Academic literature on the topic 'Neurone intermediaire'
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Journal articles on the topic "Neurone intermediaire"
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Itazawa, Shun-Ichi, Tadashi Isa, and Seiji Ozawa. "Inwardly Rectifying and Ca2+-Permeable AMPA-Type Glutamate Receptor Channels in Rat Neocortical Neurons." Journal of Neurophysiology 78, no. 5 (1997): 2592–601. http://dx.doi.org/10.1152/jn.1997.78.5.2592.
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Itazawa, Shun-Ichi, Tadashi Isa, and Seiji Ozawa. Inwardly rectifying and Ca2+-permeable AMPA-type glutamate receptor channels in rat neocortical neurons. J. Neurophysiol. 78: 2592–2605, 1997. Current-voltage ( I-V) relations and Ca2+ permeability of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)type glutamate receptor channels were investigated in neurons of rat neocortex by using the whole cell patch-clamp technique in brain slices. To activate AMPA receptor channels, kainate was used as a nondesensitizing agonist. A patch pipette was filled with solution containing 100 μM spermine to maintain the inward rectification of Ca2+-permeable AMPA receptor channels. Three types of responses to kainate were observed: type I response with outwardly rectifying I-V relation, type II response with I-V relation of marked inward rectification, and intermediate response with I-V relation of weaker inward rectification. Neurons with type I, type II and intermediate I-V relations were referred to as type I, type II, and intermediate neurons, respectively. Of a total of 223 recorded cells, 90 (40.4%) were type I, 129 (57.8%) intermediate, and 4 (1.8%) type II neurons. Properties of AMPA receptor channels were examined in the former two types of neurons. The value of PCa:PCs, the ratio of the permeability coefficients of Ca2+ and Cs+, was estimated from the reversal potentials of kainate responses in the outside-out patches bathed in Na+-free solution containing 100 mM Ca2+ according to the constant-field equation. They ranged from 0.05 to 0.10 (0.08 ± 0.02, mean ± SD, n = 8) for type I neurons and from 0.14 to 1.29 (0.60 ± 0.37, n = 11) for the intermediate neurons. There was a close correlation between the inward rectification and the Ca2+ permeability in AMPA receptor channels in these neurons. Intermediate neurons stained with biocytin were nonpyramidal cells with ellipsoidal-shaped somata. Type I neurons had either triangular- or ellipsoidal-shaped somata. Excitatory postsynaptic currents (EPSCs) recorded in both type I and intermediate neurons had 6-cyano-7-nitroquinoxaline-2,3-dione-sensitive fast and d−2-amino-5-phosphonovalerate-sensitiveslow components. The I-V relation of the fast component exhibited inward rectification in the intermediate neuron, whereas that in the type I neuron showed slight outward rectification. The fast component of EPSCs in the intermediate neuron was suppressed more prominently (to 56 ± 15% of the control, n = 12) than that in the type I neuron (to 78 ± 6% of the control, n = 6) by bath application of 1 mM spermine. These results indicate that inwardly rectifying and Ca2+-permeable AMPA receptor channels are expressed in a population of neurons of rat neocortex and are involved in excitatory synaptic transmission.
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Nuding, Sarah C., Lauren S. Segers, David M. Baekey, et al. "Pontine–Ventral Respiratory Column Interactions Through Raphé Circuits Detected Using Multi-Array Spike Train Recordings." Journal of Neurophysiology 101, no. 6 (2009): 2943–60. http://dx.doi.org/10.1152/jn.91305.2008.
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Recently, Segers et al. identified functional connectivity between the ventrolateral respiratory column (VRC) and the pontine respiratory group (PRG). The apparent sparseness of detected paucisynaptic interactions motivated consideration of other potential functional pathways between these two regions. We report here evidence for “indirect” serial functional linkages between the PRG and VRC via intermediary brain stem midline raphé neurons. Arrays of microelectrodes were used to record sets of spike trains from a total of 145 PRG, 282 VRC, and 340 midline neurons in 11 decerebrate, vagotomized, neuromuscularly blocked, ventilated cats. Spike trains of 13,843 pairs of neurons that included at least one raphé cell were screened for respiratory modulation and short-time scale correlations. Significant correlogram features were detected in 7.2% of raphé–raphé (291/4,021), 4.3% of VRC–raphé (292/6,755), and 4.0% of the PRG–raphé (124/3,067) neuron pairs. Central peaks indicative of shared influences were the most common feature in correlations between pairs of raphé neurons, whereas correlated raphé–PRG and raphé–VRC neuron pairs displayed predominantly offset peaks and troughs, features suggesting a paucisynaptic influence of one neuron on the other. Overall, offset correlogram features provided evidence for 33 VRC-to-raphé-to-PRG and 45 PRG-to-raphé-to-VRC correlational linkage chains with one or two intermediate raphé neurons. The results support a respiratory network architecture with parallel VRC-to-PRG and PRG-to-VRC links operating through intervening midline circuits, and suggest that raphé neurons contribute to the respiratory modulation of PRG neurons and shape the respiratory motor pattern through coordinated divergent actions on both the PRG and VRC.
