Academic literature on the topic 'Hippocampe (anatomie) – Physiologie'
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Journal articles on the topic "Hippocampe (anatomie) – Physiologie"
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Hsia, Albert Y., Robert C. Malenka, and Roger A. Nicoll. "Development of Excitatory Circuitry in the Hippocampus." Journal of Neurophysiology 79, no. 4 (April 1, 1998): 2013–24. http://dx.doi.org/10.1152/jn.1998.79.4.2013.
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Hsia, Albert Y., Robert C. Malenka, and Roger A. Nicoll. Development of excitatory circuitry in the hippocampus. J. Neurophysiol. 79: 2013–2024, 1998. Assessing the development of local circuitry in the hippocampus has relied primarily on anatomic studies. Here we take a physiological approach, to directly evaluate the means by which the mature state of connectivity between CA3 and CA1 hippocampal pyramidal cells is established. Using a technique of comparing miniature excitatory postsynaptic currents (mEPSCs) to EPSCs in response to spontaneously occurring action potentials in CA3 cells, we found that from neonatal to adult ages, functional synapses are created and serve to increase the degree of connectivity between CA3-CA1 cell pairs. Neither the probability of release nor mean quantal size was found to change significantly with age. However, the variability of quantal events decreases substantially as synapses mature. Thus in the hippocampus the developmental strategy for enhancing excitatory synaptic transmission does not appear to involve an increase in the efficacy at individual synapses, but rather an increase in the connectivity between cell pairs.
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Sabolek, Helen R., Stephanie C. Penley, James R. Hinman, Jamie G. Bunce, Etan J. Markus, Monty Escabi, and James J. Chrobak. "Theta and Gamma Coherence Along the Septotemporal Axis of the Hippocampus." Journal of Neurophysiology 101, no. 3 (March 2009): 1192–200. http://dx.doi.org/10.1152/jn.90846.2008.
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Theta and gamma rhythms synchronize neurons within and across brain structures. Both rhythms are widespread within the hippocampus during exploratory behavior and rapid-eye-movement (REM) sleep. How synchronous are these rhythms throughout the hippocampus? The present study examined theta and gamma coherence along the septotemporal (long) axis of the hippocampus in rats during REM sleep, a behavioral state during which theta signals are unaffected by external sensory input or ongoing behavior. Unilateral entorhinal cortical inputs are thought to play a prominent role in the current generation of theta, whereas current generation of gamma is primarily due to local GABAergic neurons. The septal 50% (4–5 mm) of the dentate gyrus (DG) receives a highly divergent, unilateral projection from any focal point along a lateral band of entorhinal neurons near the rhinal sulcus. We hypothesized that theta coherence in the target zone (septal DG) of this divergent entorhinal input would not vary, while gamma coherence would significantly decline with distance in this zone. However, both theta and gamma coherence decreased significantly along the long axis in the septal 50% of the hippocampus across both DG and CA1 electrode sites. In contrast, theta coherence between homotypic (e.g., DG to DG) sites in the contralateral hemisphere (∼3–5 mm distant) were quite high (∼0.7–0.9), much greater than theta coherence between homotypic sites 3–5 mm distant (∼0.4–0.6) along the long axis. These findings define anatomic variation in both rhythms along the longitudinal axis of the hippocampus, indicate the bilateral CA3/mossy cell projections are the major determinant of theta coherence during REM, and demonstrate that theta coherence varies as a function of anatomical connectivity rather than physical distance. We suggest CA3 and entorhinal inputs interact dynamically to generate theta field potentials and advance the utility of theta and gamma coherence as indicators of hippocampal dynamics.
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Carnevale, Nicholas T., Kenneth Y. Tsai, Brenda J. Claiborne, and Thomas H. Brown. "Comparative Electrotonic Analysis of Three Classes of Rat Hippocampal Neurons." Journal of Neurophysiology 78, no. 2 (August 1, 1997): 703–20. http://dx.doi.org/10.1152/jn.1997.78.2.703.
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Carnevale, Nicholas T., Kenneth Y. Tsai, Brenda J. Claiborne, and Thomas H. Brown. Comparative electrotonic analysis of three classes of rat hippocampal neurons. J. Neurophysiol. 78: 703–720, 1997. We present a comparative analysis of electrotonus in the three classes of principal neurons in rat hippocampus: pyramidal cells of the CA1 and CA3c fields of the hippocampus proper, and granule cells of the dentate gyrus. This analysis used the electrotonic transform, which combines anatomic and biophysical data to map neuronal anatomy into electrotonic space, where physical distance between points is replaced by the logarithm of voltage attenuation (log A). The transforms were rendered as “neuromorphic figures” by redrawing the cell with branch lengths proportional to log A along each branch. We also used plots of log A versus anatomic distance from the soma; these reveal features that are otherwise less apparent and facilitate comparisons between dendritic fields of different cells. Transforms were always larger for voltage spreading toward the soma ( V in) than away from it ( V out). Most of the electrotonic length in V out transforms was along proximal large diameter branches where signal loss for somatofugal voltage spread is greatest. In V in transforms, more of the length was in thin distal branches, indicating a steep voltage gradient for signals propagating toward the soma. All transforms lengthened substantially with increasing frequency. CA1 neurons were electrotonically significantly larger than CA3c neurons. Their V out transforms displayed one primary apical dendrite, which bifurcated in some cases, whereas CA3c cell transforms exhibited multiple apical branches. In both cell classes, basilar dendrite V out transforms were small, indicating that somatic potentials reached their distal ends with little attenuation. However, for somatopetal voltage spread, attenuation along the basilar and apical dendrites was comparable, so the V in transforms of these dendritic fields were nearly equal in extent. Granule cells were physically and electrotonically most compact. Their V out transforms at 0 Hz were very small, indicating near isopotentiality at DC and low frequencies. These transforms resembled those of the basilar dendrites of CA1 and CA3c pyramidal cells. This raises the possibility of similar functional or computational roles for these dendritic fields. Interpreting the anatomic distribution of thorny excrescences on CA3 pyramidal neurons with this approach indicates that synaptic currents generated by some mossy fiber inputs may be recorded accurately by a somatic patch clamp, providing that strict criteria on their time course are satisfied. Similar accuracy may not be achievable in somatic recordings of Schaffer collateral synapses onto CA1 pyramidal cells in light of the anatomic and biophysical properties of these neurons and the spatial distribution of synapses.
