lésions est indispensable au processus pathologique. Son polymorphisme influence considérablement le devenir de l’infection, mais elle ne peut être tenue pour seule responsable de la transmission de la maladie.

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5

Verkhratsky, Alexei, and Frank Kirchhoff. "Glutamate-mediated neuronal?glial transmission." Journal of Anatomy 210, no. 6 (June 2007): 651–60. http://dx.doi.org/10.1111/j.1469-7580.2007.00734.x.

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6

Macarthur, H., G. H. Wilken, T. C. Westfall, and L. L. Kolo. "Neuronal and non-neuronal modulation of sympathetic neurovascular transmission." Acta Physiologica 203, no. 1 (March 1, 2011): 37–45. http://dx.doi.org/10.1111/j.1748-1716.2010.02242.x.

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7

SHAPIRO, KAREN, MELISSA A. MILLER, ANDREA E. PACKHAM, BEATRIZ AGUILAR, PATRICIA A. CONRAD, ELIZABETH VANWORMER, and MICHAEL J. MURRAY. "Dual congenital transmission ofToxoplasma gondiiandSarcocystis neuronain a late-term aborted pup from a chronically infected southern sea otter (Enhydra lutris nereis)." Parasitology 143, no. 3 (October 23, 2015): 276–88. http://dx.doi.org/10.1017/s0031182015001377.

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SUMMARYToxoplasma gondiiandSarcocystis neuronaare protozoan parasites with terrestrial definitive hosts, and both pathogens can cause fatal disease in a wide range of marine animals. Close monitoring of threatened southern sea otters (Enhydra lutris nereis) in California allowed for the diagnosis of dual transplacental transmission ofT. gondiiandS. neuronain a wild female otter that was chronically infected with both parasites. Congenital infection resulted in late-term abortion due to disseminated toxoplasmosis.Toxoplasma gondiiandS. neuronaDNA was amplified from placental tissue culture, as well as from fetal lung tissue. Molecular characterization ofT. gondiirevealed a Type X genotype in isolates derived from placenta and fetal brain, as well as in all tested fetal organs (brain, lung, spleen, liver and thymus). This report provides the first evidence for transplacental transmission ofT. gondiiin a chronically infected wild sea otter, and the first molecular and immunohistochemical confirmation of concurrent transplacental transmission ofT. gondiiandS. neuronain any species. Repeated fetal and/or neonatal losses in the sea otter dam also suggested thatT. gondiihas the potential to reduce fecundity in chronically infected marine mammals through parasite recrudescence and repeated fetal infection.

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8

Wu, Xiaoyin, Jun Gao, Jin Yan, Jing Fan, Chung Owyang, and Ying Li. "Role for NMDA receptors in visceral nociceptive transmission in the anterior cingulate cortex of viscerally hypersensitive rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 294, no. 4 (April 2008): G918—G927. http://dx.doi.org/10.1152/ajpgi.00452.2007.

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We have identified colorectal distension (CRD)-responsive neurons in the anterior cingulate cortex (ACC) and demonstrated that persistence of a heightened visceral afferent nociceptive input to the ACC induces ACC sensitization. In the present study, we confirmed that rostral ACC neurons of sensitized rats [induced by chicken egg albumin (EA)] exhibit enhanced spike responses to CRD. Simultaneous in vivo recording and reverse microdialysis of single ACC neurons showed that a low dose of glutamate (50 μM) did not change basal ACC neuronal firing in normal rats but increased ACC neuronal firing in EA rats from 18 ± 2 to 32 ± 3.8 impulses/10 s. A high dose of glutamate (500 μM) produced 1.95-fold and a 4.27-fold increases of ACC neuronal firing in sham-treated rats and in EA rats, respectively, suggesting enhanced glutamatergic transmission in the ACC neurons of EA rats. Reverse microdialysis of the 3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)/kainite receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 μM) reduced basal and abolished CRD-induced ACC neuronal firing in normal rats. In contrast, microdialysis of N-methyl-d-aspartate (NMDA) receptor antagonist AP5 had no effect on ACC neuronal firing in normal rats. However, AP5 produced 86% inhibition of ACC neuronal firing evoked by 50 mmHg CRD in the EA rats. In conclusion, ACC nociceptive transmissions are mediated by glutamate AMPA receptors in the control rats. ACC responses to CRD are enhanced in viscerally hypersensitive rats. The enhancement of excitatory glutamatergic transmission in the ACC appears to mediate this response. Furthermore, NMDA receptors mediate ACC synaptic responses after the induction of visceral hypersensitivity.

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Tsai, M. C., K. Tanaka, L. Overstreet-Wadiche, and J. I. Wadiche. "Neuronal Glutamate Transporters Regulate Glial Excitatory Transmission." Journal of Neuroscience 32, no. 5 (February 1, 2012): 1528–35. http://dx.doi.org/10.1523/jneurosci.5232-11.2012.