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Saito, Yasuhiko, and Tadashi Isa. "Laminar Specific Distribution of Lateral Excitatory Connections in the Rat Superior Colliculus." Journal of Neurophysiology 92, no. 6 (2004): 3500–3510. http://dx.doi.org/10.1152/jn.00033.2004.
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Premovement activities in neurons in the intermediate gray layer [stratum griseum intermediale (SGI)] of the mammalian superior colliculus (SC) are essential for initiation of orienting behaviors such as saccades. Our previous study demonstrated that burst activities are induced by synchronous activation of SGI neurons communicating within a local excitatory network, which depends on NMDA-receptor–dependent synaptic transmission and release from GABAA inhibition. Furthermore, dual whole cell recordings from adjacent neurons in SGI revealed that application of 10 μM bicuculline (Bic) and reduction of extracellular Mg2+ concentration (to 0.1 mM) induce spontaneous depolarization that is synchronous between neuron pairs, suggesting the recruitment of a large number of neurons communicating through intense excitatory connections. In the present study, we investigated the properties of synchronous depolarization and the fundamental structure of the lateral excitatory network that recruits a neuronal population in SC to synchronous activation, by analyzing the synchronicity of spontaneous depolarization induced in the presence of Bic plus low Mg2+. We found that 1) spontaneous depolarization exhibits bidirectional horizontal propagation among the SGI neuron pairs; 2) induction of spontaneous depolarization is not caused by activation of intrinsic voltage-dependent conductances; 3) neurons exposed to low Mg2+ alone exhibit spontaneous depolarization, although in this case the depolarization is less synchronous; and 4) neurons exposed to Bic alone exhibit synchronous depolarization, but less frequently than those exposed to both Bic and low Mg2+. Analysis of the synchronicity of spontaneous depolarization indicates that the distribution of lateral excitatory connections is markedly different among layers of SC; the SGI neurons form extensive lateral excitatory connections, whereas they are sparse or limited within subsets of neurons in the stratum griseum superficiale (SGS). Wide-field vertical neurons in the stratum opticum have features intermediate between neurons in the SGS and SGI. Such differences in the structure of lateral excitatory connections may reflect the different way signal processing is achieved in each layer of SC.
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Trojanowski, J. Q. "Neurofilament proteins and human nervous system tumors." Journal of Histochemistry & Cytochemistry 35, no. 9 (1987): 999–1003. http://dx.doi.org/10.1177/35.9.3611738.
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Neoplasms that arise in the peripheral (e.g., carotid body tumors, neuroblastomas, pheochromocytomas) or central (gangliocytomas, medulloblastomas) nervous system express a number of neuron-specific gene products. Presumably, these tumors are derived from precursor cells that are or have the potential to develop into neurons or neuron-like cells. This report provides a critical examination of the hypothesis that cytoskeletal proteins of normal neurons, in particular the neuron-specific class of intermediate filaments (neurofilaments), are present but are abnormal in neoplasms derived from neurons or neuron-like cells. The implications of these findings for understanding tumor promotion and progression, and for development of molecular probes for the diagnostic assessment of these neoplasms, are discussed.
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Weinstein, D. E., M. L. Shelanski, and R. K. Liem. "Suppression by antisense mRNA demonstrates a requirement for the glial fibrillary acidic protein in the formation of stable astrocytic processes in response to neurons." Journal of Cell Biology 112, no. 6 (1991): 1205–13. http://dx.doi.org/10.1083/jcb.112.6.1205.
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The glial fibrillary acidic protein (GFAP) is a glial-specific intermediate filament protein, which is expressed in astrocytes in the central nervous system, as well as in astrocytoma cell lines. To investigate the function of GFAP, we have studied the human astrocytoma cell line, U251, which constitutively expresses GFAP and vimentin in the same 10-nm filaments. These cells respond to neurons in vitro in the same way as primary astrocytes: they withdraw from the cell cycle, support neuronal cell survival and neurite outgrowth, and they extend complex, GFAP-positive processes. To determine the role of GFAP in these responses, we have specifically suppressed its expression by stably transfecting the U251 cells with an antisense GFAP construct. Two stable antisense cell lines from separate transfections were isolated and were shown to be GFAP negative by Northern and Western blot analyses, and by immunofluorescence studies. The antisense cell lines were inhibited in their ability to extend significant glial processes in response to neurons. In culture with primary neurons, the average increase in process length of the U251 cells was nearly 400%, as compared to only 14% for the antisense transfectants. The other neuron induced responses of astrocytes, i.e., proliferative arrest and neuronal support, were not affected in these cell lines. These data support the conclusion that the glial-specific intermediate filament protein, GFAP, is required for the formation of stable astrocytic processes in response to neurons.
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Newland, Philip L., and Yasuhiro Kondoh. "Dynamics of Neurons Controlling Movements of a Locust Hind Leg II. Flexor Tibiae Motor Neurons." Journal of Neurophysiology 77, no. 4 (1997): 1731–46. http://dx.doi.org/10.1152/jn.1997.77.4.1731.