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Smith, K. L., D. H. Szarowski, J. N. Turner, and J. W. Swann. "Diverse neuronal populations mediate local circuit excitation in area CA3 of developing hippocampus." Journal of Neurophysiology 74, no. 2 (August 1, 1995): 650–72. http://dx.doi.org/10.1152/jn.1995.74.2.650.
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1. Studies were undertaken to better understand why the developing hippocampus has a marked capacity to generate prolonged synchronized discharges when exposed to gamma-aminobutyric acid-A (GABAA) receptor antagonists. 2. Excitatory synaptic interactions were studied in small microdissected segments of hippocampal area CA3. Slices were obtained from 10- to 16-day-old rats. Application of the GABAA receptor antagonist penicillin produced prolonged synchronized discharges in minislices that were very similar, if not identical, to those recorded in intact slices. The sizes of minislices were systematically varied. Greater than 90% of those that measured 600 microns along the cell body layer produced prolonged synchronized discharges, whereas most minislices measuring 300 microns produced only brief interictal spikes. 3. Action potentials in the majority (75%, 158 of 254) of cells impaled with microelectrodes were able to entrain the entire CA3 population. They were also able to increase (on average 26%) the frequency of spontaneous population discharges. The population discharges were followed by a refractory period that lasted 5–60 s, during which single cells were unable to initiate a population discharge. 4. The majority (87%) of neurons with intrinsic burst properties were found to entrain the CA3 population. The electrophysiological characteristics of these cells were reminiscent of recordings obtained from more mature rats. Action potentials were quite prolonged and demonstrated a secondary shoulder or hump on the down-slope of the spike. 5. When bursting cells were filled with Lucifer yellow and imaged during recording sessions by videomicroscopy and later using confocal microscopy, they showed the anatomic features of CA3 hippocampal pyramidal cells. Confocal microscopy permitted detailed characterization of individual neurons and showed substantial variation in cellular microanatomy. 6. Another class of cells that were found to entrain the CA3 population but did not demonstrate intrinsic bursts were termed regular-firing cells. These cells possessed many of the anatomic and physiological features of bursting cells with the exception of burst firing. They were rarely encountered in intracellular recordings. 7. The third physiological class of cells was termed fast-spiking cells. These had action potentials that were shorter in duration than the other two cell types. They were distinct in the rapid rate of spike repolarization. They demonstrated modest degrees of spike frequency adaptation and fired repeatedly and at relatively high frequencies. Compared with reports on fast-spiking cells in mature hippocampus and neocortex, action potentials appear to be slower and repetitive discharging appeared to be of a lower frequency.(ABSTRACT TRUNCATED AT 400 WORDS)
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Biella, Gerardo, and Marco de Curtis. "Olfactory Inputs Activate the Medial Entorhinal Cortex Via the Hippocampus." Journal of Neurophysiology 83, no. 4 (April 1, 2000): 1924–31. http://dx.doi.org/10.1152/jn.2000.83.4.1924.
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The lateral and medial regions of the entorhinal cortex differ substantially in terms of connectivity and pattern of activation. With regard to olfactory input, a detailed and extensive physiological map of the olfactory projection to the entorhinal cortex is missing, even if anatomic studies suggest that the olfactory afferents are confined to the lateral and rostral entorhinal region. We studied the contribution of the medial and lateral entorhinal areas to olfactory processing by analyzing the responses induced by lateral olfactory tract stimulation in different entorhinal subfields of the in vitro isolated guinea pig brain. The pattern of synaptic activation of the medial and lateral entorhinal regions was reconstructed either by performing simultaneous multisite recordings or by applying current source density analysis on field potential laminar profiles obtained with 16-channel silicon probes. Current source density analysis demonstrated the existence of a direct monosynaptic olfactory input into the superficial 300 μm of the most rostral part of the lateral entorhinal cortex exclusively, whereas disynaptic sinks mediated by associative fibers arising from the piriform cortex were observed at 100–350 μm depth in the entire lateral aspect of the cortex. No local field responses were recorded in the medial entorhinal region unless a large population spike was generated in the hippocampus (dentate gyrus and CA1 region) by a stimulus 3–5× the intensity necessary to obtain a maximal monosynaptic response in the piriform cortex. In these conditions, a late sink was recorded at a depth of 600-1000 μm in the medial entorhinal area (layers III–V) 10.6 ± 0.9 (SD) msec after a population spike was simultaneously recorded in CA1. Diffuse activation of the medial entorhinal region was also obtained by repetitive low-intensity stimulation of the lateral olfactory tract at 2–8 Hz. Higher or lower stimulation frequencies did not induce hippocampal-medial entorhinal cortex activation. These results suggest that the medial and the lateral entorhinal regions have substantially different roles in processing olfactory sensory inputs.
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Abrous, Djoher Nora, Muriel Koehl, and Michel Le Moal. "Adult Neurogenesis: From Precursors to Network and Physiology." Physiological Reviews 85, no. 2 (April 2005): 523–69. http://dx.doi.org/10.1152/physrev.00055.2003.
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The discovery that the adult mammalian brain creates new neurons from pools of stemlike cells was a breakthrough in neuroscience. Interestingly, this particular new form of structural brain plasticity seems specific to discrete brain regions, and most investigations concern the subventricular zone (SVZ) and the dentate gyrus (DG) of the hippocampal formation (HF). Overall, two main lines of research have emerged over the last two decades: the first aims to understand the fundamental biological properties of neural stemlike cells (and their progeny) and the integration of the newly born neurons into preexisting networks, while the second focuses on understanding its relevance in brain functioning, which has been more extensively approached in the DG. Here, we propose an overview of the current knowledge on adult neurogenesis and its functional relevance for the adult brain. We first present an analysis of the methodological issues that have hampered progress in this field and describe the main neurogenic sites with their specificities. We will see that despite considerable progress, the levels of anatomic and functional integration of the newly born neurons within the host circuitry have yet to be elucidated. Then the intracellular mechanisms controlling neuronal fate are presented briefly, along with the extrinsic factors that regulate adult neurogenesis. We will see that a growing list of epigenetic factors that display a specificity of action depending on the neurogenic site under consideration has been identified. Finally, we review the progress accomplished in implicating neurogenesis in hippocampal functioning under physiological conditions and in the development of hippocampal-related pathologies such as epilepsy, mood disorders, and addiction. This constitutes a necessary step in promoting the development of therapeutic strategies.