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10

Laduron, Pierre M. "Presynaptic heteroreceptors in regulation of neuronal transmission." Biochemical Pharmacology 34, no. 4 (February 1985): 467–70. http://dx.doi.org/10.1016/0006-2952(85)90176-5.

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11

Haydon, Philip G., and Giorgio Carmignoto. "Astrocyte Control of Synaptic Transmission and Neurovascular Coupling." Physiological Reviews 86, no. 3 (July 2006): 1009–31. http://dx.doi.org/10.1152/physrev.00049.2005.

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From a structural perspective, the predominant glial cell of the central nervous system, the astrocyte, is positioned to regulate synaptic transmission and neurovascular coupling: the processes of one astrocyte contact tens of thousands of synapses, while other processes of the same cell form endfeet on capillaries and arterioles. The application of subcellular imaging of Ca2+ signaling to astrocytes now provides functional data to support this structural notion. Astrocytes express receptors for many neurotransmitters, and their activation leads to oscillations in internal Ca2+. These oscillations induce the accumulation of arachidonic acid and the release of the chemical transmitters glutamate, d-serine, and ATP. Ca2+ oscillations in astrocytic endfeet can control cerebral microcirculation through the arachidonic acid metabolites prostaglandin E2 and epoxyeicosatrienoic acids that induce arteriole dilation, and 20-HETE that induces arteriole constriction. In addition to actions on the vasculature, the release of chemical transmitters from astrocytes regulates neuronal function. Astrocyte-derived glutamate, which preferentially acts on extrasynaptic receptors, can promote neuronal synchrony, enhance neuronal excitability, and modulate synaptic transmission. Astrocyte-derived d-serine, by acting on the glycine-binding site of the N-methyl-d-aspartate receptor, can modulate synaptic plasticity. Astrocyte-derived ATP, which is hydrolyzed to adenosine in the extracellular space, has inhibitory actions and mediates synaptic cross-talk underlying heterosynaptic depression. Now that we appreciate this range of actions of astrocytic signaling, some of the immediate challenges are to determine how the astrocyte regulates neuronal integration and how both excitatory (glutamate) and inhibitory signals (adenosine) provided by the same glial cell act in concert to regulate neuronal function.

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12

Renart, Alfonso, and Mark C. W. van Rossum. "Transmission of Population-Coded Information." Neural Computation 24, no. 2 (February 2012): 391–407. http://dx.doi.org/10.1162/neco_a_00227.

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As neural activity is transmitted through the nervous system, neuronal noise degrades the encoded information and limits performance. It is therefore important to know how information loss can be prevented. We study this question in the context of neural population codes. Using Fisher information, we show how information loss in a layered network depends on the connectivity between the layers. We introduce an algorithm, reminiscent of the water filling algorithm for Shannon information that minimizes the loss. The optimal connection profile has a center-surround structure with a spatial extent closely matching the neurons’ tuning curves. In addition, we show how the optimal connectivity depends on the correlation structure of the trial-to-trial variability in the neuronal responses. Our results explain how optimal communication of population codes requires the center-surround architectures found in the nervous system and provide explicit predictions on the connectivity parameters.

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13

Rossi, Silvia, Valeria Studer, Caterina Motta, Valentina De Chiara, Francesca Barbieri, Giorgio Bernardi, and Diego Centonze. "Inflammation inhibits GABA transmission in multiple sclerosis." Multiple Sclerosis Journal 18, no. 11 (March 14, 2012): 1633–35. http://dx.doi.org/10.1177/1352458512440207.

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Abnormal glutamate-dependent synaptic excitation contributes to neuronal damage in multiple sclerosis (MS). Little is known about the involvement of the GABA system in this disorder. Here we found that cerebrospinal fluid (CSF) from MS patients with enhanced brain lesions on magnetic resonance imaging inhibited GABA transmission in mouse brain slices. Enhanced IL-1β neuronal action was responsible for this effect, because IL-1β receptor antagonist blocked, and exogenous IL-1β mimicked the synaptic effect of inflamed CSF. Our results provide evidence that focal inflammation in MS perturbs the cytokine milieu within the circulating CSF, resulting in diffuse GABAergic alteration in neurons.

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14

Martínez-Lozada, Zila, and Arturo Ortega. "Glutamatergic Transmission: A Matter of Three." Neural Plasticity 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/787396.

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Glutamatergic transmission in the vertebrate brain requires the involvement of glia cells, in a continuous molecular dialogue. Glial glutamate receptors and transporters are key molecules that sense synaptic activity and by these means modify their physiology in the short and long term. Posttranslational modifications that regulate protein-protein interactions and modulate transmitter removal are triggered in glial cells by neuronal released glutamate. Moreover, glutamate signaling cascades in these cells are linked to transcriptional and translational control and are critically involved in the control of theso-calledglutamate/glutamine shuttle and by these means in glutamatergic neurotransmission. In this contribution, we summarize our current understanding of the biochemical consequences of glutamate synaptic activity in their surrounding partners and dissect the molecular mechanisms that allow neurons to take control of glia physiology to ensure proper glutamate-mediated neuronal communication.