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Newland, Philip L. and Yasuhiro Kondoh. Dynamics of neurons controlling movements of a locust hind leg. II. Flexor tibiae motor neurons. J. Neurophysiol. 77: 1731–1746, 1997. Imposed movements of a proprioceptor that monitors the relative position of the tibia about the femur, the femorotibial chordotonal organ (FeCO), evoke resistance reflexes in the motor neurons that control the movements of the tibia of the locust. The response dynamics of one pool of motor neurons, the flexor tibiae motor neurons, which are located in three groups (anterior, lateral, and posterior), have been analyzed by the Wiener kernel method. First- and second-order kernels that represent the linear and nonlinear responses, respectively, were computed by a cross-correlation between the intracellularly recorded synaptic responses in the motor neurons and the white noise stimulus applied to the FeCO, and were used to define the input-output characteristics of the motor neurons. The posterior fast, intermediate, and slow and the anterior fast and intermediate flexor tibiae motor neurons had biphasic first-order kernels with initial negative phases, indicating that they are velocity sensitive. The falling phases of the kernels had distinct shoulders, indicating that the responses of the motor neurons also had delayed low-pass components, i.e., position sensitivity. The anterior slow flexor motor neuron had a monophasic, low-passed, first-order kernel, indicating that it is position sensitive. The linear component of the motor neuron responses, predicted by convolving the first-order kernels with the stimulus signal, strongly resembled the actual response, whereas the second-order nonlinear component was small, particularly at >10 Hz. The power spectra of the fast motor neurons showed that they had the highest cutoff frequencies (at >8 Hz), whereas the slow flexor motor neurons had a gradual roll-off at 1 Hz. The intermediate flexor motor neuron had an intermediate cutoff frequency of ∼2–3 Hz. The linear responses of the flexor motor neurons could be decomposed into low- and high-frequency components. The high-frequency components (>10 Hz) were velocity dependent and linear, whereas the low-frequency components (<10 Hz) were position dependent and nonlinear. The nonlinearity was a signal compression (or half-wave rectification). The results show that although the flexor motor neurons receive many common inputs during FeCO stimulation, each individual has specific dynamic response properties. The responses of the motor neurons are fractionated so that a given individual within the pool will respond best to position, whereas others will respond better to velocity. Likewise, some motor neurons respond best at low frequencies, whereas others respond best at higher frequencies of stimulation.
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Walker, M. F., E. J. Fitzgibbon, and M. E. Goldberg. "Neurons in the monkey superior colliculus predict the visual result of impending saccadic eye movements." Journal of Neurophysiology 73, no. 5 (1995): 1988–2003. http://dx.doi.org/10.1152/jn.1995.73.5.1988.
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1. Previous experiments have shown that visual neurons in the lateral intraparietal area (LIP) respond predictively to stimuli outside their classical receptive fields when an impending saccade will bring those stimuli into their receptive fields. Because LIP projects strongly to the intermediate layers of the superior colliculus, we sought to demonstrate similar predictive responses in the monkey colliculus. 2. We studied the behavior of 90 visually responsive neurons in the superficial and intermediate layers of the superior colliculus of two rhesus monkeys (Macaca mulatta) when visual stimuli or the locations of remembered stimuli were brought into their receptive fields by a saccade. 3. Thirty percent (18/60) of intermediate layer visuomovement cells responded predictively before a saccade outside the movement field of the neuron when that saccade would bring the location of a stimulus into the receptive field. Each of these neurons did not respond to the stimulus unless an eye movement brought it into its receptive field, nor did it discharge in association with the eye movement unless it brought a stimulus into its receptive field. 4. These neurons were located in the deeper parts of the intermediate layers and had relatively larger receptive fields and movement fields than the cells at the top of the intermediate layers. 5. The predictive responses of most of these neurons (16/18, 89%) did not require that the stimulus be relevant to the monkey's rewarded behavior. However, for some neurons the predictive response was enhanced when the stimulus was the target of a subsequent saccade into the neuron's movement field. 6. Most neurons with predictive responses responded with a similar magnitude and latency to a continuous stimulus that remained on after the saccade, and to the same stimulus when it was only flashed for 50 ms coincident with the onset of the saccade target and thus never appeared within the cell's classical receptive field. 7. The visual response of neurons in the intermediate layers of the colliculus is suppressed during the saccade itself. Neurons that showed predictive responses began to discharge before the saccade, were suppressed during the saccade, and usually resumed discharging after the saccade. 8. Three neurons in the intermediate layers responded tonically from stimulus appearance to saccade without a presaccadic burst. These neurons responded predictively to a stimulus that was going to be the target for a second saccade, but not to an irrelevant flashed stimulus. 9. No superficial layer neuron (0/27) responded predictively when a stimulus would not be brought into their receptive fields by a saccade.(ABSTRACT TRUNCATED AT 400 WORDS)
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Pettit, Diana L., Matthew C. Helms, Psyche Lee, George J. Augustine, and William C. Hall. "Local Excitatory Circuits in the Intermediate Gray Layer of the Superior Colliculus." Journal of Neurophysiology 81, no. 3 (1999): 1424–27. http://dx.doi.org/10.1152/jn.1999.81.3.1424.