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Berényi, Antal, Zoltán Somogyvári, Anett J. Nagy, Lisa Roux, John D. Long, Shigeyoshi Fujisawa, Eran Stark, Anthony Leonardo, Timothy D. Harris, and György Buzsáki. "Large-scale, high-density (up to 512 channels) recording of local circuits in behaving animals." Journal of Neurophysiology 111, no. 5 (March 1, 2014): 1132–49. http://dx.doi.org/10.1152/jn.00785.2013.
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Monitoring representative fractions of neurons from multiple brain circuits in behaving animals is necessary for understanding neuronal computation. Here, we describe a system that allows high-channel-count recordings from a small volume of neuronal tissue using a lightweight signal multiplexing headstage that permits free behavior of small rodents. The system integrates multishank, high-density recording silicon probes, ultraflexible interconnects, and a miniaturized microdrive. These improvements allowed for simultaneous recordings of local field potentials and unit activity from hundreds of sites without confining free movements of the animal. The advantages of large-scale recordings are illustrated by determining the electroanatomic boundaries of layers and regions in the hippocampus and neocortex and constructing a circuit diagram of functional connections among neurons in real anatomic space. These methods will allow the investigation of circuit operations and behavior-dependent interregional interactions for testing hypotheses of neural networks and brain function.
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Lynch, Michael, and Thomas Sutula. "Recurrent Excitatory Connectivity in the Dentate Gyrus of Kindled and Kainic Acid–Treated Rats." Journal of Neurophysiology 83, no. 2 (February 1, 2000): 693–704. http://dx.doi.org/10.1152/jn.2000.83.2.693.
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Repeated seizures induce mossy fiber axon sprouting, which reorganizes synaptic connectivity in the dentate gyrus. To examine the possibility that sprouted mossy fiber axons may form recurrent excitatory circuits, connectivity between granule cells in the dentate gyrus was examined in transverse hippocampal slices from normal rats and epileptic rats that experienced seizures induced by kindling and kainic acid. The experiments were designed to functionally assess seizure-induced development of recurrent circuitry by exploiting information available about the time course of seizure-induced synaptic reorganization in the kindling model and detailed anatomic characterization of sprouted fibers in the kainic acid model. When recurrent inhibitory circuits were blocked by the GABAAreceptor antagonist bicuculline, focal application of glutamate microdrops at locations in the granule cell layer remote from the recorded granule cell evoked trains of excitatory postsynaptic potentials (EPSPs) and population burst discharges in epileptic rats, which were never observed in slices from normal rats. The EPSPs and burst discharges were blocked by bath application of 1 μM tetrodotoxin and were therefore dependent on network-driven synaptic events. Excitatory connections were detected between blades of the dentate gyrus in hippocampal slices from rats that experienced kainic acid–induced status epilepticus. Trains of EPSPs and burst discharges were also evoked in granule cells from kindled rats obtained after ≥1 wk of kindled seizures, but were not evoked in slices examined 24 h after a single afterdischarge, before the development of sprouting. Excitatory connectivity between blades of the dentate gyrus was also assessed in slices deafferented by transection of the perforant path, and bathed in artificial cerebrospinal fluid (ACSF) containing bicuculline to block GABAA receptor–dependent recurrent inhibitory circuits and 10 mM [Ca2+]o to suppress polysynaptic activity. Low-intensity electrical stimulation of the infrapyramidal blade under these conditions failed to evoke a response in suprapyramidal granule cells from normal rats ( n = 15), but in slices from epileptic rats evoked an EPSP at a short latency (2.59 ± 0.36 ms) in 5 of 18 suprapyramidal granule cells. The results are consistent with formation of monosynaptic excitatory connections between blades of the dentate gyrus. Recurrent excitatory circuits developed in the dentate gyrus of epileptic rats in a time course that corresponded to the development of mossy fiber sprouting and demonstrated patterns of functional connectivity corresponding to anatomic features of the sprouted mossy fiber pathway.
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Xiang, Zixiu, and Thomas H. Brown. "Complex Synaptic Current Waveforms Evoked in Hippocampal Pyramidal Neurons by Extracellular Stimulation of Dentate Gyrus." Journal of Neurophysiology 79, no. 5 (May 1, 1998): 2475–84. http://dx.doi.org/10.1152/jn.1998.79.5.2475.
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Xiang, Zixiu and Thomas H. Brown. Complex synaptic current waveforms evoked in hippocampal pyramidal neurons by extracellular stimulation of dentate gyrus. J. Neurophysiol. 79: 2475–2484, 1998. Excitatory postsynaptic currents (EPSCs) evoked in hippocampal CA3 pyramidal neurons by extracellular stimulation of the dentate gyrus typically exhibit complex waveforms. They commonly have inflections or notches on the rising phase; the decay phase may exhibit notches or other obvious departures from a simple monoexponential decline; they often display considerable variability in the latency from stimulation to the peak current; and the rise times tend to be long. One hypothesis is that these complex EPSC waveforms might result from excitation via other CA3 pyramidal cells that were recruited antidromically or trans-synaptically by the stimulus due to the complex anatomy of this region. An alternative hypothesis is that EPSC complexity does not emerge from the functional anatomy but rather reflects an unusual physiological property, intrinsic to excitation-secretion coupling in mossy-fiber (mf) synaptic terminals, that causes asynchronous quantal release. We evaluated certain predictions of our anatomic hypothesis by adding a pharmacological agent to the normal bathing medium that should suppress di- or polysynaptic responses. For this purpose we used baclofen (3 μM), a selective agonist for the γ-aminobutyric acid B receptor. The idea was that baclophen should discriminate against polysynaptic versus monosynaptic inputs by hyperpolarizing the cells, bringing them further from spike threshold and possibly also through inhibitory presynaptic actions. Whole cell recordings were done from visually preselected CA3 pyramidal neurons and EPSCs were evoked by fine bipolar electrodes positioned into the granule cell layer of the dentate. To the extent that the EPSC complexity reflects di- or polysynaptic responses, we predicted baclofen to reduce the number of notches on the rising and decay phases, reduce the variance in latency to peak of the EPSCs, decrease the amplitudes and rise times of the individual and averaged EPSCs, and increase the apparent failures in evoked EPSCs. All of these predictions were confirmed, in support of the hypothesis that these complex EPSC waveforms commonly reflect di- or polysynaptic responses. We also documented a distinctly different, intermittent, form of EPSC complexity, which also is predicted and easily explained by our anatomic hypothesis. In particular, the results were in accord with the suggestion that stimulation of the dentate gyrus might antidromically stimulate axon collaterals of CA3 neurons that make recurrent synapses onto the recorded cell. We conclude that the overall pattern of results is consistent with expectations based on the functional anatomy. The explanation does not demand a special type of intrinsic asynchronous mechanism for excitation-secretion coupling in the mf synapses.