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15

STOCKS, N. G., D. ALLINGHAM, and R. P. MORSE. "THE APPLICATION OF SUPRATHRESHOLD STOCHASTIC RESONANCE TO COCHLEAR IMPLANT CODING." Fluctuation and Noise Letters 02, no. 03 (September 2002): L169—L181. http://dx.doi.org/10.1142/s0219477502000774.

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In this paper we explore the possibility of using a recently discovered form of stochastic resonance - termed suprathreshold stochastic resonance - to improve speech comprehension in patients fitted with cochlear implants. A leaky-integrate-and-fire (LIF) neurone is used to model cochlear nerve activity when subject to electrical stimulation. This model, in principle, captures key aspects of temporal coding in analogue cochlear implants. Estimates for the information transmitted by a population of nerve fibres is obtained as a function of internal (neuronal) noise level. We conclude that SSR does indeed provide a possible mechanism by which information transmission along the cochlear nerve can be improved - and thus may well lead to improved speech comprehension.

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16

Yoshihara, Motojiro, Kazuhiro Suzuki, and Yoshiaki Kidokoro. "Neuromuscular synaptic transmission in neuronal-synaptobrevin null mutants." Neuroscience Research 31 (January 1998): S104. http://dx.doi.org/10.1016/s0168-0102(98)81943-3.

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17

Hossmann, K. A. "Recovery of Neuronal Transmission after Prolonged Cerebral Ischemia." Gerontology 33, no. 3-4 (1987): 213–19. http://dx.doi.org/10.1159/000212880.

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18

TSUDA, Masaaki. "Genetical Responses of Neuronal Cells to Synaptic Transmission." YAKUGAKU ZASSHI 112, no. 5 (1992): 283–98. http://dx.doi.org/10.1248/yakushi1947.112.5_283.

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19

Araque, Alfonso, Rita P. Sanzgiri, Vladimir Parpura, and Philip G. Haydon. "Astrocyte-induced modulation of synaptic transmission." Canadian Journal of Physiology and Pharmacology 77, no. 9 (October 10, 1999): 699–706. http://dx.doi.org/10.1139/y99-076.

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The idea that astrocytes simply provide structural and trophic support to neurons has been challenged by recent evidence demonstrating that astrocytes exhibit a form of excitability and communication based on intracellular Ca2+ variations and intercellular Ca2+ waves, which can be initiated by neuronal activity. These astrocyte Ca2+ variations have now been shown to induce glutamate-dependent Ca2+ elevations and slow inward currents in neurons. More recently, it has been demonstrated that synaptic transmission between cultured hippocampal neurons can be directly modulated by astrocytes. We have reported that astrocyte stimulation can increase the frequency of miniature synaptic currents. Furthermore, we also have demonstrated that an elevation in the intracellular Ca2+ in astrocytes induces a reduction in both excitatory and inhibitory evoked synaptic transmission through the activation of selective presynaptic metabotropic glutamate receptors.Key words: astrocyte-neuron signaling, glutamate receptors, calcium waves, neuronal electrical activity, synaptic transmission.

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20

Jiang, Chang-Yu, Tsugumi Fujita, and Eiichi Kumamoto. "Synaptic modulation and inward current produced by oxytocin in substantia gelatinosa neurons of adult rat spinal cord slices." Journal of Neurophysiology 111, no. 5 (March 1, 2014): 991–1007. http://dx.doi.org/10.1152/jn.00609.2013.

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Cellular mechanisms for antinociception produced by oxytocin in the spinal dorsal horn have not yet been investigated thoroughly. We examined how oxytocin affects synaptic transmission in substantia gelatinosa neurons, which play a pivotal role in regulating nociceptive transmission, by applying the whole-cell patch-clamp technique to the substantia gelatinosa neurons of adult rat spinal cord slices. Bath-applied oxytocin did not affect glutamatergic spontaneous, monosynaptically-evoked primary-afferent Aδ-fiber and C-fiber excitatory transmissions. On the other hand, oxytocin produced an inward current at −70 mV and enhanced GABAergic and glycinergic spontaneous inhibitory transmissions. These activities were repeated with a slow recovery from desensitization, concentration-dependent and mimicked by oxytocin-receptor agonist. The oxytocin current was inhibited by oxytocin-receptor antagonist, intracellular GDPβS, U-73122, 2-aminoethoxydiphenyl borate, but not dantrolene, chelerythrine, dibutyryl cyclic-AMP, CNQX, Ca2+-free and tetrodotoxin, while the spontaneous inhibitory transmission enhancements were depressed by tetrodotoxin. Current-voltage relation for the oxytocin current reversed at negative potentials more than the equilibrium potential for K+, or around 0 mV. The oxytocin current was depressed in high-K+, low-Na+ or Ba2+-containing solution. Vasopressin V1A-receptor antagonist inhibited the oxytocin current, but there was no correlation in amplitude between a vasopressin-receptor agonist [Arg8]vasopressin and oxytocin responses. It is concluded that oxytocin produces a membrane depolarization mediated by oxytocin but not vasopressin-V1A receptors, which increases neuronal activity, resulting in the enhancement of inhibitory transmission, a possible mechanism for antinociception. This depolarization is due to a change in membrane permeabilities to K+ and/or Na+, which is possibly mediated by phospholipase C and inositol 1,4,5-triphosphate-induced Ca2+-release.