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Local excitatory circuits in the intermediate gray layer of the superior colliculus. We have used photostimulation and whole cell patch-clamp recording techniques to examine local synaptic interactions in slices from the superior colliculus of the tree shrew. Uncaging glutamate 10–75 μm from the somata of neurons in the intermediate gray layer elicited a long-lasting inward current, due to direct activation of glutamate receptors on these neurons, and brief inward currents caused by activation of presynaptic neurons. The synaptic responses occurred as individual currents or as clusters that lasted up to several hundred milliseconds. Excitatory synaptic responses, which reversed at membrane potentials near 0 mV, could be evoked by uncaging glutamate anywhere within 75 μm of an intermediate layer neuron. Our results indicate the presence of extensive local excitatory circuits in the intermediate layer of the superior colliculus and support the hypothesis that such intrinsic circuitry contributes to the development of presaccadic command bursts.
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Rozovsky, Irina, Min Wei, David J. Stone, et al. "Estradiol (E2) Enhances Neurite Outgrowth by Repressing Glial Fibrillary Acidic Protein Expression and Reorganizing Laminin." Endocrinology 143, no. 2 (2002): 636–46. http://dx.doi.org/10.1210/endo.143.2.8615.
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Abstract Neuronal remodeling in response to deafferenting lesions in the brain can be enhanced by estradiol (E2). Astrocytes are among the targets of E2 in complex interactions with neurons and may support or inhibit neuronal remodeling. In ovariectomized female rats given entorhinal cortex lesions, E2 replacement inhibited the increase of glial fibrillary acidic protein (GFAP) protein. To model the role of E2 in these complex processes, we used the “wounding-in-a-dish” of astrocyte-neuron cocultures. Low physiological E2 (1 pm) blocks the wound-induced increase of GFAP expression (transcription and protein) and enhances neurite outgrowth. The transcriptional responses to E2 during wounding are mediated by sequences in the 5′-upstream region of the rat GFAP promoter. Concurrently, E2 reorganized astrocytic laminin into extracellular fibrillar arrays, which others have shown support neurite outgrowth. The inhibition of GFAP expression by E2 in this model is consistent with in vivo findings that E2 enhanced recovery from deafferenting cortical lesions by increased neurite outgrowth in association with decreased GFAP expression. More generally, we hypothesize that physiological variations in E2 levels modulate neuronal plasticity through direct effects on GFAP transcription that, in turn, modify GFAP-containing intermediate filaments and reorganize astrocytic laminin.
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Page, Keri L., Jure Zakotnik, Volker Dürr, and Thomas Matheson. "Motor Control of Aimed Limb Movements in an Insect." Journal of Neurophysiology 99, no. 2 (2008): 484–99. http://dx.doi.org/10.1152/jn.00922.2007.
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Limb movements that are aimed toward tactile stimuli of the body provide a powerful paradigm with which to study the transformation of motor activity into context-dependent action. We relate the activity of excitatory motor neurons of the locust femoro-tibial joint to the consequent kinematics of hind leg movements made during aimed scratching. There is posture-dependence of motor neuron activity, which is stronger in large amplitude (putative fast) than in small (putative slow and intermediate) motor neurons. We relate this posture dependency to biomechanical aspects of the musculo-skeletal system and explain the occurrence of passive tibial movements that occur in the absence of agonistic motor activity. There is little recorded co-activation of antagonistic tibial extensor and flexor motor neurons, and there is differential recruitment of proximal and distal flexor motor neurons. Large-amplitude motor neurons are often recruited soon after a switch in joint movement direction. Motor bursts containing large-amplitude spikes exhibit high spike rates of small-amplitude motor neurons. The fast extensor tibiae neuron, when recruited, exhibits a pattern of activity quite different to that seen during kicking, jumping, or righting: there is no co-activation of flexor motor neurons and no full tibial flexion. Changes in femoro-tibial joint angle and angular velocity are most strongly dependent on variations in the number of motor neuron spikes and the duration of motor bursts rather than on firing frequency. Our data demonstrate how aimed scratching movements result from interactions between biomechanical features of the musculo-skeletal system and patterns of motor neuron recruitment.
Dissertations / Theses on the topic "Neurone intermediaire"
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Cavallari, Paolo. "Organisation des circuits transmettant inhibition et excitation entre les muscles antagonistes du poignet chez l'homme." Paris 6, 1988. http://www.theses.fr/1988PA066126.
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Djabali, Karima. "Dynamiques et interactions specifiques de la peripherine, proteine de filament intermediaire neuronale." Paris 7, 1991. http://www.theses.fr/1991PA077161.
