Journal articles: 'Neurones humains'

1

Bohler, Sébastien. "Des neurones humains à sens unique." Cerveau & Psycho N° 166, no. 6 (May 14, 2024): 11. http://dx.doi.org/10.3917/cerpsy.166.0011.

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Barbotin, Anne-Laure, Vincent Prévot, and Paolo Giacobini. "Développement des neurones à GnRH dans le cerveau d’embryons humains." médecine/sciences 33, no. 4 (April 2017): 376–79. http://dx.doi.org/10.1051/medsci/20173304003.

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Scordel, Chloé, and Muriel Coulpier. "La phosphoprotéine P du virus de la maladie de Borna altère le développement des neurones GABAergiques humains." médecine/sciences 31, no. 12 (December 2015): 1060–63. http://dx.doi.org/10.1051/medsci/20153112003.

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Mallet, L. "∑njeux de la πsychiatrie ℂomputationnelle." European Psychiatry 30, S2 (November 2015): S50—S51. http://dx.doi.org/10.1016/j.eurpsy.2015.09.143.

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La psychiatrie computationnelle est un champ émergent qui, dans le prolongement des évolutions récentes en neurosciences cognitives, cherche à comprendre les pathologies mentales par la modélisation des processus élémentaires de pensée et leurs dysfonctionnements. En explicitant l’implémentation neurobiologique des algorithmes utilisés par le cerveau humain pour choisir, percevoir, ou ressentir… D’une certaine façon, cette nouvelle approche de la physiopathologie psychiatrique a pour ambition de combler le « fossé explicatif » entre cerveau et esprit. L’approche computationnelle se base sur la confrontation entre des données neurophysiologiques (IRM, EEG, MEG, électrophysiologie) acquises à chaque niveau de description du cerveau (récepteurs, neurones, réseaux, aires corticales) et les variables cachées prédites par des modèles ajustés aux comportements humains observables. Ce point de vue permet une approche transnosographique des symptômes psychiatriques qui peuvent être reconsidérés et caractérisés en termes de traitements pathologiques de l’information. Ces principes seront illustrés pour montrer :– comment cette approche permet de mieux comprendre l’émergence des processus élémentaires de pensée à partir de réseaux neuraux distribués, à contre-pied des approches néophrénologiques ;– illustrer comment ce type d’approche permet l’étude de l’architecture neurobiologique des processus de prise de décision chez l’homme ;– montrer l’intérêt des modèles bayésiens pour comprendre l’émergence des idées délirantes dans la schizophrénie.

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Epstein, Alberto L. "Maladie d’Alzheimer, neuro-inflammation et virus herpétiques." médecine/sciences 36, no. 5 (May 2020): 479–86. http://dx.doi.org/10.1051/medsci/2020090.

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L’infection du cerveau par divers types d’agents pathogènes, et les réponses inflammatoires qui s’en suivent, occupent une place grandissante dans notre compréhension de l’étiologie de la maladie d’Alzheimer (MA). Le fait que, parmi la vingtaine de gènes identifiés comme étant des facteurs à risque, plusieurs soient impliqués dans la modulation de la réponse immunitaire, ainsi que la diversité même des agents infectieux identifiés comme étant des acteurs possibles dans l’évolution de cette maladie, plaident en faveur de l’hypothèse neuro-inflammatoire, tout comme la prise de conscience que la protéine Aβ, l’un des marqueurs les plus importants de la MA, peut agir comme un système de défense antimicrobienne, capable de neutraliser des bactéries et des virus. Différent types de pathogènes, incluant des bactéries, des champignons, des protozoaires et des virus, ont été identifiés dans le cerveau malade, souvent près des lésions caractéristiques de la MA. Parmi eux, les virus herpétiques (surtout, mais pas seulement, HSV-1), qui se caractérisent par l’établissement d’infections latentes dans les neurones, ponctuées par des épisodes de réactivation suite à des stress ou des immunodépressions, apparaissent comme des candidats très solides à un rôle étiologique, ne serait-ce qu’en tant que cofacteurs, de la MA. La présence de génomes HSV-1 latents dans le cerveau, et donc le risque de réactivation, augmentent significativement avec l’âge. Des résultats récents montrent que, dans des neurones humains et de rat, l’infection par HSV-1 augmente l’expression de la β-sécrétase et de la nicastrine, deux enzymes impliquées dans la formation des Aβ selon la voie amyloïdogénique, ainsi que de celle de GSK3β et PKA, deux kinases impliquées dans la phosphorylation des protéines Tau, un autre marqueur essentiel de la MA. Les preuves croissantes obtenues, selon lesquelles les infections chroniques et les mécanismes de défense suscités, y compris les processus inflammatoires, sont au cœur de la MA, justifient de revoir les médicaments antiviraux tels que l’acyclovir, et peut-être aussi la vaccination, comme des voies potentielles de lutte contre la MA.

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Deydier, N., N. Lebonvallet, M. Talagas, L. Misery, and C. Le Gall-Ianotto. "Étude de la neuroprotection dans un modèle de co-culture 2D de keratinocytes primaires humains avec des neurones sensoriels de rat soumis à un stress inflammatoire mimant la dermatite atopique." Annales de Dermatologie et de Vénéréologie - FMC 3, no. 8 (December 2023): A104. http://dx.doi.org/10.1016/j.fander.2023.09.113.

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Sienkiewicz, W., A. Chrószcz, A. Dudek, M. Janeczek, and J. Kaleczyc. "Caudal mesenteric ganglion in the sheep – macroanatomical and immunohistochemical study." Polish Journal of Veterinary Sciences 18, no. 2 (June 1, 2015): 379–89. http://dx.doi.org/10.1515/pjvs-2015-0049.