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21

Lomax, Alan E., Sabindra Pradhananga, and Paul P. Bertrand. "Plasticity of neuroeffector transmission during bowel inflammation1." American Journal of Physiology-Gastrointestinal and Liver Physiology 312, no. 3 (March 1, 2017): G165—G170. http://dx.doi.org/10.1152/ajpgi.00365.2016.

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Altered gastrointestinal (GI) function contributes to the debilitating symptoms of inflammatory bowel diseases (IBD). Nerve circuits contained within the gut wall and outside of the gut play important roles in modulating motility, mucosal fluid transport, and blood flow. The structure and function of these neuronal populations change during IBD. Superimposed on this plasticity is a diminished responsiveness of effector cells — smooth muscle cells, enterocytes, and vascular endothelial cells — to neurotransmitters. The net result is a breakdown in the precisely orchestrated coordination of motility, fluid secretion, and GI blood flow required for health. In this review, we consider how inflammation-induced changes to the effector innervation of these tissues, and changes to the tissues themselves, contribute to defective GI function in models of IBD. We also explore the evidence that reversing neuronal plasticity is sufficient to normalize function during IBD.

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Dorval, Alan D., and Warren M. Grill. "Deep brain stimulation of the subthalamic nucleus reestablishes neuronal information transmission in the 6-OHDA rat model of parkinsonism." Journal of Neurophysiology 111, no. 10 (May 15, 2014): 1949–59. http://dx.doi.org/10.1152/jn.00713.2013.

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Pathophysiological activity of basal ganglia neurons accompanies the motor symptoms of Parkinson's disease. High-frequency (>90 Hz) deep brain stimulation (DBS) reduces parkinsonian symptoms, but the mechanisms remain unclear. We hypothesize that parkinsonism-associated electrophysiological changes constitute an increase in neuronal firing pattern disorder and a concomitant decrease in information transmission through the ventral basal ganglia, and that effective DBS alleviates symptoms by decreasing neuronal disorder while simultaneously increasing information transfer through the same regions. We tested these hypotheses in the freely behaving, 6-hydroxydopamine-lesioned rat model of hemiparkinsonism. Following the onset of parkinsonism, mean neuronal firing rates were unchanged, despite a significant increase in firing pattern disorder (i.e., neuronal entropy), in both the globus pallidus and substantia nigra pars reticulata. This increase in neuronal entropy was reversed by symptom-alleviating DBS. Whereas increases in signal entropy are most commonly indicative of similar increases in information transmission, directed information through both regions was substantially reduced (>70%) following the onset of parkinsonism. Again, this decrease in information transmission was partially reversed by DBS. Together, these results suggest that the parkinsonian basal ganglia are rife with entropic activity and incapable of functional information transmission. Furthermore, they indicate that symptom-alleviating DBS works by lowering the entropic noise floor, enabling more information-rich signal propagation. In this view, the symptoms of parkinsonism may be more a default mode, normally overridden by healthy basal ganglia information. When that information is abolished by parkinsonian pathophysiology, hypokinetic symptoms emerge.

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23

Gwak, Young S., Claire E. Hulsebosch, and Joong Woo Leem. "Neuronal-Glial Interactions Maintain Chronic Neuropathic Pain after Spinal Cord Injury." Neural Plasticity 2017 (2017): 1–14. http://dx.doi.org/10.1155/2017/2480689.

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The hyperactive state of sensory neurons in the spinal cord enhances pain transmission. Spinal glial cells have also been implicated in enhanced excitability of spinal dorsal horn neurons, resulting in pain amplification and distortions. Traumatic injuries of the neural system such as spinal cord injury (SCI) induce neuronal hyperactivity and glial activation, causing maladaptive synaptic plasticity in the spinal cord. Recent studies demonstrate that SCI causes persistent glial activation with concomitant neuronal hyperactivity, thus providing the substrate for central neuropathic pain. Hyperactive sensory neurons and activated glial cells increase intracellular and extracellular glutamate, neuropeptides, adenosine triphosphates, proinflammatory cytokines, and reactive oxygen species concentrations, all of which enhance pain transmission. In addition, hyperactive sensory neurons and glial cells overexpress receptors and ion channels that maintain this enhanced pain transmission. Therefore, post-SCI neuronal-glial interactions create maladaptive synaptic circuits and activate intracellular signaling events that permanently contribute to enhanced neuropathic pain. In this review, we describe how hyperactivity of sensory neurons contributes to the maintenance of chronic neuropathic pain via neuronal-glial interactions following SCI.