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La peripherine, proteine neuronale de filament intermediaire de type iii est co-exprimee avec les neurofilaments dans certaines populations neuronales et avec la vimentine dans les lignees de neuroblastome. Nous avons montre que la peripherine est co-localisee avec les neurofilaments dans les neurones de ganglions sympathiques et sensoriels ainsi qu'avec la vimentine dans des cellules de neuroblastome. Nous avons etudie les interactions moleculaires entre la peripherine et les lamines nucleaires. Nous avons montre que la peripherine purifiee interagit specifiquement in vitro avec la lamine b de mammifere. Nous avons egalement demontre qu'un peptide synthetique (pi) representant la partie proximale du domaine carboxy-terminal de la peripherine est aussi capable d'association avec la lamine b de maniere specifique et saturable et de facon cooperative. Des animaux de laboratoire immunises avec le peptide i developpent spontanement des anticorps idiotypiques et anti-idiotypiques capables de reconnaitre respectivement la peripherine et la lamine b. Ces resultats demontrent in vivo que la lamine b est le recepteur nucleaire de la peripherine
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Giasson, Benoit I. "Regulatory and aberrant phosphorylation of neuronal intermediate filament proteins." Thesis, McGill University, 1997. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=37546.
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The activation of cyclic AMP-dependent protein kinase (PKA) in rat dorsal root ganglion (DRG) cultures, treated concomitantly with low concentrations of okadaic acid that selectively inhibit protein phosphatase-2A, enhanced the disassembly of neuronal intermediate filaments (IFs). The latter disassembly correlated with phosphorylation of the peripherin head domain and a novel, identified PKA site, Ser-2, in the low molecular mass neurofilament (NF) subunit (NFL). On the other hand. insignificant levels of 32P were incorporated into alpha-internxin under control and experimental conditions that promote disassembly. These findings indicate that phosphorylation of the latter protein is not directly involved in the fragmentation of neuronal IFs Phosphopeptide mapping of the mid-size (NF) subunit (NFM) revealed that 32P-labelling of one of its many phosphopeptides is correlated with neuronal IF fragmentation.<br>The expression and Triton X-100 (Triton) solubility of neuronal IF proteins were determined in the developing rat cerebral cortex. The level of expression of alpha-internexin was unchanged from embryonic day 15 (E15) to postnatal day 15 (P15), whereas expression of (NF) subunits increased during this time interval. NFL was largely insoluble in Triton from the time, P5, when there were sufficient amounts for its solubility to be assayed. There was a continual reduction in the Triton solubility of NFM and alpha-internexin during the E15-P15 developmental period. Similar expression patterns and Triton solubility profiles were obtained for neuronal IF proteins in cultured neurons from E15 cerebral cortex. These results suggest that alpha-internexin is expressed earlier than (NF) proteins to provide a more plastic network in the early developing brain.<br>Correlative studies and direct, in vivo activation of stress-activated protein kinases (SAPKs) were used to demonstrate that SAPKs are involved in aberrant phosphorylation of the perikaryal high molecular mass (NF) subunit (NFH). It was also shown that hyperphosphorylation of perikaryal NFH is a reversible process that does not involve p38 kinases or extracellular signal-regulated kinases (ERKs). The use of defined peptide substrates indicated that SAPKgamma preferentially phosphorylates KSPXE motifs in NFH. SAPKgamma was shown to be located both in the cell body and neurites of cultured DRG neurons, suggesting that it is likely to be involved in the phosphorylation of cytoplasmic proteins. Collectively, these findings strongly support the notion that activation of SAPKs causes the aberrant hyperphosphorylation of perikaryal NFH reported in many neurological diseases.
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Giasson, Benoit I. "Regulatory and aberrant phosphorylation of neuronal intermediate filament proteins." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0003/NQ44440.pdf.
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Mosaheb, Sabrina. "Investigations of neuronal Pin1 protein in neurodegeneration, focusing on neuronal intermediate fillament inclusion disease." Thesis, University of Sussex, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.488585.
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Following reports that in Alzheimer's disease (AD) Pin I associates with intraneuronal neurofibrillary tangles (NFTs; a hallmark pathological feature), Pin I has become a protem of interest in this disorder.
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ESCURAT, MICHEL. "Etude de l'expression dynamique de la peripherine, proteine constitutive de filament intermediaire neuronale." Paris 6, 1992. http://www.theses.fr/1992PA066137.