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Abstract The caudal mesenteric ganglion (CaMG) is a prevetrebral ganglion which provides innervation to a number of organs in the abdominal and pelvic cavity. The morphology of CaMG and the chemical coding of neurones in this ganglion have been described in humans and many animal species, but data on this topic in the sheep are entirely lacking. This prompted us to undertake a study to determine the localization and morphology of sheep CaMG as well as immunohistochemical properties of its neurons. The study was carried out on 8 adult sheep, weighing from 40 to 60 kg each. The sheep were deeply anaesthetised and transcardially perfused with 4% paraformaldehyde. CaMG-s were exposed and their location was determined. Macroanatomical observations have revealed that the ovine CaMG is located at the level of last two lumbar (L5 or L6) and the first sacral (S1) vertebrae. The ganglion represents an unpaired structure composed of several, sequentially arranged aggregates of neurons. Immunohistochemical investigations revealed that nearly all (99.5%) the neurons were DβH-IR and were richly supplied by VACHT-IR nerve terminals forming „basket-like” structures around the perikarya. VACHT-IR neurones were not determined. Many neurons (55%) contained immunoreactivity to NPY, some of them (10%) stained for Met-ENK and solitary nerve cells were GAL-positive. CGRP-IR nerve fibres were numerous and a large number of them simultaneously expressed immunoreactivity to SP. Single, weakly stained neurones were SP-IR and only very few nerve cells weakly stained for VIP.

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Verkhratsky, Alexei, and Arthur Butt. "The History of the Decline and Fall of the Glial Numbers Legend." Neuroglia 1, no. 1 (July 17, 2018): 188–92. http://dx.doi.org/10.3390/neuroglia1010013.

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In the field of neuroscience and, more specifically glial cell biology, one of the most fundamentally intriguing and enduring questions has been “how many neuronal cells—neurones and glia—are there in the human brain?”. From the outset, the driving force behind this question was undoubtedly the scientific quest for knowledge of why humans are more intelligent than even our nearest relatives; the ‘neuronal doctrine’ dictated we must have more neurones than other animals. The early histological studies indicated a vast space between neurones that was filled by ‘nervenkitt’, later identified as neuroglia; arguably, this was the origin of the myth that glia massively outnumber neurones in the human brain. The myth eventually became embedded in ideology when later studies seemed to confirm that glia outnumber neurones in the human cortex—the seat of humanity—and that there was an inevitable rise in the glia-to-neurone ratio (GNR) as we climbed the evolutionary tree. This could be described as the ‘glial doctrine’—that the rise of intelligence and the rise of glia go hand-in-hand. In many ways, the GNR became a mantra for working on glial cells at a time when the neuronal doctrine ruled the world. However, the work of Suzana Herculano-Houzel which she reviews in this first volume of Neuroglia has led the way in demonstrating that neurones and glia are almost equal in number in the human cortex and there is no inexorable phylogenetic rise in the GNR. In this commentary we chart the fall and decline of the mythology of the GNR.

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Curran, William, and Catherine Lynn. "Monkey and humans exhibit similar motion-processing mechanisms." Biology Letters 5, no. 6 (July 22, 2009): 743–45. http://dx.doi.org/10.1098/rsbl.2009.0407.

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Single cell recording studies have resulted in a detailed understanding of motion-sensitive neurons in non-human primate visual cortex. However, it is not known to what extent response properties of motion-sensitive neurons in the non-human primate brain mirror response characteristics of motion-sensitive neurons in the human brain. Using a motion adaptation paradigm, the direction aftereffect, we show that changes in the activity of human motion-sensitive neurons to moving dot patterns that differ in dot density bear a strong resemblance to data from macaque monkey. We also show a division-like inhibition between neural populations tuned to opposite directions, which also mirrors neural-inhibitory behaviour in macaque. These findings strongly suggest that motion-sensitive neurons in human and non-human primates share common response and inhibitory characteristics.

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Zee, D. S., E. J. Fitzgibbon, and L. M. Optican. "Saccade-vergence interactions in humans." Journal of Neurophysiology 68, no. 5 (November 1, 1992): 1624–41. http://dx.doi.org/10.1152/jn.1992.68.5.1624.

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1. We recorded eye movements in four normal human subjects during refixations between targets calling for various combinations of saccades and vergence. We confirmed and extended prior observations of 1) transient changes in horizontal ocular alignment during both pure horizontal saccades (relative divergence followed by relative convergence) and pure vertical saccades (usually divergence for upward and convergence for downward saccades); 2) occasional, high-frequency (20-25 Hz), conjugate oscillations along the axis orthogonal to the main saccade; and 3) the speeding up of horizontal vergence by both horizontal and vertical saccades. 2. To interpret these findings, we developed a hypothesis for the generation of vergence to step changes in target depth, both with and without associated saccades. The essential features of this hypothesis are 1) the transient changes in horizontal ocular alignment during pure horizontal saccades reflect asymmetries in the mechanical properties of the lateral and medial rectus muscles causing adduction to lag abduction; 2) pure vergence movements in response to step changes in target depth are generated by a neural network that uses a desired change in vergence position as its input command and instantaneous vergence motor error (the difference between the desired change and the actual change in vergence) to drive vergence premoter neurons; and 3) the facilitation of horizontal vergence by saccades arises from nonlinear interactions in central premotor circuits. 3. The hypothetical network for generating pure vergence to step changes in target depth is analogous in structure to the local feedback model for the generation of saccades and has the same conceptual appeal. With the assumption of a single nonlinearity describing the relationship between a vergence motor error signal and the output of the neurons that generate promoter vergence velocity commands, this model generates pure vergence movements with peak velocity-amplitude relationships and trajectories that closely match those of experimental data. 4. Several types of models are proposed for the central, nonlinear interaction that occurs when saccades and vergence are combined. Common to all models is the idea that omnidirectional pause neurons (OPN), which are thought to gate activity for saccade burst neurons, also gate activity for saccade-related vergence. In one model we hypothesize the existence of a separate class of saccade-related vergence burst neurons, which generate premotor horizontal vergence commands but only during saccades. In a second model we hypothesize separate right eye and left eye saccadic burst neurons that receive not only conjugate, but also equal but oppositely directed vergence error signals.(ABSTRACT TRUNCATED AT 400 WORDS)

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Peyron, C. "Les neurones à hypocrétine (orexine) et la narcolepsie humaine." Revue Neurologique 168 (April 2012): A199. http://dx.doi.org/10.1016/j.neurol.2012.01.517.