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24

Akkentli, Fatih, Yusuf P. Tan, and Hale Saybasili. "Common Pesticide Rotenone Interference with Neuronal Transmission in Hippocampus." American Journal of Biomedical Engineering 2, no. 6 (January 7, 2013): 212–17. http://dx.doi.org/10.5923/j.ajbe.20120206.01.

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KURUP, RAVI KUMAR, and PARAMESWARA ACHUTHA KURUP. "HYPOTHALAMIC DIGOXIN, REGULATION OF NEURONAL TRANSMISSION, AND CEREBRAL DOMINANCE." International Journal of Neuroscience 113, no. 6 (January 2003): 821–30. http://dx.doi.org/10.1080/00207450390200891.

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26

Chen, Chun, ZhiYing Jiang, Xin Fu, Diankun Yu, Hai Huang, and Jeffrey G. Tasker. "Astrocytes Amplify Neuronal Dendritic Volume Transmission Stimulated by Norepinephrine." Cell Reports 29, no. 13 (December 2019): 4349–61. http://dx.doi.org/10.1016/j.celrep.2019.11.092.

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27

Otmakhov, Nikolai, Aneil M. Shirke, and Roberto Malinow. "Measuring the impact of probabilistic transmission on neuronal output." Neuron 10, no. 6 (June 1993): 1101–11. http://dx.doi.org/10.1016/0896-6273(93)90058-y.

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28

Hirokawa, Nobutaka. "The neuronal cytoskeleton-morphogenesis, organelle transport, and synaptic transmission." Neuroscience Research Supplements 15 (January 1990): S5. http://dx.doi.org/10.1016/0921-8696(90)90055-8.

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Hirokawa, Nobutaka. "The neuronal cytoskeleton-morphogenesis, organelle transport, and synaptic transmission." Neuroscience Research Supplements 11 (January 1990): S5. http://dx.doi.org/10.1016/0921-8696(90)90478-l.

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Wu, Zhen, Xiao Fei Xia, and Jun Song Wang. "EEG Autocorrelation Analysis of Neuronal Population at Criticality." Applied Mechanics and Materials 482 (December 2013): 363–66. http://dx.doi.org/10.4028/www.scientific.net/amm.482.363.

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The brain operates at criticality not only at resting state but also with some recognition tasks. Researches have shown that the information transmission efficiency is maximized when brain operates at criticality, however, the underlined mechanism remains some unknown. In this study, we elucidate the underlined mechanism of neuronal information transmission at criticality through a computational study. Firstly, a bifurcation analysis is conducted, by which we can obtain the Hopf bifurcation curve, responding the critical state. Secondly, we compute the autocorrelation function of the EEG (Electroencephalography) signals. The results have demonstrated that the autocorrelation function at criticality decay slowly and is much larger than other states, meaning long range dependence of the EEG signals at criticality, which reveals that the large autocorrelation function results that the information transmission efficiency is maximized at criticality.

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Woo, Junsung, Joo Ok Min, Dae-Si Kang, Yoo Sung Kim, Guk Hwa Jung, Hyun Jung Park, Sunpil Kim, et al. "Control of motor coordination by astrocytic tonic GABA release through modulation of excitation/inhibition balance in cerebellum." Proceedings of the National Academy of Sciences 115, no. 19 (April 24, 2018): 5004–9. http://dx.doi.org/10.1073/pnas.1721187115.

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Tonic inhibition in the brain is mediated through an activation of extrasynaptic GABAA receptors by the tonically released GABA, resulting in a persistent GABAergic inhibitory action. It is one of the key regulators for neuronal excitability, exerting a powerful action on excitation/inhibition balance. We have previously reported that astrocytic GABA, synthesized by monoamine oxidase B (MAOB), mediates tonic inhibition via GABA-permeable bestrophin 1 (Best1) channel in the cerebellum. However, the role of astrocytic GABA in regulating neuronal excitability, synaptic transmission, and cerebellar brain function has remained elusive. Here, we report that a reduction of tonic GABA release by genetic removal or pharmacological inhibition of Best1 or MAOB caused an enhanced neuronal excitability in cerebellar granule cells (GCs), synaptic transmission at the parallel fiber-Purkinje cell (PF-PC) synapses, and motor performance on the rotarod test, whereas an augmentation of tonic GABA release by astrocyte-specific overexpression of MAOB resulted in a reduced neuronal excitability, synaptic transmission, and motor performance. The bidirectional modulation of astrocytic GABA by genetic alteration of Best1 or MAOB was confirmed by immunostaining and in vivo microdialysis. These findings indicate that astrocytes are the key player in motor coordination through tonic GABA release by modulating neuronal excitability and could be a good therapeutic target for various movement and psychiatric disorders, which show a disturbed excitation/inhibition balance.

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Shefa, Ulfuara, Dokyoung Kim, Min-Sik Kim, Na Young Jeong, and Junyang Jung. "Roles of Gasotransmitters in Synaptic Plasticity and Neuropsychiatric Conditions." Neural Plasticity 2018 (2018): 1–15. http://dx.doi.org/10.1155/2018/1824713.