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Cette these represente une etude de l'expression de la peripherine, proteine neurospecifique constitutive de filament intermediaire de type iii. Trois types de recherches ont ete abordees: 1) l'etude de sa distribution spatio-temporelle de la peripherine comparee a celle de la proteine de neurofilament nf-l au cours du developpement chez le rat; 2) l'effet de l'environnement cellulaire sur l'expression de cette proteine; 3) l'effet de l'inhibition de son expression. Il en resulte que l'expression de la peripherine est contemporaine de celle de nf-l mais qu'elle reste limitee a certaines populations neuronales. Sa distribution ne depend ni d'une origine embryonnaire commune, ni d'une fonction neuronale particuliere. En effet, le seul point commun aux differents neurones exprimant la peripherine est qu'ils projettent tous leurs neurites a l'exterieur de l'axe encephale-moelle epiniere. Cette distribution pourrait donc dependre d'elements epigenetiques associes a l'environnement glial; et peut laisser supposer que cette proteine interviendrait dans la dynamique d'extension neuritique. L'etude in vivo et in vitro de la modulation de l'expression de la peripherine en fonction de l'exposition de differents neurones a divers environnements cellulaires a revele que l'expression de cette proteine pouvait etre induite par la presence de fibroblastes. Les observations obtenues lors de l'etude de l'inhibition de son expression, a l'aide d'oligodeoxynucleotides antisens, dans des neurones sensoriels en culture ne permettent pas actuellement de confirmer ou d'infirmer l'hypothese de l'extension neuritique
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Larivière, Roxanne. "Transgenic approach to study the role of intermediate filaments in motor neuron disease." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=84279.
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Amyotrophic lateral sclerosis (ALS) is a late-onset neurodegenerative disorder characterized by the loss of upper and lower motor neurons. Many reports lead to the hypothesis that a high axonal neurofilament burden and a large axonal caliber account for the selective vulnerability of motor neurons affected in ALS (Kawamura et al., 1981; Sobue et al., 1981; 1987). Transgenic mice expressing a mutant form of SOD1-linked to familial ALS and having one disrupted allele for each neurofilament gene were generated to address this issue. Despite a 40% reduction in neurofilament content and a decrease of large axonal caliber from 5--9 mum to 1--5 mum, these mice did not show an extended life span, nor did they display an alleviated loss of motor axons. These results do not support the idea that high neurofilament content and large axonal caliber are responsible for the selective vulnerability of motor neurons in ALS.<br>Peripherin, a type III intermediate filament (IF) protein is also expressed in spinal motor neurons, and is present together with neurofilaments in axonal spheroids of ALS patients, suggesting that this protein could be involved in the pathogenesis of ALS. Moreover, mice overexpressing a peripherin transgene develop a late-onset motor neuron death characterized by the presence of IF inclusion bodies (Beaulieu et al., 1999a). In a first attempt to clarify the role of peripherin in ALS, peripherin knockout mice were generated. Peripherin null mice were viable, reproduce normally and did not exhibit overt phenotype. However, they did show a 34% reduction in the number of L5 unmyelinated sensory fibers demonstrating a requirement of peripherin for the proper development of a subset of sensory neurons.<br>Finally, in order to investigate whether peripherin contributes to the pathogenesis of ALS, mutant SOD1 mice were generated in a peripherin overexpressing background and a peripherin depleted background. Unexpectedly, upregulation or suppression of peripherin expression had no effect on disease onset, mortality and motor neuron loss in mutant SOD1 mice. Taken together, these results provide compelling evidence that peripherin is not a key contributor of motor neuron degeneration associated with toxicity of mutant SOD1.
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Yazdani, Armin A. "The Smn-Independent Beneficial Effects of Trichostatin A on an Intermediate Mouse Model of Spinal Muscular Atrophy." Thèse, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/30703.
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Trichostatin A (TSA) is a histone deacetylase inhibitor with beneficial effects in spinal muscular atrophy mouse models that carry the human SMN2 transgene. Whether TSA specifically targets the upregulation of the SMN2 gene or whether other genes respond to TSA and in turn provide neuroprotection in SMA mice is unclear. We have taken advantage of the Smn2B/- mouse model that does not harbor the human SMN2 transgene, to test the hypothesis that TSA has its beneficial effects through a non-Smn mediated pathway. Daily intraperitoneal injection of TSA from postnatal day 12 to 25 was performed in the Smn2B/- mice and littermate controls. Previous work from our laboratory demonstrated that treatment with TSA increased the median lifespan of Smn2B/- mice from twenty days to eight weeks. As well, there was a significant attenuation of weight loss and improved motor behavior. Pen test and righting reflex both showed significant improvement, and motor neurons in the spinal cord of Smn2B/-mice were protected from degeneration. Both the size and maturity of neuromuscular junctions were significantly improved in TSA treated Smn2B/- mice. Here, we have shown that TSA treatment does not increase the levels of Smn protein in mouse embryonic fibroblasts or myoblasts obtained from the Smn2B/- mice. Further, qPCR analysis revealed no changes in the level of Smn transcripts in the brain or spinal cord of TSA-treated SMA mice. Similarly, western blot analysis revealed no significant increase in Smn protein levels in the brain, spinal cord, hind limb muscle, heart muscle, or the liver of TSA treated Smn2B/- mice. However, TSA has beneficial effects in the muscles of Smn2B/- mice and improves motor behavior and myofiber size. TSA improves muscle development by enhancing the activity of myogenic regulatory factors independent of the Smn gene. The beneficial effect of TSA is therefore likely through an Smn-independent manner. Identification of these protective pathways will be of therapeutic value for the treatment of SMA.
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Bahia, Parmvir Kaur. "A study of small and intermediate conductance calcium-activated potassium channels in sensory neurones." Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1445301/.