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Chen, Pan, Sudipta Chakraborty, Tanara V. Peres, Aaron B. Bowman, and Michael Aschner. "Manganese-induced neurotoxicity: from C. elegans to humans." Toxicology Research 4, no. 2 (2015): 191–202. http://dx.doi.org/10.1039/c4tx00127c.

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Manganese (Mn) is neurotoxic, and its effect is mediated by net transport across cell membranes. (WT: the intact dopaminergic (DAergic) neurons in the head ofC. elegans, in the absence of Mn exposure; + Mn: the DAergic neurons undergo neurodegeneration upon Mn exposure.)

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Fabbri-Destro, Maddalena, and Giacomo Rizzolatti. "Mirror Neurons and Mirror Systems in Monkeys and Humans." Physiology 23, no. 3 (June 2008): 171–79. http://dx.doi.org/10.1152/physiol.00004.2008.

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Mirror neurons are a distinct class of neurons that transform specific sensory information into a motor format. Mirror neurons have been originally discovered in the premotor and parietal cortex of the monkey. Subsequent neurophysiological (TMS, EEG, MEG) and brain imaging studies have shown that a mirror mechanism is also present in humans. According to its anatomical locations, mirror mechanism plays a role in action and intention understanding, imitation, speech, and emotion feeling.

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Thomson, Helen. "Mirror neurons recorded in humans at last." New Scientist 206, no. 2756 (April 2010): 12. http://dx.doi.org/10.1016/s0262-4079(10)60911-6.

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Keysers, Christian, and Valeria Gazzola. "Social Neuroscience: Mirror Neurons Recorded in Humans." Current Biology 20, no. 8 (April 2010): R353—R354. http://dx.doi.org/10.1016/j.cub.2010.03.013.

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Verguts, Tom, and Wim Fias. "Representation of Number in Animals and Humans: A Neural Model." Journal of Cognitive Neuroscience 16, no. 9 (November 2004): 1493–504. http://dx.doi.org/10.1162/0898929042568497.

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This article addresses the representation of numerical information conveyed by nonsymbolic and symbolic stimuli. In a first simulation study, we show how number-selective neurons develop when an initially uncommitted neural network is given nonsymbolic stimuli as input (e.g., collections of dots) under unsupervised learning. The resultant network is able to account for the distance and size effects, two ubiquitous effects in numerical cognition. Furthermore, the properties of the network units conform in detail to the characteristics of recently discovered number-selective neurons. In a second study, we simulate symbol learning by presenting symbolic and nonsymbolic input simultaneously. The same number-selective neurons learn to represent the numerical meaning of symbols. In doing so, they show properties reminiscent of the originally available number-selective neurons, but at the same time, the representational efficiency of the neurons is increased when presented with symbolic input. This finding presents a concrete proposal on the linkage between higher order numerical cognition and more primitive numerical abilities and generates specific predictions on the neural substrate of number processing.

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Dąmbska, Maria, and Izabela Kuchna. "Different developmental rates of selected brain structures in humans." Acta Neurobiologiae Experimentalis 56, no. 1 (March 31, 1996): 83–93. http://dx.doi.org/10.55782/ane-1996-1107.

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Various rates of development are characteristic for particular structures of the human central nervous system (CNS). The differences of the maturing brain stern and telencephalon are evident in a routine neuropathological examination. The fetal and postnatal archi- and neocortex also reveals uneven levels of maturation. In order to precisely describe those differences in humans we performed a morphological and morphometric study on the dorsal vagal nucleus of the medulla oblongata, on Ammon's horn and on neocortex from midgestation to the 18th postnatal month. The numerical density of neurones, cell perikarya and nuclear cross-sectional area, and the ratio of nucleus to perikaryon area were measured. The results demonstrate a development-dependent decrease in cell density and progressive differentiation of neurones according to their changing size. They express a process of maturation which differs in rate across the CNS structures examined.

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Conson, Massimiliano, Francesco Polito, Alessandro Di Rosa, Luigi Trojano, Gennaro Cordasco, Anna Esposito, and Marco Turi. "‘Not only faces’: specialized visual representation of human hands revealed by adaptation." Royal Society Open Science 7, no. 12 (December 2020): 200948. http://dx.doi.org/10.1098/rsos.200948.

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Classical neurophysiological studies demonstrated that the monkey brain is equipped with neurons selectively representing the visual shape of the primate hand. Neuroimaging in humans provided data suggesting that a similar representation can be found in humans. Here, we investigated the selectivity of hand representation in humans by means of the visual adaptation technique. Results showed that participants' judgement of human-likeness of a visual probe representing a human hand was specifically reduced by a visual adaptation procedure when using a human hand adaptor but not when using an anthropoid robotic hand or a non-primate animal paw adaptor. Instead, human-likeness of the anthropoid robotic hand was affected by both human and robotic adaptors. No effect was found when using a non-primate animal paw as adaptor or probe. These results support the existence of specific neural mechanisms encoding human hand in the human's visual system.

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Bergmann, Olaf, Jakob Liebl, Samuel Bernard, Kanar Alkass, Maggie S. Y. Yeung, Peter Steier, Walter Kutschera, et al. "The Age of Olfactory Bulb Neurons in Humans." Neuron 74, no. 4 (May 2012): 634–39. http://dx.doi.org/10.1016/j.neuron.2012.03.030.

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TURELLA, L., A. PIERNO, F. TUBALDI, and U. CASTIELLO. "Mirror neurons in humans: Consisting or confounding evidence?" Brain and Language 108, no. 1 (January 2009): 10–21. http://dx.doi.org/10.1016/j.bandl.2007.11.002.