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Buckmaster, Paul S., and F. Edward Dudek. "Network Properties of the Dentate Gyrus in Epileptic Rats With Hilar Neuron Loss and Granule Cell Axon Reorganization." Journal of Neurophysiology 77, no. 5 (May 1, 1997): 2685–96. http://dx.doi.org/10.1152/jn.1997.77.5.2685.
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Buckmaster, Paul S. and F. Edward Dudek. Network properties of the dentate gyrus in epileptic rats with hilar neuron loss and granule cell axon reorganization. J. Neurophysiol. 77: 2685–2696, 1997. Neuron loss in the hilus of the dentate gyrus and granule cell axon reorganization have been proposed as etiologic factors in human temporal lobe epilepsy. To explore these possible epileptogenic mechanisms, electrophysiological and anatomic methods were used to examine the dentate gyrus network in adult rats that had been treated systemically with kainic acid. All kainate-treated rats, but no age-matched vehicle-treated controls, were observed to have spontaneous recurrent motor seizures beginning weeks to months after exposure to kainate. Epileptic kainate-treated rats and control animals were anesthetized for field potential recording from the dentate gyrus in vivo. Epileptic kainate-treated rats displayed spontaneous positivities (“dentate electroencephalographic spikes”) with larger amplitude and higher frequency than those in control animals. After electrophysiological recording, rats were perfused and their hippocampi were processed for Nissl and Timm staining. Epileptic kainate-treated rats displayed significant hilar neuron loss and granule cell axon reorganization. It has been hypothesized that hilar neuron loss reduces lateral inhibition in the dentate gyrus, thereby decreasing seizure threshold. To assess lateral inhibition, simultaneous recordings were obtained from the dentate gyrus in different hippocampal lamellae, separated by 1 mm. The perforant path was stimulated with paired-pulse paradigms, and population spike amplitudes were measured. Responses were obtained from one lamella while a recording electrode in a distant lamella leaked saline or the γ-aminobutyric acid-A receptor antagonist bicuculline. Epileptic kainate-treated and control rats both showed significantly more paired-pulse inhibition when a lateral lamella was hyperexcitable. To assess seizure threshold in the dentate gyrus, two techniques were used. Measurement of stimulus threshold for evoking maximal dentate activation revealed significantly higher thresholds in epileptic kainate-treated rats compared with controls. In contrast, epileptic kainate-treated rats were more likely than controls to discharge spontaneous bursts of population spikes and to display stimulus-triggered afterdischarges when a focal region of the dentate gyrus was disinhibited with bicuculline. These spontaneous bursts and afterdischarges were confined to the disinhibited region and did not spread to other septotemporal levels of the dentate gyrus. Epileptic kainate-treated rats that displayed spontaneous bursts and/or afterdischarges had significantly larger percentages of Timm staining in the granule cell and molecular layers than epileptic kainate-treated rats that failed to show spontaneous bursts or afterdischarges. In summary, this study reveals functional abnormalities in the dentate gyri of epileptic kainate-treated rats; however, lateral inhibition persists, suggesting that vulnerable hilar neurons are not necessary for generating lateral inhibition in the dentate gyrus.
Dissertations / Theses on the topic "Hippocampe (anatomie) – Physiologie"
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Liautard, Camille. "Mécanismes physiopathologiques dans deux modèles murins d'épilepsie liée à la mutation des canaux sodiques 1. 1." Nice, 2012. http://www.theses.fr/2012NICE4080.
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L’épilepsie est caractérisée par la récurrence de crises épileptiques résultant d’une activité neuronale hyper synchrone et excessive. Les canaux sodiques dépendants du potentiel (Nav), en participant à l’initiation et la propagation des potentiels d’action, sont des acteurs essentiels dans l’excitabilité neuronale. A l’heure actuelle, de nombreuses mutations épileptogéniques ont été identifiées au niveau du gène SCN1A codant la sous-unité α des canaux Nav1. 1. Ces canaux seraient particulièrement impliqués dans l’excitabilité des interneurones GABAergiques inhibiteurs du cerveau (Yu et al. , 2006). Au cours de ma thèse, j’ai étudié deux épilepsies génétiques liées à des mutations des canaux Nav1. 1 : le syndrome de Dravet (SD), une épilepsie pharmaco-résistante très grave de l’enfance ; et l’Epilepsie Génétique avec Convulsions Fébriles Plus (EGCF+), une épilepsie présentant un phénotype hétérogène plus modéré. Afin de comprendre les mécanismes physiopathologiques impliqués dans ces épilepsies, nous avons réalisé des enregistrements électrophysiologiques dans des tranches de cerveau. Ces enregistrements ont été réalisés au niveau de différents circuits neuronaux dans deux modèles murins présentant des altérations au niveau du gène SCN1A : les souris invalidées pour ce gène (souris Knock-Out-KO-) mimant le SD et les souris portant la mutation R1648H (souris Knock-In-KI-) mimant l’EGCF+. Nos travaux ont mis en avant une implication particulière de l’hippocampe dans la génération des crises épileptiques chez les souris KO. Cette structure présente une hyperexcitabilité du réseau neuronal entraînée par un défaut de la transmission synaptique liée à la perte de fonction des Nav1. 1. De plus, dans des conditions épileptogènes, une activité spécifique à notre modèle a été mise en évidence. Enfin, l’utilisation in vitro d’antiépileptiques a montré des effets similaires à ceux retrouvés chez les patients. L’ensemble de ces résultats placent ce modèle murin comme un outil de choix dans la recherche sur le SD. Chez la souris KI, nous avons étudié l’activité de la boucle thalamo-corticale, un réseau neuronal qui serait impliqué dans la génération de crises généralisées type absence présentes chez les patients EGCF+. L’hyperexcitabilité neuronale spontanée enregistrée au niveau de la boucle a mis en avant un fort impact de la mutation R1648H. Cette hyperexcitabilité serait corrélée à une altération spécifique de l’excitabilité des neurones inhibiteurs des différentes structures impliquées dans le circuit thalamo-corticale. Cette altération serait alors à l’origine du dysfonctionnement de la transition inhibitrice observée dans la boucle. En conclusion, nos résultats ont permis de caractériser les mécanismes physiopathologiques présents dans des circuits neuronaux qui pourraient être impliqués dans la génération des crises épileptiques. Les modèles murins permettront par la suite le développement de nouvelles stratégies thérapeutiques et l’étude des troubles cognitifs observés chez les patients présentant un phénotype très sévèreDravet Syndrome (DS), a very severe pharmaco-resistant epilepsy of infancy, and Genetic Epilepsy with febrile Seizures Plus (GEFS+), presenting a moderate phenotype, are two epilepsies linked to an heterozygous mutation of SCN1A, the gene coding for voltage-dependent sodium channels 1. 1. To better understand the pathogenic mechanisms in these epilepsies, electrophysiological recordings in brain slices from two animal models with altered SCN1A were performed. Our data have shown a specific implication of the hippocampus in the generation of epileptic seizures in mice models of DS. This structure presents a hyperexcitability of the neuronal network due to an inhibitory transmission defect linked to the Nav1. 1 loss of function. In epileptogenic conditions, an activity specific to our model was identified. In GEFS+ mice models, the thalamo-cortical network, implied in the generation of absence seizures observed in patients, was studied. A spontaneous neuronal hyperexcitability in the circuit was detected. This hyperexcitability could be correlated to the specific alteration of the inhibitory neurons present in the different structures of the circuit. This alteration may be responsible for the inhibitory transmission dysfunction observed in the thalamo-cortical network. In conclusion, we have characterized the pathogenic mechanisms present in these neuronal networks. These mice models will be used in the future to develop new therapeutic strategies
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Ledoux, Erwan. "Etude théorique de la dynamique des réseaux de neurones et application aux oscillations physiologiques de l'hippocampe." Paris 6, 2012. http://www.theses.fr/2012PA066234.