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Synaptic plasticity is important for maintaining normal neuronal activity and proper neuronal functioning in the nervous system. It is crucial for regulating synaptic transmission or electrical signal transduction to neuronal networks, for sharing essential information among neurons, and for maintaining homeostasis in the body. Moreover, changes in synaptic or neural plasticity are associated with many neuropsychiatric conditions, such as schizophrenia (SCZ), bipolar disorder (BP), major depressive disorder (MDD), and Alzheimer’s disease (AD). The improper maintenance of neural plasticity causes incorrect neurotransmitter transmission, which can also cause neuropsychiatric conditions. Gas neurotransmitters (gasotransmitters), such as hydrogen sulfide (H2S), nitric oxide (NO), and carbon monoxide (CO), play roles in maintaining synaptic plasticity and in helping to restore such plasticity in the neuronal architecture in the central nervous system (CNS). Indeed, the upregulation or downregulation of these gasotransmitters may cause neuropsychiatric conditions, and their amelioration may restore synaptic plasticity and proper neuronal functioning and thereby improve such conditions. Understanding the specific molecular mechanisms underpinning these effects can help identify ways to treat these neuropsychiatric conditions.

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Riquelme, Julio, Mario Wellmann, Ramón Sotomayor-Zárate, and Christian Bonansco. "Gliotransmission: A Novel Target for the Development of Antiseizure Drugs." Neuroscientist 26, no. 4 (January 24, 2020): 293–309. http://dx.doi.org/10.1177/1073858420901474.

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For more than a century, epilepsy has remained an incapacitating neurological disorder with a high incidence worldwide. Mesial temporal lobe epilepsy (TLE) is a common type of epilepsy without an effective pharmacological treatment. An increase in excitability and hypersynchrony of electrical neuronal activity during development are typically associated with an excitatory/inhibitory imbalance in the neuronal network. Astrocytes release gliotransmitters, which can regulate neuronal excitability and synaptic transmission; therefore, the classical neurocentric vision of the cellular basis of epileptogenesis has begun to change. Growing evidence suggests that the key contribution of astrocyte-to-neuron signaling in the mechanisms underlies the initiation, propagation, and recurrence of seizure activity. The aim of this review was to summarize current evidence obtained from experimental models that suggest how alterations in astroglial modulation of synaptic transmission and neuronal activity contribute to the development of this brain disease. In this article, we will summarize the main pharmacological, Ca2+-imaging, and electrophysiological findings in the gliotransmitter-mediated modulation of neuronal activity and their possible regulation as a novel cellular target for the development of pharmacological strategies for treating refractory epilepsies.

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Seagard, J. L., C. Dean, and F. A. Hopp. "Activity-dependent role of NMDA receptors in transmission of cardiac mechanoreceptor input to the NTS." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 3 (March 1, 2003): H884—H891. http://dx.doi.org/10.1152/ajpheart.00601.2002.

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Evidence suggests that transmission of barosensitive input from arterial baroreceptors and cardiac mechanoreceptors at nucleus tractus solitarius (NTS) neurons involves non- N-methyl-d-aspartate (NMDA) glutamate receptors, but there is a possibility that the contribution of NMDA receptors might increase during periods of increased afferent input, when enhanced neuronal depolarization could increase the activation of NMDA receptors by removal of a Mg2+ block. Thus the effects of NMDA on cardiac mechanoreceptor-modulated NTS neuronal discharges were examined at different levels of arterial pressure used to change cardiac mechanoreceptor afferent input. To determine whether the response was specific to NMDA, (±)-α-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA) was also administered at different levels of neuronal discharge. In anesthetized dogs, neuronal activity was recorded from the NTS while NMDA or AMPA was picoejected at high versus low arterial stimulating pressures. NMDA, but not AMPA, produced a significantly greater discharge of mechanoreceptor-driven NTS neurons at higher versus lower levels of stimulating pressure. These data suggest that the role played by NMDA receptors is greater during periods of enhanced neuronal depolarization, which could be produced by increases in afferent barosensitive input.

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Feinerman, Ofer, Menahem Segal, and Elisha Moses. "Signal Propagation Along Unidimensional Neuronal Networks." Journal of Neurophysiology 94, no. 5 (November 2005): 3406–16. http://dx.doi.org/10.1152/jn.00264.2005.

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Dissociated neurons were cultured on lines of various lengths covered with adhesive material to obtain an experimental model system of linear signal transmission. The neuronal connectivity in the linear culture is characterized, and it is demonstrated that local spiking activity is relayed by synaptic transmission along the line of neurons to develop into a large-scale population burst. Formally, this can be treated as a one-dimensional information channel. Directional propagation of both spontaneous and stimulated bursts along the line, imaged with the calcium indicator Fluo-4, revealed the existence of two different propagation velocities. Initially, a small number of neighboring neurons fire, leading to a slow, small and presumably asynchronous wave of activity. The signal then spontaneously develops to encompass much larger and further populations, and is characterized by fast propagation of high-amplitude activity, which is presumed to be synchronous. These results are well described by an existing theoretical framework for propagation based on an integrate-and-fire model.