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Allman, John M., Nicole A. Tetreault, Atiya Y. Hakeem, and Soyoung Park. "The von economo neurons in apes and humans." American Journal of Human Biology 23, no. 1 (December 7, 2010): 5–21. http://dx.doi.org/10.1002/ajhb.21136.

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Macefield, Vaughan G., and B. Gunnar Wallin. "Physiological and pathophysiological firing properties of single postganglionic sympathetic neurons in humans." Journal of Neurophysiology 119, no. 3 (March 1, 2018): 944–56. http://dx.doi.org/10.1152/jn.00004.2017.

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It has long been known from microneurographic recordings in human subjects that the activity of postganglionic sympathetic axons occurs as spontaneous bursts, with muscle sympathetic nerve activity (MSNA) exhibiting strong cardiac rhythmicity via the baroreflex and skin sympathetic nerve activity showing much weaker cardiac modulation. Here we review the firing properties of single sympathetic neurons, obtained using highly selective microelectrodes. Individual vasoconstrictor neurons supplying muscle or skin, or sudomotor neurons supplying sweat glands, always discharge with a low firing probability (~30%) and at very low frequencies (~0.5 Hz). Moreover, they usually fire only once per cardiac interval but can fire greater than four times within a burst. Modeling has shown that this pattern can best be explained by individual neurons being driven by, on average, two preganglionic inputs. Unitary recordings of muscle vasoconstrictor neurons have been made in several pathophysiological states, including heart failure, hypertension, obstructive sleep apnea, bronchiectasis, chronic obstructive pulmonary disease, depression, and panic disorder. The augmented MSNA in each of these diseases features an increase in firing probability and discharge frequency of individual muscle vasoconstrictor neurons above that seen in healthy subjects, yet firing rates rarely exceed 1 Hz. However, unlike patients with heart failure, all patients with respiratory disease or panic disorder, and patients with hyperhidrosis, exhibited an increase in multiple within-burst firing, which emphasizes the different modes by which the sympathetic nervous system grades its output in pathophysiological states of high sympathetic nerve activity.

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Andreae, Laura C. "Adult neurogenesis in humans: Dogma overturned, again and again?" Science Translational Medicine 10, no. 436 (April 11, 2018): eaat3893. http://dx.doi.org/10.1126/scitranslmed.aat3893.

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Hirai, T., C. Ohye, Y. Nagaseki, and M. Matsumura. "Cytometric analysis of the thalamic ventralis intermedius nucleus in humans." Journal of Neurophysiology 61, no. 3 (March 1, 1989): 478–87. http://dx.doi.org/10.1152/jn.1989.61.3.478.

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1.The cytoarchitecture and the exact borders of the thalamic ventralis intermedius (Vim) nucleus of humans as originally delineated by Hassler (17) have been studied on the basis of stereotaxic coordinates correlated with Nissl- and Golgi-impregnated sections, using a microscopic image analyzer. 2. The Vim nucleus forms part of a relatively “cell-sparse zone” which includes the other ventrolateral thalamic subnuclei. It is distinguished by the presence of darkly stained, large and medium sized, angular cells with areas of approximately 500–1,000 microns 2 and 300-400 microns 2, respectively, and a cell density of approximately 50-90 (mean 65)/mm2 in 50-microns-thick sections. 3. Both sets of neurons have the characteristics of thalamocortical relay neurons in Golgi preparations. Large neurons have rectangular or square somata 30-50 microns diam and are concentrated mainly in the lateral and ventral two-thirds of the nucleus. The medium neurons have square to round somata, 15–25 microns diam, and are distributed homogeneously through the nucleus. The total dendritic arborization of both types is usually symmetrical in all directions and at least 500–600 microns diam. 4. The borders between the Vim nucleus and the Nucleus ventrooralis (Vo) and between the Vim nucleus and the Nucleus ventrocaudalis internus (Vci) are clearly identified by clearcut differences in cell size and cell density. The borders between the Vim nucleus and the Nucleus ventrooralis internus (Voi) and between the Vim nucleus and the Nucleus zentrolateralis intermedius (Zim) are quite obscure, and these nuclei, with Vim, seem to be parts of the large cell sparse zone comparable to that described in monkeys as VLp or VL. The border between the Vim nucleus and the Nucleus ventrocaudalis externus anterior (Vcea) is also unclear but the increased cell density and intermingling of small and medium-to-small neurons with large neurons are the major features that distinguish the Vcea nucleus from the Vim nucleus cytometrically. 5. The position and anatomic organization of the human Vim nucleus make it likely that it is the region in which kinesthetic response were recorded in the accompanying paper but extension of the recording sites into the Vcea nucleus cannot be ruled out.

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Galletti, C., PP Battaglini, and P. Fattori. "The Posterior Parietal Cortex in Humans and Monkeys." Physiology 12, no. 4 (August 1, 1997): 166–71. http://dx.doi.org/10.1152/physiologyonline.1997.12.4.166.

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The recently reported existence of neurons able to encode visual space in the superior parietal lobule of the monkey brain suggests that human and monkey superior parietal lobules are homologous structures.

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Lu, Thomas, Li Liang, and Xiaoqin Wang. "Neural Representations of Temporally Asymmetric Stimuli in the Auditory Cortex of Awake Primates." Journal of Neurophysiology 85, no. 6 (June 1, 2001): 2364–80. http://dx.doi.org/10.1152/jn.2001.85.6.2364.