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Dans le sysème nerveux central, les réseaux de neurones reçoivent au niveau de leurs entrées un grand nombre de stimulations aux dynamiques très variables, dont les échelles de temps vont de la milliseconde à plusieurs minutes. La réponse du réseau à des entrées variables dans le temps dépend des propriétés cellulaires, mais aussi de la connectivité entre les neurones. La manière dont la connectivité synaptique entre les différentes populations de neurones affecte la dynamique globale du réseau reste encore à être déterminée. Dans ce travail, nous calculons analytiquement la fonction de transfert d'un réseau de neurones. Cette fonction permet de reconstruire la réponse de celui-ci pour n'importe quelle entrée variable dans le temps, en considérant le comportement du système comme approximativement linéaire. Les calculs furent réalisés pour deux classes de modèles : les modèles à taux de décharge et un réseau de neurones Intègre-Et-Décharge en présence de bruit blanc. Dans ce cadre, nous avons pu d'une part étudier comment la connectivité façonne la fonction de transfert. D'autre part, nous avons utilisé ces outils analytiques pour déterminer la connectivité du réseau CA1 dans l'hippocampe permettant de reproduire les différents rythmes physiologiques enregistrés dans ce système.
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Daoudal, Gaël. "Plasticité bidirectionnelle de l'intégration synaptique dans la région CA1 de l'hippocampe." Aix-Marseille 2, 2003. http://www.theses.fr/2003AIX20655.
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Demont-Guignard, Sophie. "Interprétation des évènements inter critiques dans les signaux EEG intra cérébraux : apport des modèles détaillés de réseaux neuronaux." Rennes 1, 2009. http://www.theses.fr/2009REN1S068.
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Cette thèse porte sur l’analyse d’événements électrophysiologiques particuliers rencontrés dans les signaux intracérébraux acquis chez les patients souffrant d’épilepsie partielle et candidats à la chirurgie. L’objectif est d’identifier certains mécanismes impliqués dans la génération d’événements observés en dehors des crises. Pour ce faire, nous avons développé un modèle, à l’échelle cellulaire, de réseau de neurones incluant cellules principales et interneurones qui permet, à partir de la reconstruction du potentiel de champ, de faire le lien entre les signaux enregistrés sur les électrodes intracérébrales et l’activité du réseau. Les travaux sont focalisés sur le champ CA1 de l’hippocampe, structure très impliquée dans les épilepsies du lobe temporal. Au niveau cellulaire, un modèle de neurone pyramidal à deux compartiments a été développé par comparaison à des enregistrements intracellulaires réels obtenus en conditions normale et pathologique. Au niveau du réseau (plusieurs milliers de neurones), le modèle est capable de simuler des évènements ressemblant à des événements paroxystiques réelsThis work deals with the analysis of particular electrophysiological events of intracerebral signals recorded in the pre-surgical evaluation of patients with drug-resistant epilepsy. Our objective was to to explain specific mechanisms involved in the interictal transient events production (epileptic spikes). In order to meet this objective, we have developed a model, at the cellular level, of neuronal network including pyramidal cells and interneurons. This model was able to bridge between recorded signals with intracerebral electrodes and network activity, from the reconstruction of the local field potential (dipole theory). This work is focused on the CA1 subfield of the hippocampus, a structure often involved in temporal lobe epilepsy. At cellular level, a new pyramidal neuron model with two compartments was proposed and validated by comparison with real intracellular recordings, in normal and pathological conditions. At network level (including a large number of cells), the model was able to simulate events that closely resemble actual epileptic spikes
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Djebaili, Myriam. "Etude des phénomènes de mort neuronale induits in-vivo et in-vitro après l'action de l'acide kai͏̈nique ou du N-méthyl-D-aspartate dans l'hippocampe de souris : implication des protéines p53, bax et caspase-3 dans les phénomènes de mort neuronale par apoptose." Montpellier 2, 2001. http://www.theses.fr/2001MON20088.
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Gastrein, Philippe. "Courant H et rythmes 0 dans les structures corticales : un exemple du rôle des courants intrinsèques dans l'organisation temporelle de l'activité de réseau." Aix-Marseille 2, 2007. http://www.theses.fr/2007AIX20665.