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The role of small and intermediate conductance calcium-activated potassium channels (SK and IK channels) in dorsal root ganglion (DRG) neurones was examined. Sixteen antibodies raised against human or rat SK/IK channel peptide epitopes were tested for their ability to stain cells expressing channel protein. Of sixteen antibodies, 12 (6 to SKI, 1 to SK2, 2 to SK3 and 3 to IK) were deemed suitable for immunohistochemistry in human or rat tissue. Real-time quantitative PCR (qPCR) of rat DRG cDNA was performed to examine SK/IK expression levels. DRG neurones produce mRNA for all SK/IK channels and these mRNA levels were found to increase during development. Antibody staining experiments using DRG neurones cultured from different aged animals produced a positive stain with the anti-SK3 antibody only. The number of cells that stained positively and the intensity of staining for SK3 increased with age. To investigate possible functional roles for SK/IK channels sensory neurones, action potential afterhyperpolarisations (AHPs) were recorded from cultured DRG and nodose cells. The majority of these AHPs proved to be insensitive to the SK channel blocker UCL 1848. Attempts to block medium duration AHPs in DRG cells using IK and calcium channel blockers, also failed in most cases, suggesting that some other potassium conductances) are responsible. The possibility that SK3 is functional at the terminals of primary afferents was examined next. Spinal cord slices stained with SK/EK channel antibodies revealed positive SK3 staining in the outer laminae of the dorsal horn, where small and large diameter DRG fibres are expected to terminate. In vivo experiments (done by Dr Rie Suzuki, Department of Pharmacology, UCL) using UCL 1848 and l-ethyl-2- benzimidazolinone (1-EBIO an SK channel opener) showed that SK channels are likely to be active at these terminals where they have a functional role in mediating innocuous mechanical and nociceptive responses.
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Athlan, Eric S. "Study of in vivo and in vitro associations between neuronal intermediate filament proteins." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq44352.pdf.
Full textBooks on the topic "Neurone intermediaire"
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Chromatin motion in neuronal interphase nuclei: Changes induced by disruption of intermediate filaments. National Library of Canada, 1990.
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Banerjee, Ashis, and Clara Oliver. Neurological emergencies. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198786870.003.0011.
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A number of neurological conditions can present to the emergency department in a variety of presentations. This chapter summarizes the common neurological problems that may be examined in the Intermediate FRCEM short-answer question (SAQ) paper. This chapter includes the pathophysiology and management of an unconscious patient which may commonly appear in the SAQ paper. In addition, it also includes sections of epilepsy, headaches and strokes, and their subclassification and diagnosis. Many individuals find the differentiation of the cause of motor weakness complicated. This chapter summarizes the different causes of motor weakness, in terms of upper and lower motor neurones lesions and the clinical features associated to aid diagnosis. There is also a section on spinal cord pathology and hydrocephalus knowledge of which is essential for the SAQ paper.
Book chapters on the topic "Neurone intermediaire"
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Giordano, Suzanne, Eric Glasgow, Robert Druger, and Nisson Schechter. "Intermediate Filaments." In Neuron—Glia Interrelations During Phylogeny. Humana Press, 1995. http://dx.doi.org/10.1007/978-1-59259-468-9_15.
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Young, Kevin G., and Rashmi Kothary. "Intermediate Filament Interactions in Neurons." In Advances in Neurobiology. Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6787-9_17.
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Cairns, Nigel J. "Neuronal Intermediate Filament Inclusion Disease." In Neurodegeneration: The Molecular Pathology of Dementia and Movement Disorders. Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444341256.ch42.
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Sajda, Paul, and Leif H. Finkel. "Construction of Illusory Surfaces by Intermediate-Level Visual Cortical Networks." In Computation in Neurons and Neural Systems. Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2714-5_20.
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Oblinger, Monica M., Susanne A. Kost, and Leelabai D. Singh. "Regulation of Type III Intermediate Filament Protein Genes in Astrocytes during Development and after Injury." In Biology and Pathology of Astrocyte-Neuron Interactions. Springer US, 1993. http://dx.doi.org/10.1007/978-1-4757-9486-1_26.
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Rudrabhatla, Parvathi, and Harish C. Pant. "Topographic Regulation of Neuronal Intermediate Filament Proteins by Phosphorylation: In Health and Disease." In Advances in Neurobiology. Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6787-9_26.
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Liem, Ronald K. H., and Vikash Verma. "Neurons | Neuronal Intermediate Filaments." In Encyclopedia of Biological Chemistry III. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-819460-7.00198-5.
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Liem, Ronald K. H. "Neuronal Intermediate Filaments." In Encyclopedia of Biological Chemistry. Elsevier, 2004. http://dx.doi.org/10.1016/b0-12-443710-9/00421-x.
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Liem, R. K. H. "Neuronal Intermediate Filaments." In Encyclopedia of Biological Chemistry. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-378630-2.00436-9.
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Cairns, Nigel J. "Neuronal Intermediate Filament Inclusion Disease." In Dementias. Elsevier, 2008. http://dx.doi.org/10.1016/s0072-9752(07)01240-7.