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The representation of rapid acoustic transients by the auditory cortex is a fundamental issue that is still unresolved. Auditory cortical neurons have been shown to be limited in their stimulus-synchronized responses, yet the perceptual performances of humans and animals in discriminating temporal variations in complex sounds are better than what existing neurophysiological data would predict. This study investigated the neural representation of temporally asymmetric stimuli in the primary auditory cortex of awake marmoset monkeys. The stimuli, ramped and damped sinusoids, were systematically manipulated (by means of half-life of the exponential envelope) within a cortical neuron's presumed temporal integration window. The main findings of this study are as follows: 1) temporal asymmetry in ramped and damped sinusoids with a short period (25 ms) was clearly reflected by average discharge rate but not necessarily by temporal discharge patterns of auditory cortical neurons. There was considerable response specificity to these stimuli such that some neurons were strongly responsive to a ramped sinusoid but almost completely unresponsive to its damped counterpart or vice versa. Of 181 neurons studied, 140 (77%) showed significant response asymmetry in at least one of the tested half-life values of the exponential envelope. Forty-six neurons showed significant response asymmetry over all half-lives tested. Sustained firing, commonly observed under awake conditions, contributed to greater response asymmetry than that of onset responses in many neurons. 2) A greater proportion of the neurons (32/46) that exhibited significant overall response asymmetry showed stronger responses to the ramped sinusoids than to the damped sinusoids, possibly contributing to the difference in the perceived loudness between these two classes of sounds. 3) The asymmetry preference of a neuron to ramped or damped sinusoids did not appear to be correlated with its characteristic frequency or minimum response latency, suggesting that this is a general phenomenon that exists across populations of cortical neurons. Moreover, the intensity of the stimuli did not have significant effects on the measure of the asymmetry preference based on discharge rate. 4) A population measure of response preference, based on discharge rate, of cortical neurons to the temporally asymmetric stimuli was qualitatively similar to the performance of human listeners in discriminating ramped versus damped sinusoids at different half-life values. These findings suggest that rapid acoustic transients embedded in complex sounds can be represented by discharge rates of cortical neurons instead of or in the absence of stimulus-synchronized discharges.

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Agrochao, Margarida, Ryosuke Tanaka, Emilio Salazar-Gatzimas, and Damon A. Clark. "Mechanism for analogous illusory motion perception in flies and humans." Proceedings of the National Academy of Sciences 117, no. 37 (August 24, 2020): 23044–53. http://dx.doi.org/10.1073/pnas.2002937117.

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Visual motion detection is one of the most important computations performed by visual circuits. Yet, we perceive vivid illusory motion in stationary, periodic luminance gradients that contain no true motion. This illusion is shared by diverse vertebrate species, but theories proposed to explain this illusion have remained difficult to test. Here, we demonstrate that in the fruit fly Drosophila, the illusory motion percept is generated by unbalanced contributions of direction-selective neurons’ responses to stationary edges. First, we found that flies, like humans, perceive sustained motion in the stationary gradients. The percept was abolished when the elementary motion detector neurons T4 and T5 were silenced. In vivo calcium imaging revealed that T4 and T5 neurons encode the location and polarity of stationary edges. Furthermore, our proposed mechanistic model allowed us to predictably manipulate both the magnitude and direction of the fly’s illusory percept by selectively silencing either T4 or T5 neurons. Interestingly, human brains possess the same mechanistic ingredients that drive our model in flies. When we adapted human observers to moving light edges or dark edges, we could manipulate the magnitude and direction of their percepts as well, suggesting that mechanisms similar to the fly’s may also underlie this illusion in humans. By taking a comparative approach that exploits Drosophila neurogenetics, our results provide a causal, mechanistic account for a long-known visual illusion. These results argue that this illusion arises from architectures for motion detection that are shared across phyla.

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Nau, Jean-Yves. "De nouveaux neurones naissent en permanence au sein du cerveau humain." Revue Médicale Suisse 3, no. 100 (2007): 563. http://dx.doi.org/10.53738/revmed.2007.3.100.0563.

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Parola, Abraham H., Aviv Cohen, Ilana Nathan, and Roni Kasher. "Humanin inhibits necrotic cell death in neurons." Biophysical Journal 121, no. 3 (February 2022): 271a. http://dx.doi.org/10.1016/j.bpj.2021.11.1390.

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Davis, Karen D., Andres M. Lozano, Marosh Manduch, Ronald R. Tasker, Zelma H. T. Kiss, and Jonathan O. Dostrovsky. "Thalamic Relay Site for Cold Perception in Humans." Journal of Neurophysiology 81, no. 4 (April 1, 1999): 1970–73. http://dx.doi.org/10.1152/jn.1999.81.4.1970.

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Thalamic relay site for cold perception in humans. The neural pathways subserving the sensation of temperature are virtually unknown. However, recent findings in the monkey suggest that the sensation of cold may be mediated by an ascending pathway relaying in the posterior part of the thalamic ventromedial nucleus (VMpo). To test this hypothesis we examined the responses of neurons to thermal stimulation of the skin and determined the perceptual effects of microstimulation in the VMpo region in awake patients undergoing functional stereotactic surgery. In 16 patients, microstimulation in the VMpo region evoked cold sensations in a circumscribed body part. Furthermore, at some of these sites thalamic neurons were found that responded to innocuous cooling of the skin area corresponding to the stimulation-evoked cold sensations. These data provide the first direct demonstration of a pathway mediating cold sensation and its location in the human thalamus.

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McGeer, Edith G., and Patrick L. McGeer. "Aging, Neurodegenerative Disease and the Brain." Canadian Journal on Aging / La Revue canadienne du vieillissement 16, no. 2 (1997): 218–36. http://dx.doi.org/10.1017/s071498080001432x.