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Le courant cationique activé par l’hyperpolarisation (courant H) est impliqué dans l’organisation temporelle de l’activité neuronale. Nous montrons que le courant H améliore la synchronisation et la régularité des oscillations thêta dans l’hippocampe et dans le néocortex in vitro. Il détermine les oscillations thêta par la définition de résonance intrinsèque de membrane, la fidélité de décharge et le couplage entre potentiels postsynaptiques et décharge. Les cinétiques du courant H sont modulées par l’AMPc. Nous montrons que l’augmentation de l’activité synaptique provoque une augmentation de la concentration en AMPc intracellulaire qui pourrait réguler les oscillations de l’activité de réseau. Ces résultats illustrent le rôle clef d’un courant intrinsèque dans l’organisation temporelle de l’activité des neurones en réseau. La modulation des propriétés cinétiques du courant H peut agir comme un régulateur de fréquenceDer durch Hyperpolarisation aktivierte, kationische Einwärtsstrom (H-Strom) ist in die zeitliche Organisation neuronaler Aktivität involviert. Wir zeigen, dass der H-Strom die Synchronisation und die Regelmäßigkeit der Theta-Oszillationen im Hippocampus und im Neocortex in vitro verbessert. Er beeinflußt die Theta-Oszillationen durch die Vorgabe einer intrinsischen elektrischen Resonanz, desweiteren durch die Genauigkeit der Aktionspotentialausl ¨osung sowie durch die Kopplung zwischen den postsynaptischen Potentialen und der Aktionspotentialausl¨osung. Die Kinetik des H-Stromes wird durch cAMP moduliert. Wir zeigen, dass die Steigerung der synaptischen Aktivität eine Steigerung der intrazellulären cAMP-Konzentration verursacht, welche die oszillierende Netzwerkaktivität regulieren könnte. Diese Ergebnisse veranschaulichen die Schlüsselrolle eines intrinsischen Stromes wie der IH in der zeitlichen Organisation einer Netzwerkaktivität von Nervenzellen wie die kortikale Theta-Oszillationen. Unsere Studium läßt uns vorschlagen, dass die Modulation der kinetischen Eigenschaften des H-Stromes hierbei wie ein Frequenzstimmer wirken
The hyperpolarisation-activated current (h-current) is involved in the temporal organisation of neuronal activity. We show that h-current enhances synchronisation and regularity of theta oscillations in the hippocampus and in the neocortex in vitro. It locks theta oscillations via intrinsic resonance and enhanced temporal spiking fidelity. Kinetics of h-current is modulated by cAMP. We show that increased synaptic activity evokes an increase in intracellular cAMP concentration which could regulate network activity oscillations. These results illustrate the key role of an intrinsic current in the temporal organisation of neuronal network activity. The modulation of h-current kinetics can act as a frequency tuner
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Lucas, Morgan. "Sustrats neuronaux des mémoires émotionnelles associées au sevrage des opiacés : analyse des réseaux de l'amygdale et des structures associées." Bordeaux 2, 2007. http://www.theses.fr/2007BOR21470.
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Dans la dépendance aux opiacés, l'arrêt de la prise de drogue entraîne l'émergence d'un syndrome de sevrage, dont les propriétés aversives peuvent être conditionnées à l'environnement dans lequel il est vécu. D'une manière générale, les stimuli conditionnés associés à la drogue ou à son sevrage sont connus pour influencer les comportements addictifs, via des processus d'apprentissage et de mémoire à long terme. Ces processus impliquent des circuits neuronaux qu'il est nécessaire de caractériser pour mieux comprendre la persistance de cette pathologie. Notre objectif a été par des approches anatomo-fonctionnelles de préciser au niveau de l'amygdale et des structures associées, certains des processus neuronaux sous-tendant les effets conditionnés du sevrage des opiacés chez des animaux dépendants et abstinents. Nous avons utilisé un modèle d'aversion de place conditionnée induite par le sevrage chez le rat morphino-dépendant, permettant l'étude de la mémoire de cet état aversif par la réexposition ultérieure à l'environnement. Nos travaux ont mis en évidence, au cours du conditionnement, des processus de plasticité dans les noyaux de l'amygdale, qui pourraient sous-tendre la formation de la mémoire du sevrage, mais aussi son rappel par la réexposition aux stimuli confitionnés. Nous montrons aussi que la dopamine est impliquée dans ce processus mais, dans l'amygdale, n'est pas nécessaire au conditionnement. Enfin, le rappel de la mémoire du sevrage à long terme chez des rats abstinents, implique des circuits en partie différents de ceux recrutés chez des rats dépendants, suggérant un remodelage des circuits qui sous-tendent cette mémoire en fonction de l'état de dépendanceIn opiate addiction, a withdrawal syndrome emerges when stopping drug consumption, and the aversive properties of the withdrawal state can be conditioned to the environment. Indeed, environmental stimuli associated with drug taking or withdrawal are known to influence addictive behaviours, via associative learning and long term memory processes. The processes involved neural networks that must be characterized to better understand the persistence of this pathology. Our work intended to analyze, by using anatomo-functional approaches, the neuronal processes underlying opiate withdrawal conditioning within amygdala nuclei and associated stuctures. For this, we used a conditioned place aversion model induced by opiate withdrawal in morphine-dependent rats that allowed the study of withdrawal aversive state memory by reexposure to the conditioned environment, in both dependent and abstinent rats. During morphine withdrawal conditioning, our data reveal neuronal plasticity processes in the amygdala nuclei which could underlie withdrawal memory formation, but also the retrieval of this memory in dependent rats during reexposure to the conditioned stimuli. We also show a dopaminergic activation in such processes, although it seems not necessary in the amygdala for withdrawal memory formation. Finally, the retrieval aversive memories in abstinent ats involves neuronal networks partly different from those in dependent rats. This suggests an anatomo-functional reorganization of the networks underlying the retrieval memories associated with morphine withdrawal depending on the dependance state
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Renaudineau, Sophie. "Flexibilité fonctionnelle des cellules de lieu et mémoire spatiale : étude des mécanismes d’adaptation et des aspects moléculaires." Aix-Marseille 1, 2008. http://www.theses.fr/2008AIX11084.