Full textConference papers on the topic "Neurone intermediaire"
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Melikov, Rustamzhon, Shashi Bhushan Srivastava, Mohammad Mohammadi Aria, Ugur Meric Dikbas, Ibrahim Halil Kavakli, and Sedat Nizamoglu. "Control over capacitive and Faradaic extracellular photostimulation of neurons using intermediate ZnO layer for organic bio-interfaces." In Colloidal Nanoparticles for Biomedical Applications XV, edited by Marek Osiński and Antonios G. Kanaras. SPIE, 2020. http://dx.doi.org/10.1117/12.2545571.
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Begonia, Mark G. T., Jun Liao, Mark F. Horstemeyer, and Lakiesha N. Williams. "Strain Rate Dependence in the Structure Property Relationship of Porcine Brain." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206371.
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The brain is the control center for the central nervous system (CNS), and it is composed of specialized divisions that are attributed to a vast assortment of structural, homeostatic, and cognitive functions. These distinct regions are surrounded by supportive tissue and comprised of a complex arrangement of neurons that can be further categorized as either gray or white matter. The cerebrum constitutes the larger surrounding portion of the forebrain and includes sinuous ridges called gyri that are separated by grooves or fissures called sulci. The intermediate layer of the cerebrum primarily consists of white matter tracts that are responsible for integrating various regions throughout the cerebrum. The innermost and outermost layers of tissue mainly contain gray matter and are collectively known as the subcortical nuclei and cerebral cortex, respectively, which are crucial integrating components of the CNS [1]. An investigation into the mechanical properties of this vital organ coupled with microstructural characterization of its constituents under varying deformation levels is therefore crucial for implementing more accurate prediction and prevention of traumatic brain injury (TBI).
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Nakamura, Morimasa, Masahiko Nishiyama, and Ichiro Moriwaki. "Gear Noise Diagnosis System for Automobile Transmission Using Artificial Intelligence (Effect of Number of Intermediate Layers on Judgement Performance)." In ASME 2013 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/detc2013-12864.
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The present paper describes a digitizing method for the measured gear noise and a construction of a neural network system for gear noise diagnosis. Gear noise emitted from automobile transmissions should be evaluated by gear noise experts. Although quietness performance estimates from measured noise levels of the transmissions on some production lines, the estimation must be very difficult. There is not a certain relationship between the measured noise levels and the evaluations by the gear noise experts. Therefore, the estimation should be severe. As a result, such an automatic gear noise diagnosis system must yield transmissions with over-quality. The present study deals with a new gear noise diagnosis system to which an artificial intelligence, that is, a neural network system is applied. The previous evaluations by the new gear noise diagnosis system were good when the statistical property of the teacher signals from which the neural network system learned was similar to that of population. This fact means that many teacher signals are necessary on the practical use. Proposed digitizing method of gear noise levels provided good evaluations of neural network system even when the statistical properties of the teacher signals were not similar to that of the population. In addition, a new method, “Moment method” for determining the construction of the neural network system was introduced instead of “Back Propagation Method”. The Moment Method contributed to the improvement of the system judgments. The neural network system constructed using the Moment Method brought good performance. And the number of intermediate layers in the neural network system could be small enough to obtain good performance. It was found that the Moment method provided good learning because of connecting weights update function. When the Moment method was used for determining the connection weights between neurons in the neural network system, the developed gear noise diagnosis system achieved high and stable correct answer ratio. And the number of intermediate layers in the neural network system was only one enough for obtaining good performance of the system. Four intermediate layers, which was the maximum in this paper, did not provide much good performance.
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Nikolaeva, Elena I. "Genetics and psychophysiology of ADHD and autism." In 2nd International Neuropsychological Summer School named after A. R. Luria “The World After the Pandemic: Challenges and Prospects for Neuroscience”. Ural University Press, 2020. http://dx.doi.org/10.15826/b978-5-7996-3073-7.12.
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The paper discusses the brain mechanisms of autism and attention deficit hyperactivity disorder. It is shown that these disorders are associated with different genetic causes that create certain psychophysiological mechanisms. Nevertheless, their diagnosis is interrelated. Moreover, a child is often first diagnosed with ADHD, and then the diagnosis is changed to “autism spectrum disease”. Among the most common causes of the disease is the behavior of retrotransposons. Retrotransposons (also called transposons via intermediate RNA) are genetic elements that can amplify themselves in the genome. These DNA sequences use a “copy and paste” mechanism, whereby they are first transcribed into RNA and then converted back to identical DNA sequences via reverse transcription, and these sequences are then inserted into the genome at target sites. In humans, retro elements take up 42 % of the DNA. The conclusion is made that for the formation of an individual profile of gene expression in the neuron, the most important is the phenomenon of somatic mosaicism, due to the process of L1 retrotransposition, in addition to the classical described mechanisms of differentiation. The number of such events and their localization is significant as they are likely to contribute to the development of both autism and ADHD.