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RésuméL'eorganisation anatomique et chimique du cerveau humain subit de nombreux changements au cours du vieillissement. Certains neurons meurent, d'autres s'atrophient et ily a une réduction marquée du nombre de synapses dans des régions spécifiques du cerveau. Des diminutions du métabolisme du glucose et des effets pré- et post-synaptiques des neurotransmetteurs ont aussi été rapportées. À l'exception de certaines structures sous-corticales, il existe cependant une controverse quant à la sévérité des changements dans l'ensemble du cerveau. De plus, les effets du vieillissement sont très variables d'une région du cerveau à l'autre ainsi que d'un individu à l'autre. Certains phénomènes observès dans le vieillissement normal, tels la perte des neurones dopaminergique de la substance noire et celle des neurones cholinergiques du prosencé;phale basal, apparaissent sous une forme grandement exacerbées dans diverses pathologies neurodégénératives comme les maladies de Parkinson et d'Alzeimer. Les faibles altérations qui surviennent au niveau de ces systémes lors du vieillissement normal pourraient étre responsables des troubles d'équilibre, de la pauvreté de mouvement et des pertes de mémoires que l'on observent chez les gens âgés. Cependant, l'inflammation chronique du cerveau semble être une caractéristique typique des individus atteints de maladies neurodégénératives. L'hypothèse voulant que cette inflammation puisse être ralentie par un traitement avec des agents anti-inflammatoires a été supportée par les résultats de 19 études épidémiologiques ainsi que par un essai clinique de moindre envergure. Cependant, d'Autres études cliniques devront ètre réalisées et une attention particulière devra être portée aux effets secondaires de la thérapie anti-inflammatoire conventionnelle afin d'en arriver à une conclusion définitive.

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Walton, J. R. "Aluminum in hippocampal neurons from humans with Alzheimer's disease." NeuroToxicology 27, no. 3 (May 2006): 385–94. http://dx.doi.org/10.1016/j.neuro.2005.11.007.

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Sani, Sepehr, Shoichi Shimamoto, Robert S. Turner, Nadja Levesque, and Philip A. Starr. "Microelectrode recording in the posterior Hypothalamic Region in Humans." Operative Neurosurgery 64, suppl_1 (March 1, 2009): ONS161—ONS169. http://dx.doi.org/10.1227/01.neu.0000334051.91501.e3.

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Abstract Introduction: Deep brain stimulation of the posterior hypothalamic region (PHR) is an emerging technique for the treatment of medically intractable cluster headache. Few reports have analyzed single unit neuronal recordings in the human PHR. We report properties of spontaneous neuronal discharge in PHR for 6 patients who underwent DBS for cluster headaches. Methods: Initial target coordinates, determined by magnetic resonance imaging stereotactic localization, were 2 mm lateral, 3 mm posterior, and 5 mm inferior to the midpoint of the anterior commissure-posterior commissure plane. A single microelectrode penetration was performed beginning 10 mm above the anatomic target, without systemic sedation. Single units were discriminated off-line by cluster cutting in principal components space. Discharge rates, interspike intervals, and oscillatory activity were analyzed and compared between ventromedial thalamic and hypothalamic units. Results: Six patients and 24 units were evaluated. Units in the PHR had a slow, regular spontaneous discharge with wide, low-amplitude action potentials. The mean discharge rate of hypothalamic neurons was significantly lower (mean ± standard deviation, 13.2 ± 12.2) than that of medial thalamic units (28.0 ± 8.2). Oscillatory activity was not detected. Microelectrode recording in this region caused no morbidity. Conclusion: The single-unit discharge rate of neurons in the PHR of awake humans was 13.2 Hz and was significantly lower than medial thalamic neurons recorded dorsal to the target. The findings will be of use for microelectrode localization of the cluster headache target and for comparison with animal studies.

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Keerthana B, Yuvaraj Babu K, and Gayathri R. "Rosehip Neuron - A Review." International Journal of Research in Pharmaceutical Sciences 11, SPL3 (September 8, 2020): 53–59. http://dx.doi.org/10.26452/ijrps.v11ispl3.2890.

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Rosehip neuron is a special type of neuron present only in humans. It has inhibitory actions over other cells. It is present in the first layer of the human cerebral cortex. These neurons have an inhibitory action over other neuronal cells. This research is seen as a scoping literature review. In seeking to identify the relevant literature from the past twenty years, we used common databases such as Pubmed, Google scholar online websites. Nearly 30 reference articles are collected related to the topic. The obtained articles were later read thoroughly and understood. Rosehip neurons are unique neurons and can treat neuronal disorders. It can also maintain the activities of other neuronal cells. It is concluded that more research has to be done on the actions of rosehip neurons and about its functions. This review is an attempt to understand the various functions of Rosehip neurons in humans. Further research is needed to know about its full use of humanity.

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Hickok, Gregory. "Eight Problems for the Mirror Neuron Theory of Action Understanding in Monkeys and Humans." Journal of Cognitive Neuroscience 21, no. 7 (July 2009): 1229–43. http://dx.doi.org/10.1162/jocn.2009.21189.

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The discovery of mirror neurons in macaque frontal cortex has sparked a resurgence of interest in motor/embodied theories of cognition. This critical review examines the evidence in support of one of these theories, namely, that mirror neurons provide the basis of action understanding. It is argued that there is no evidence from monkey data that directly tests this theory, and evidence from humans makes a strong case against the position.

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Cohen, Aviv, Jenny Lerner-Yardeni, David Meridor, Roni Kasher, Ilana Nathan, and Abraham H. Parola. "Humanin Derivatives Inhibit Necrotic Cell Death in Neurons." Molecular Medicine 21, no. 1 (January 2015): 505–14. http://dx.doi.org/10.2119/molmed.2015.00073.

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Zheng, Jie, Andrea G. P. Schjetnan, Mar Yebra, Bernard A. Gomes, Clayton P. Mosher, Suneil K. Kalia, Taufik A. Valiante, Adam N. Mamelak, Gabriel Kreiman, and Ueli Rutishauser. "Neurons detect cognitive boundaries to structure episodic memories in humans." Nature Neuroscience 25, no. 3 (March 2022): 358–68. http://dx.doi.org/10.1038/s41593-022-01020-w.

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Wessler, I., and C. J. Kirkpatrick. "Acetylcholine beyond neurons: the non-neuronal cholinergic system in humans." British Journal of Pharmacology 154, no. 8 (August 2008): 1558–71. http://dx.doi.org/10.1038/bjp.2008.185.