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L’objectif de ce travail a été d’étudier deux aspects de la flexibilité du système des cellules de lieu de l’hippocampe : la réponse adaptative des cellules de lieu à des changements environnementaux, et les aspects moléculaires impliqués dans cette flexibilité. Dans une première étude, nous avons évalué la capacité de ces cellules à maintenir une représentation spatiale stable malgré des changements des repères de l’environnement. Nous avons pour cela produit un conflit en tournant deux types d’indices dans des directions opposées : des indices proches et des indices distants. La majorité des cellules montre une réorganisation de la représentation (remapping), ce qui suggère qu’elles sont contrôlées par la configuration d’ensemble des indices. Moins souvent, les cellules sont contrôlées par les indices proches, et encore moins souvent par les indices distants. En retirant un des ensemble d’indices, nous observons la compétition entre les processus de pattern completion et pattern separation. Dans un deuxième ensemble d’études, nous avons cherché à comprendre l’implication du gène zif268 dans la mémoire spatiale à court terme et à long terme. Ce gène, membre de la famille des facteurs de transcription Egr, jouerait le rôle de « commutateur moléculaire » permettant le remodelage durable des réseaux neuronaux à la base de la formation de traces mnésiques stables, qui a lieu lors des processus de potentialisation à long terme (PLT). Nous avons testé une souche de souris mutantes chez laquelle le gène zif268 (Krox24) est invalidé dans l’ensemble du cerveau. D’abord, nous avons voulu identifier comment ce gène contrôle la stabilité des champs d’activité des cellules de lieu de CA1 hippocampiques. Nos résultats montrent que les souris mutantes zif268 ont des cellules de lieu fonctionnelles, avec des paramètres de décharges comparables aux souris contrôles. Nous avons trouvé que la délétion de ce gène n’interfère pas avec la formation, ni avec le maintien à court terme (1h) d’une nouvelle représentation, mais affecte seulement son maintien à long terme (24h). Zif268 est donc nécessaire pour le maintien à long terme de la représentation spatiale. Ensuite, dans une tâche d’exploration d’objets, nous avons montré que les souris mutantes zif268 présentaient des déficits dans la détection d’un changement spatial, après la réactivation du contexte initial, ce qui suggère un rôle de zif268 dans la re-consolidation. Ensemble, ces résultats indiquent que zif268 est un élément clef de la voie de signalisation moléculaire responsable de la formation de souvenirs à long termeThe objective of this work was to study two hippocampal aspects of the flexibility of the hippocampal place cell system and its contribution to spatial memory: the adaptative response to environmental change and the molecular determinants of synaptic plasticity. In a first study, we investigated the ability of place cells to maintain a stable spatial representation following various manipulations of environmental cues. In particular, we asked how place fields could be controlled by a configuration of a distal and proximal set of cues. To do this, a conflict was produced by rotating the two kinds of cues in opposite direction. The results show a reorganization of the representation (remapping) in a majority of cells suggesting a control by the whole cue configuration. Less often, cells were controlled by proximal cues only, and yet more rarely, by distal cues only. Furthermore, additional tests involving removal of a specific set of cues revealed a competition between pattern completion and pattern separation processes. In a second set of study, we examined the impact of zif268 on short term and long term spatial memory. Zif268 is an immediate early gene of the Egr family, that plays a crucial role in late LTP and in long term memory. First, we tested the hypothesis that place cell long term spatial memory would require activation of Zif268 gene, by recording CA1 place cells in mice lacking the Zif268 gene. Zif268 gene deletion did not prevent formation of the representation of a novel environment and did not affect its stability after a short delay (1 h). Stability of the representation of the novel environment was affected after a long delay (24 h). The results suggest that Zif268 gene is a critical element for expression of long term memory in hippocampal place cells and support the notion that place cell activity requires LTP-like mechanisms to maintain spatial representation. Thus, the absence of Zif268 prevents the normal consolidation process. Second, using an object exploration task, we showed that zif268 mutant mice displayed a deficit in detecting spatial novelty after reactivation of the initial context. This suggests a role of zif268 in re-consolidation processes. Together, these results suggest that zif268 is as a key element of a universal molecular pathway responsible for long term memory formation
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Fiorentino, Hervé. "Rôle de l'activité synaptique dans la maturation fonctionnelle des synapses gabaergiques de l'hippocampe en développement." Aix-Marseille 2, 2009. http://theses.univ-amu.fr.lama.univ-amu.fr/2009AIX22071.pdf.
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L'activité neuronale est un facteur essentiel dans le développement des réseaux neuronaux. Dans l'hippocampe, la majorité de l'activité développementale est présente sous la forme de bouffées d'activité synchrone, les GDPs (Giant Depolarizing Potentials), dont la fonction n'est pas clairement établie. J'expose dans ce travail de thèse deux mécanismes distincts liant activité et maturation synaptique. Dans le premier, l'activation endogène des récepteurs GABAB au cours des GDPs entraîne une libération de BDNF (Brain Derived Neurotrophic Factor) qui est nécessaire au développement d'une population de synapses GABAergiques. L'autre décrit le rôle joué par l'activité synaptique glutamatergique spontanée dans une forme de plasticité des synapses GABAergiques, également liée à la libération de BDNF; les GDPs ne sont cependant pas impliqués dans ce phénomène. Ces deux mécanismes décrivent donc des aspects complémentaires de la maturation synaptique fonctionnelle dans l'hippocampeNeuronal activity is required for the correct development of neuronal networks. In the hippocampus, most of the developmental activity exists as bursts of synchronous activity known as GDPs (Giant Depolarizing Potentials), whose function remains to be determined. I present in my thesis two distinct mechanisms that establish a link between activity and synaptic maturation. I first show that endogenous activation of GABAB receptors during GDPs induces a BDNF (Brain Derived Neurotrophic Factor) release that is necessary for the development of a population of GABAergic synapses. Next, I show that spontaneous glutamatergic activity plays a role in the plasticity of GABAergic synapses, whose induction also required BDNF release; GDPs are not involved in this phenomenon though. Thus, both mechanisms are complementary aspects of the functional synaptic maturation in the developing hippocampus
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Koenig, Julie. "Implication des récepteurs 5-HT1A du septum médian dans la mémoire spatiale chez le rat." Université Louis Pasteur (Strasbourg) (1971-2008), 2007. https://publication-theses.unistra.fr/public/theses_doctorat/2007/KOENIG_Julie_2007.pdf.
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Ce travail de thèse vise à caractériser l’implication des récepteurs 5-HT1A du septum médian dans la mémoire spatiale chez le Rat en étudiant les effets d’une instillation intra-septale de 8-OH-DPAT, un agoniste des récepteurs 5-HT1A et 5-HT7, sur les performances de mémoire de référence dans le test de la piscine de Morris. Les déficits de performances induits par la 8-OH-DPAT dans ce test ne sont pas attribuables à une perturbation de l’anxiété, de l’activité locomotrice, des capacités sensorimotrices ou motivationnelles. En revanche, la 8-OH-DPAT perturbe l’encodage des informations spatiales ou leur consolidation dans une fenêtre de temps limitée après l’acquisition. De plus, les déficits induits par la 8-OH-DPAT sont attribuables à l’activation des récepteurs 5-HT1A du septum médian et non pas des récepteurs 5-HT7 et ces déficits n’impliquent pas les neurones cholinergiques septo-hippocampiques chez des rats naïfs, et ne les impliquent que légèrement chez des rats entraînésThis thesis aims at characterizing the implication of 5-HT1A receptors of the medial septum in spatial memory in the Rat. We investigated the effects of an intraseptal infusion of 8-OH-DPAT, a mixed 5HT1A and 5-HT7 receptors agonist, on reference memory performances in the Morris Water Maze. The 8-OH-DPAT-induced deficits in this test cannot be explained by a perturbation of anxiety, locomotor activity, sensorimotor or motivational abilities. However, our results show that 8-OH-DPAT impairs declarative-like information encoding or consolidation within a given postacquisition time window. Moreover, 8-OH-DPAT-induced deficits involve activation of 5-HT1A receptors but not of 5-HT7 receptors by a mechanism to which cholinergic neurons of the medial septum are not essential
Books on the topic "Hippocampe (anatomie) – Physiologie"
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R, Jefferys John G., and Whittington Miles A, eds. Fast oscillations in cortical circuits. Cambridge, Mass: MIT Press, 1999.