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Henley, Jeremy M., Tim J. Craig, and Kevin A. Wilkinson. "Neuronal SUMOylation: Mechanisms, Physiology, and Roles in Neuronal Dysfunction." Physiological Reviews 94, no. 4 (October 2014): 1249–85. http://dx.doi.org/10.1152/physrev.00008.2014.

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Protein SUMOylation is a critically important posttranslational protein modification that participates in nearly all aspects of cellular physiology. In the nearly 20 years since its discovery, SUMOylation has emerged as a major regulator of nuclear function, and more recently, it has become clear that SUMOylation has key roles in the regulation of protein trafficking and function outside of the nucleus. In neurons, SUMOylation participates in cellular processes ranging from neuronal differentiation and control of synapse formation to regulation of synaptic transmission and cell survival. It is a highly dynamic and usually transient modification that enhances or hinders interactions between proteins, and its consequences are extremely diverse. Hundreds of different proteins are SUMO substrates, and dysfunction of protein SUMOylation is implicated in a many different diseases. Here we briefly outline core aspects of the SUMO system and provide a detailed overview of the current understanding of the roles of SUMOylation in healthy and diseased neurons.

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Gonzalez-Sulser, Alfredo, Jing Wang, Bridget N. Queenan, Massimo Avoli, Stefano Vicini, and Rhonda Dzakpasu. "Hippocampal neuron firing and local field potentials in the in vitro 4-aminopyridine epilepsy model." Journal of Neurophysiology 108, no. 9 (November 1, 2012): 2568–80. http://dx.doi.org/10.1152/jn.00363.2012.

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Excessive synchronous neuronal activity is a defining feature of epileptic activity. We previously characterized the properties of distinct glutamatergic and GABAergic transmission-dependent synchronous epileptiform discharges in mouse hippocampal slices using the 4-aminopyridine model of epilepsy. In the present study, we sought to identify the specific hippocampal neuronal populations that initiate and underlie these local field potentials (LFPs). A perforated multielectrode array was used to simultaneously record multiunit action potential firing and LFPs during spontaneous epileptiform activity. LFPs had distinct components based on the initiation site, extent of propagation, and pharmacological sensitivity. Individual units, located in different hippocampal subregions, fired action potentials during these LFPs. A specific neuron subgroup generated sustained action potential firing throughout the various components of the LFPs. The activity of this subgroup preceded the LFPs observed in the presence of antagonists of ionotropic glutamatergic synaptic transmission. In the absence of ionotropic glutamatergic and GABAergic transmission, LFPs disappeared, but units with shorter spike duration and high basal firing rates were still active. These spontaneously active units had an increased level of activity during LFPs and consistently preceded all LFPs recorded before blockade of synaptic transmission. Our findings reveal that neuronal subpopulations with interneuron properties are likely responsible for initiating synchronous activity in an in vitro model of epileptiform discharges.

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Cachope, Roger, and Alberto E. Pereda. "Opioids potentiate electrical transmission at mixed synapses on the Mauthner cell." Journal of Neurophysiology 114, no. 1 (July 2015): 689–97. http://dx.doi.org/10.1152/jn.00165.2015.

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Opioid receptors were shown to modulate a variety of cellular processes in the vertebrate central nervous system, including synaptic transmission. While the effects of opioid receptors on chemically mediated transmission have been extensively investigated, little is known of their actions on gap junction-mediated electrical synapses. Here we report that pharmacological activation of mu-opioid receptors led to a long-term enhancement of electrical (and glutamatergic) transmission at identifiable mixed synapses on the goldfish Mauthner cells. The effect also required activation of both dopamine D1/5 receptors and postsynaptic cAMP-dependent protein kinase A, suggesting that opioid-evoked actions are mediated indirectly via the release of dopamine from varicosities known to be located in the vicinity of the synaptic contacts. Moreover, inhibitory inputs situated in the immediate vicinity of these excitatory synapses on the lateral dendrite of the Mauthner cell were not affected by activation of mu-opioid receptors, indicating that their actions are restricted to electrical and glutamatergic transmissions co-existing at mixed contacts. Thus, as their chemical counterparts, electrical synapses can be a target for the modulatory actions of the opioid system. Because gap junctions at these mixed synapses are formed by fish homologs of the neuronal connexin 36, which is widespread in mammalian brain, it is likely that this regulatory property applies to electrical synapses elsewhere as well.

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Skrebitskii, V. G., and M. B. Shtark. "THE FUNDAMENTS OF NEURONAL PLASTICITY." Annals of the Russian academy of medical sciences 67, no. 9 (September 10, 2012): 39–44. http://dx.doi.org/10.15690/vramn.v67i9.405.