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Nishio, Takeshi, Shoei Furukawa, Ichiro Akiguchi, and Nobuhiko Sunohara. "Medial nigral dopamine neurons have rich neurotrophin support in humans." NeuroReport 9, no. 12 (August 1998): 2847–51. http://dx.doi.org/10.1097/00001756-199808240-00030.

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Inta, Dragos, Heather A. Cameron, and Peter Gass. "New neurons in the adult striatum: from rodents to humans." Trends in Neurosciences 38, no. 9 (September 2015): 517–23. http://dx.doi.org/10.1016/j.tins.2015.07.005.

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Kiss, Z. H. T., K. D. Davis, R. R. Tasker, A. M. Lozano, B. Hu, and J. O. Dostrovsky. "Kinaesthetic neurons in thalamus of humans with and without tremor." Experimental Brain Research 150, no. 1 (March 7, 2003): 85–94. http://dx.doi.org/10.1007/s00221-003-1399-3.

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Nishio, Takeshi, Shoei Furukawa, Ichiro Akiguchi, and Nobuhiko Sunohara. "Medial nigral dopamine neurons have rich neurotrophin support in humans." Neuroscience Research 31 (January 1998): S345. http://dx.doi.org/10.1016/s0168-0102(98)82512-1.

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Seeley, William W., Danielle A. Carlin, John M. Allman, Marcelo N. Macedo, Clarissa Bush, Bruce L. Miller, and Stephen J. DeArmond. "Early frontotemporal dementia targets neurons unique to apes and humans." Annals of Neurology 60, no. 6 (December 2006): 660–67. http://dx.doi.org/10.1002/ana.21055.

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Soni, Kiran, Han-Seong Jeong, and Sujeong Jang. "Neurons for Ejaculation and Factors Affecting Ejaculation." Biology 11, no. 5 (April 29, 2022): 686. http://dx.doi.org/10.3390/biology11050686.

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Ejaculation is a reflex and the last stage of intercourse in male mammals. It consists of two coordinated phases, emission and expulsion. The emission phase consists of secretions from the vas deferens, seminal vesicle, prostate, and Cowper’s gland. Once these contents reach the posterior urethra, movement of the contents becomes inevitable, followed by the expulsion phase. The urogenital organs are synchronized during this complete event. The L3–L4 (lumbar) segment, the spinal cord region responsible for ejaculation, nerve cell bodies, also called lumbar spinothalamic (LSt) cells, which are denoted as spinal ejaculation generators or lumbar spinothalamic cells [Lst]. Lst cells activation causes ejaculation. These Lst cells coordinate with [autonomic] parasympathetic and sympathetic assistance in ejaculation. The presence of a spinal ejaculatory generator has recently been confirmed in humans. Different types of ejaculatory dysfunction in humans include premature ejaculation (PE), retrograde ejaculation (RE), delayed ejaculation (DE), and anejaculation (AE). The most common form of ejaculatory dysfunction studied is premature ejaculation. The least common forms of ejaculation studied are delayed ejaculation and anejaculation. Despite the confirmation of Lst in humans, there is insufficient research on animals mimicking human ejaculatory dysfunction.

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Welsby, Philip D. "Emergence of free will and consciousness in humans: implications for doctor-patient interactions." Postgraduate Medical Journal 94, no. 1112 (May 2, 2018): 354–56. http://dx.doi.org/10.1136/postgradmedj-2018-135634.

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Human brains have about 100 billion neurons each with about 1000 dendritic connections with other neurons giving a total of 100 000 billion deterministic dendritic switches. Various voting systems that the brain may use can produce conflicting results from identical inputs without any indication as to which one or ones would be correct. Voting systems cannot deliver unequivocal results in any other than the simplest situations. It is hypothesised that these conflicting results provide an indeterminacy that underlies free will, self-awareness, awareness of others, consciousness and personal responsibility, all of which can influence doctor-patient interactions.

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Sakon, John J., and Wendy A. Suzuki. "A neural signature of pattern separation in the monkey hippocampus." Proceedings of the National Academy of Sciences 116, no. 19 (April 22, 2019): 9634–43. http://dx.doi.org/10.1073/pnas.1900804116.

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The CA3 and dentate gyrus (DG) regions of the hippocampus are considered key for disambiguating sensory inputs from similar experiences in memory, a process termed pattern separation. The neural mechanisms underlying pattern separation, however, have been difficult to compare across species: rodents offer robust recording methods with less human-centric tasks, while humans provide complex behavior with less recording potential. To overcome these limitations, we trained monkeys to perform a visual pattern separation task similar to those used in humans while recording activity from single CA3/DG neurons. We find that, when animals discriminate recently seen novel images from similar (lure) images, behavior indicative of pattern separation, CA3/DG neurons respond to lure images more like novel than repeat images. Using a population of these neurons, we are able to classify novel, lure, and repeat images from each other using this pattern of firing rates. Notably, one subpopulation of these neurons is more responsible for distinguishing lures and repeats—the key discrimination indicative of pattern separation.

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Lu, Van B., Peter A. Smith, and Saifee Rashiq. "The excitability of dorsal horn neurons is affected by cerebrospinal fluid from humans with osteoarthritis." Canadian Journal of Physiology and Pharmacology 90, no. 6 (June 2012): 783–90. http://dx.doi.org/10.1139/y2012-014.

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Changes in central neural processing are thought to contribute to the development of chronic osteoarthritis pain. This may be reflected as the presence of inflammatory mediators in the cerebral spinal fluid (CSF). We therefore exposed organotypically cultured slices of rat spinal cord to CSF from human subjects with osteoarthritis (OACSF) at a ratio of 1 part CSF in 9 parts culture medium for 5–6 days, and measured changes in neuronal electrophysiological properties by means of whole-cell recording. Although OACSF had no effect on the membrane properties and excitability of neurons in the substantia gelatinosa, synaptic transmission was clearly altered. The frequency of spontaneous excitatory postsynaptic currents (sEPSC) in delay-firing putative excitatory neurons was increased, as was sEPSC amplitude and frequency in tonic-firing inhibitory neurons. These changes could affect sensory processing in the dorsal horn, and may affect the transfer of nociceptive information. Although OACSF also affected inhibitory synaptic transmission (frequency of spontaneous inhibitory synaptic currents; sIPSC), this may have little bearing on sensory processing by substantia gelatinosa neurons, as sEPSC frequency is >3× greater than sIPSC frequency in this predominantly excitatory network. These results support the clinical notion that changes in nociceptive processing at the spinal level contribute to the generation of chronic osteoarthritis pain.