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Beyond the cognitive map: From place cells to episodic memory. Cambridge, Mass: MIT Press, 1999.
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Jon, Storm-Mathisen, Zimmer J, Ottersen O. P, and Blackstad Theodor W, eds. Understanding the brain through the hippocampus: The hippocampal region as a model for studying brain structure and function. Amsterdam: Elsevier, 1990.
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Ambroise, Gärtner, and Frantz Dener, eds. Hippocampus: Anatomy, functions, and neurobiology. Hauppauge, N.Y: Nova Science, 2009.
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1947-, Frotscher M., ed. Neurotransmission in the hippocampus. Berlin: Springer-Verlag, 1988.
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Mason, Peggy. Forebrain. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0007.
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The anatomy and function of forebrain circuits is described. The role of the hypothalamus as the executive center for regulating and protecting the body’s physiology is detailed. The thalamus is a necessary interpreter for subcortical inputs to cerebral cortex, which uses thalamic input to map the sensory world. The amygdala, critical to expressing and interpreting fear, has been implicated in post-traumatic stress disorder. During resting conditions, the basal ganglia suppress movement. Damage to the basal ganglia produces a hypo- or hyperkinetic disorder. The representation of visual fields in pathways from retina to striate cortex is described in detail. The student is then introduced to the invaluable use of visual field deficits for localizing forebrain lesions. Extrastriate, somatomotor, and prefrontal contributions to abstract functions are outlined in a clinically relevant way. Finally, the importance of the hippocampus to declarative memory is discussed, and common memory symptoms are described.
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Traub, Roger D., John G. R. Jefferys, and Miles A. Whittington. Fast Oscillations in Cortical Circuits. MIT Press, 1999.
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Redish, A. David. Beyond the Cognitive Map: From Place Cells to Episodic Memory. MIT Press, 2016.
Find full textBook chapters on the topic "Hippocampe (anatomie) – Physiologie"
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Coward, L. Andrew. "The Hippocampal System as the Cortical Resource Manager: A Model Connecting Psychology, Anatomy and Physiology." In Advances in Experimental Medicine and Biology, 315–64. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-79100-5_18.
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Fisch, Adam J. "The Diencephalon, Basal Ganglia, & Limbic System." In Neuroanatomy, 341–76. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190259587.003.0011.
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This chapter focuses on learning the anatomy of the diencephalon, basal ganglia, and limbic system. It provides instruction on how to draw the basal ganglia, the thalamus, the hypothalamus, diencephalon, limbic system, hippocampus, Papez circuit, parahippocampal gyrus, intrahippocampal circuitry, olfactory cortex, and basal forebrain. Also addressed is the neurocircuitry of sleep, including the anatomical location of the sleep center, the physiology of the thalamocortical circuits, the pathway for the generation of REM sleep, and the biology of sleep and wakefulness. The chapter concludes with key discoveries in the biology of sleep and wakefulness.
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Benarroch, Eduardo E., Jeremy K. Cutsforth-Gregory, and Kelly D. Flemming. "Supratentorial Level." In Mayo Clinic Medical Neurosciences, edited by Eduardo E. Benarroch, Jeremy K. Cutsforth-Gregory, and Kelly D. Flemming, 657–716. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190209407.003.0019.
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The supratentorial level consists of 2 main anatomical regions: the diencephalon and the telencephalon. The anatomy, physiology, and clinical correlations of lesions affecting the diencephalon and visual pathways are described in another chapter. The telencephalon forms the cerebral hemispheres, which consist of the cerebral cortex, basal ganglia, and subcortical white matter tracts that interconnect areas of the cerebral cortex with one another and with the basal ganglia, thalamus, brainstem, and spinal cord. The medial portion of the cerebral hemispheres includes the amygdala, hippocampal formation, and cingulate cortex. These areas are involved in emotional and memory processing. The olfactory system is intimately related to these structures. The lateral and inferior aspects of the cerebral hemispheres include most of the frontal, insular, parietal, temporal, and occipital lobes. Neurons distributed in several cortical areas interact, forming functional networks that control different cognitive functions.
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Price, Joseph L., and Wayne C. Drevets. "Neural Circuitry of Depression." In Neurobiology of Mental Illness, edited by Helen S. Mayberg, 455–69. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199934959.003.0034.
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The primary mood disorders, major depressive disorder (MDD) and bipolar disorder (BD), constitute leading causes of disability on a global scale, yet little is known about their pathogenesis. These conditions are not associated with gross brain pathology or clear animal models for spontaneous recurrent mood episodes.Thus, the development of neuroimagingtechnologies that allowin vivo characterization of anatomy, physiology, and neurochemistryin human subjects withmood disorders has enabled significant advances toward elucidating their pathophysiology. Crucially, the interpretion of abnormalities found using these technologies in mood disorders has depended upon the concomitant delineation of anatomical networks that support emotional behavior. Early studies identified the amygdala, hippocampus, and other parts of what was termed the “limbic” system as central parts of the emotional brain. Beginning in the 1970’s and 1980’s and continuing through the last 15 years, neuroanatomical techniques based on axonal transport have been applied extensively to the limbic system and prefrontal cortex of monkeys. With these methods, a system has been described that links the medial prefrontal cortex and a few related cortical areas to the amygdala, the ventral striatum and pallidum, the medial thalamus, the hypothalamus, and the periaqueductal gray and other parts of the brainstem. A large body of human data from functional and structural imaging, as well as analysis of lesions and histological material indicates that this system is centrally involved in mood disorders.