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Plasticity of the nervous system is determined by the modification of efficacy of synaptic transmission: long- term potentiation and long- term depression. Different modern technical approaches such as: registration of ionic currents in single neuron, molecular- genetic analysis, neurovisualization, and others reveal the molecular mechanisms of synaptic plasticity. The understanding of these mechanisms, in its turn, stimulates the development of methods of pharmacological correction of different forms of brain pathology such as Alzheimer disease, parkinsonism, alcoholism, aging and others.

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Masoliver, Maria, and Cristina Masoller. "Neuronal Transmission of Subthreshold Periodic Stimuli Via Symbolic Spike Patterns." Entropy 22, no. 5 (May 5, 2020): 524. http://dx.doi.org/10.3390/e22050524.

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We study how sensory neurons detect and transmit a weak external stimulus. We use the FitzHugh–Nagumo model to simulate the neuronal activity. We consider a sub-threshold stimulus, i.e., the stimulus is below the threshold needed for triggering action potentials (spikes). However, in the presence of noise the neuron that perceives the stimulus fires a sequence of action potentials (a spike train) that carries the stimulus’ information. To yield light on how the stimulus’ information can be encoded and transmitted, we consider the simplest case of two coupled neurons, such that one neuron (referred to as neuron 1) perceives a subthreshold periodic signal but the second neuron (neuron 2) does not perceive the signal. We show that, for appropriate coupling and noise strengths, both neurons fire spike trains that have symbolic patterns (defined by the temporal structure of the inter-spike intervals), whose frequencies of occurrence depend on the signal’s amplitude and period, and are similar for both neurons. In this way, the signal information encoded in the spike train of neuron 1 propagates to the spike train of neuron 2. Our results suggest that sensory neurons can exploit the presence of neural noise to fire spike trains where the information of a subthreshold stimulus is encoded in over expressed and/or in less expressed symbolic patterns.

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Kataoka, Yosky, Hiroshi Morii, and Yasuyoshi Watanabe. "822 Inhibition of the neuronal transmission by dye-mediated photooxidation." Neuroscience Research 28 (January 1997): S107. http://dx.doi.org/10.1016/s0168-0102(97)90284-4.

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Bouskila, Y., and F. E. Dudek. "Neuronal synchronization without calcium-dependent synaptic transmission in the hypothalamus." Proceedings of the National Academy of Sciences 90, no. 8 (April 15, 1993): 3207–10. http://dx.doi.org/10.1073/pnas.90.8.3207.

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Nagashino, H., and Y. Kinouchi. "Oscillatory modes in a neuronal network model with transmission latency." Neurocomputing 52-54 (June 2003): 843–48. http://dx.doi.org/10.1016/s0925-2312(02)00812-3.

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Wei, Chunyao, Elizabeth J. Thatcher, Abigail F. Olena, Diana J. Cha, Ana L. Perdigoto, Andrew F. Marshall, Bruce D. Carter, Kendal Broadie, and James G. Patton. "miR-153 Regulates SNAP-25, Synaptic Transmission, and Neuronal Development." PLoS ONE 8, no. 2 (February 25, 2013): e57080. http://dx.doi.org/10.1371/journal.pone.0057080.

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Paprocki, Bartosz, and Janusz Szczepanski. "How do the amplitude fluctuations affect the neuronal transmission efficiency." Neurocomputing 104 (March 2013): 50–56. http://dx.doi.org/10.1016/j.neucom.2012.11.001.

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Zhvania, Mzia G., Tamar Z. Bikashvili, Nadezhda J. Japaridze, Ilia I. Lazrishvili, and Mariam Ksovreli. "White noise and neuronal porosome complex: transmission electron microscopic study." Discoveries 2, no. 3 (August 19, 2014): e25. http://dx.doi.org/10.15190/d.2014.17.

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Haydon, P. "Symposium S06: Astrocytic regulation of neuronal excitability and synaptic transmission." Journal of Neurochemistry 94 (June 2005): 72. http://dx.doi.org/10.1111/j.1474-1644.2005.03230_3.x.

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48

Xin, Wendy, Yevgeniya A. Mironova, Hui Shen, Rosa A. M. Marino, Ari Waisman, Wouter H. Lamers, Dwight E. Bergles, and Antonello Bonci. "Oligodendrocytes Support Neuronal Glutamatergic Transmission via Expression of Glutamine Synthetase." Cell Reports 27, no. 8 (May 2019): 2262–71. http://dx.doi.org/10.1016/j.celrep.2019.04.094.

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Tanaka, Yufuko, Tetsuji Sadaike, Yasuo Inoshima, and Naotaka Ishiguro. "Characterization of PrPSc transmission from immune cells to neuronal cells." Cellular Immunology 279, no. 2 (October 2012): 145–50. http://dx.doi.org/10.1016/j.cellimm.2012.11.007.

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Weigel, Stefan, Petra Schulte, Simone Meffert, Peter Bräunig, and Andreas Offenhäusser. "Locust primary neuronal culture for the study of synaptic transmission." Journal of Molecular Histology 43, no. 4 (March 9, 2012): 405–19. http://dx.doi.org/10.1007/s10735-012-9395-1.

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