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Chudler, E. H., F. Anton, R. Dubner, and D. R. Kenshalo. "Responses of nociceptive SI neurons in monkeys and pain sensation in humans elicited by noxious thermal stimulation: effect of interstimulus interval." Journal of Neurophysiology 63, no. 3 (March 1, 1990): 559–69. http://dx.doi.org/10.1152/jn.1990.63.3.559.

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1. Twenty-six nociceptive neurons in the primary somatosensory cortex (SI) of anesthetized monkeys were responsive to noxious thermal stimulation applied to the face. Thermode temperature increased from a base line of 38 degrees C to temperatures ranging from 44 to 49 degrees C (T1). After a period of 5 s, the temperature increased an additional 1 degree C (T2). The neuronal responses to noxious thermal stimuli were compared when the interstimulus interval (ISI) was 30 or 180 s. 2. A linear regression analysis was applied to the stimulus-response functions of neuronal responses to T1 stimuli obtained at ISIs of 180 s. Based on the slopes and linear regression coefficients of these stimulus-response functions, two populations of nociceptive neurons were identified. The neuronal responses of one population of nociceptive SI neurons (WDR1) to T1 stimuli were characterized by steep slopes and high regression coefficients, whereas the other population (WDR2) had flatter slopes and lower regression coefficients. WDR1 neurons responded with monotonic increases in neuronal activity as the stimulus intensity increased. However, the peak frequency of WDR2 neurons often reached a plateau below 47 degrees C. Both WDR1 and WDR2 neurons had receptive fields that encompassed one or two divisions of the trigeminal nerve. 3. The T1 neuronal responses of WDR1 neurons were significantly suppressed when thermal stimuli were delivered with ISIs of 30 s. The T1 neuronal responses of WDR2 and the T2 responses of both WDR1 and WDR2 neurons were not significantly different when ISIs of 30 and 180 s were used. The T1 thresholds of WDR1 and WDR2 neurons were significantly higher when stimuli were delivered with ISIs of 30 s compared with ISIs of 180 s. 4. Most nociceptive SI neurons were located in layers III and IV of area 1-2. In a number of instances, multiple nociceptive neurons were found in the same microelectrode penetration. 5. The humans' intensity of pain sensation paralleled the neuronal responses of nociceptive SI neurons. With the use of a similar paradigm as in the monkey experiments, increases in T1 and T2 temperatures resulted in monotonic increases in pain ratings and change in pain sensation, respectively. However, the intensity of pain sensation to T1 temperatures was suppressed by ISIs of 30 s. Neither ISI produced statistically significant changes in the intensity of pain sensation to T2 stimuli. 6. These data demonstrate that manipulations that alter the intensity of pain sensation also produce concomitant changes in the responsiveness of nociceptive SI neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

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Burr, David C., and Maria Concetta Morrone. "Spatiotopic coding and remapping in humans." Philosophical Transactions of the Royal Society B: Biological Sciences 366, no. 1564 (February 27, 2011): 504–15. http://dx.doi.org/10.1098/rstb.2010.0244.

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How our perceptual experience of the world remains stable and continuous in the face of continuous rapid eye movements still remains a mystery. This review discusses some recent progress towards understanding the neural and psychophysical processes that accompany these eye movements. We firstly report recent evidence from imaging studies in humans showing that many brain regions are tuned in spatiotopic coordinates, but only for items that are actively attended. We then describe a series of experiments measuring the spatial and temporal phenomena that occur around the time of saccades, and discuss how these could be related to visual stability. Finally, we introduce the concept of the spatio-temporal receptive field to describe the local spatiotopicity exhibited by many neurons when the eyes move.

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Iannetti, G. D., A. Truini, A. Romaniello, F. Galeotti, C. Rizzo, M. Manfredi, and G. Cruccu. "Evidence of a Specific Spinal Pathway for the Sense of Warmth in Humans." Journal of Neurophysiology 89, no. 1 (January 1, 2003): 562–70. http://dx.doi.org/10.1152/jn.00393.2002.

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While research on human sensory processing shows that warm input is conveyed from the periphery by specific, unmyelinated primary sensory neurons, its pathways in the central nervous system (CNS) remain unclear. To gain physiological information on the spinal pathways that convey warmth or nociceptive sensations, in 15 healthy subjects, we studied the cerebral evoked responses and reaction times in response to laser stimuli selectively exciting Aδ nociceptors or C warmth receptors at different levels along the spine. To minimize the conduction distance along the primary sensory neuron, we directed CO2-laser pulses to the skin overlying the vertebral spinous processes. Using brain source analysis of the evoked responses with high-resolution electroencephalography and a realistic model of the head based on individual magnetic resonance imaging scans, we also studied the cortical areas involved in the cerebral processing of warm and nociceptive inputs. The activation of C warmth receptors evoked cerebral potentials with a main positive component peaking at 470–540 ms, i.e., a latency clearly longer than that of the corresponding wave yielded by Aδ nociceptive input (290–320 ms). Spinal neurons activated by the warm input had a slower conduction velocity (2.5 m/s) than the nociceptive spinal neurons (11.9 m/s). Brain source analysis of the cerebral responses evoked by the Aδ input yielded a very strong fit for one single generator in the mid portion of the cingulate gyrus; the warmth-related responses were best explained by three generators, one within the cingulate and two in the right and left opercular-insular cortices. Our results support the existence of slow-conducting second-order neurons specific for the sense of warmth.

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Journal articles on the topic 'Neurones humains'

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