Se connecter

Bibliographies thématiques / Basal ganglia model / Livres

Pour voir les autres types de publications sur ce sujet consultez le lien suivant : Basal ganglia model.

Livres sur le sujet « Basal ganglia model »

Auteur : Grafiati

Publié le 10 mars 2023

Créez une référence correcte selon les styles APA, MLA, Chicago, Harvard et plusieurs autres

Choisissez une source :

Consultez les 21 meilleurs livres pour votre recherche sur le sujet « Basal ganglia model ».

À côté de chaque source dans la liste de références il y a un bouton « Ajouter à la bibliographie ». Cliquez sur ce bouton, et nous générerons automatiquement la référence bibliographique pour la source choisie selon votre style de citation préféré : APA, MLA, Harvard, Vancouver, Chicago, etc.

Vous pouvez aussi télécharger le texte intégral de la publication scolaire au format pdf et consulter son résumé en ligne lorsque ces informations sont inclues dans les métadonnées.

Parcourez les livres sur diverses disciplines et organisez correctement votre bibliographie.

1

Pieter, Voorn, Berendse Henk W, Mulder Antonius B, Cools Alexander Rudolf 1941- et SpringerLink (Online service), dir. The Basal Ganglia IX. New York, NY : Springer-Verlag New York, 2009.

Trouver le texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

2

Chakravarthy, V. Srinivasa, et Ahmed A. Moustafa. Computational Neuroscience Models of the Basal Ganglia. Singapore : Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-8494-2.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

3

C, Houk James, Davis Joel L. 1942- et Beiser David G, dir. Models of information processing in the basal ganglia. Cambridge, Mass : MIT Press, 1994.

Trouver le texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

4

C, Houk James, Davis Joel L. 1942- et Beiser David G, dir. Models of information processing in the basal ganglia. Cambridge, Mass : MIT Press, 1995.

Trouver le texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

5

International Basal Ganglia Society. Symposium. The basal ganglia II : Structure and function : current concepts. New York : Plenum Press, 1987.

Trouver le texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

6

P, Riederer, et Wesemann W, dir. Parkinson's disease : Experimental models and therapy. Wien : Springer-Verlag, 1995.

Trouver le texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

7

Ely, Budding Deborah, dir. Subcortical structures and cognition : Implications for neuropsychological assessment. New York : Springer, 2009.

Trouver le texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

8

Subcortical functions in language and memory. New York : Guilford Press, 1992.

Trouver le texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

9

Steele, Vaughn R., Vani Pariyadath, Rita Z. Goldstein et Elliot A. Stein. Reward Circuitry and Drug Addiction. Sous la direction de Dennis S. Charney, Eric J. Nestler, Pamela Sklar et Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0044.

Texte intégral

Résumé :

Addiction is a complex neuropsychiatric syndrome related to dysregulation of brain systems including the mesocorticolimbic dopamine reward circuit. Dysregulation of reward circuitry is related to each of the three cyclical stages in the disease model of addiction: maintenance, abstinence, and relapse. Parsing reward circuitry is confounded due to the anatomical complexity of cortico-basal ganglia-thalamocortical loops, forward and backward projections within the circuit, and interactions between neurotransmitter systems. We begin by introducing the neurobiology of the reward system, specifically highlighting nodes of the circuit beyond the basal ganglia, followed by a review of the current literature on reward circuitry dysregulation in addiction. Finally, we discuss biomarkers of addiction identified with neuroimaging that could help guide neuroprediction models and development of targets for effective new interventions, such as noninvasive brain stimulation. The neurocircuitry of reward, especially non-prototypical nodes, may hold essential keys to understanding and treating addiction.

Styles APA, Harvard, Vancouver, ISO, etc.

10

Symposium, International Basal Ganglia Society. The basal ganglia II. Plenum, 1987.

Trouver le texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

11

Chakravarthy, V. Srinivasa, et Ahmed A. Moustafa. Computational Neuroscience Models of the Basal Ganglia. Springer, 2018.

Trouver le texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

12

Chakravarthy, V. Srinivasa. Computational Neuroscience Models of the Basal Ganglia. Springer, 2018.

Trouver le texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

13

Houk, James C., Joel L. Davis et David G. Beiser, dir. Models of Information Processing in the Basal Ganglia. The MIT Press, 1994. http://dx.doi.org/10.7551/mitpress/4708.001.0001.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

14

Davis, Joel L., James C. Houk et David G. Beiser. Models of Information Processing in the Basal Ganglia. MIT Press, 2019.

Trouver le texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

15

(Editor), Malcolm B. Carpenter, et A. Jayaraman (Editor), dir. The Basal Ganglia II : Structure and FunctionCurrent Concepts (Advances in Behavioral Biology). Springer, 1987.

Trouver le texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

16

Parkinson's Disease : Experimental Models And Therapy (Journal of Neural Transmission. Supplement). Springer-Verlag Telos, 1996.

Trouver le texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

17

Levine, Michael S., Elizabeth A. Wang, Jane Y. Chen, Carlos Cepeda et Véronique M. André. Altered Neuronal Circuitry. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0010.

Texte intégral

Résumé :

In mouse models of Huntington’s disease (HD), synaptic alterations in the cerebral cortex and striatum are present before overt behavioral symptoms and cell death. Similarly, in HD patients, it is now widely accepted that early deficits can occur in the absence of neural atrophy or overt motor symptoms. In addition, hyperkinetic movements seen in early stages are followed by hypokinesis in the late stages, indicating that different processes may be affected. In mouse models, such behavioral alterations parallel complex biphasic changes in glutamate-mediated excitatory, γ‎-aminobutyric acid (GABA)-mediated inhibitory synaptic transmission and dopamine modulation in medium spiny neurons of the striatum as well as in cortical pyramidal neurons. The progressive electrophysiologic changes in synaptic communication that occur with disease stage in the cortical and basal ganglia circuits of HD mouse models strongly indicate that therapeutic interventions and strategies in human HD must be targeted to different mechanisms in each stage and to specific subclasses of neurons.

Styles APA, Harvard, Vancouver, ISO, etc.

18

Koziol, Leonard F., et Deborah Ely Budding. Subcortical Structures and Cognition : Implications for Neuropsychological Assessment. Springer New York, 2010.

Trouver le texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

19

Benarroch, Eduardo E. Neuroscience for Clinicians. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.001.0001.

Texte intégral

Résumé :

The aim of this book is to provide the clinician with a comprehensive and clinical relevant survey of emerging concepts on the organization and function of the nervous system and neurologic disease mechanisms, at the molecular, cellular, and system levels. The content of is based on the review of information obtained from recent advances in genetic, molecular, and cell biology techniques; electrophysiological recordings; brain mapping; and mouse models, emphasizing the clinical and possible therapeutic implications. Many chapters of this book contain information that will be relevant not only to clinical neurologists but also to psychiatrists and physical therapists. The scope includes the mechanisms and abnormalities of DNA/RNA metabolism, proteostasis, vesicular biogenesis, and axonal transport and mechanisms of neurodegeneration; the role of the mitochondria in cell function and death mechanisms; ion channels, neurotransmission and mechanisms of channelopathies and synaptopathies; the functions of astrocytes, oligodendrocytes, and microglia and their involvement in disease; the local circuits and synaptic interactions at the level of the cerebral cortex, thalamus, basal ganglia, cerebellum, brainstem, and spinal cord transmission regulating sensory processing, behavioral state, and motor functions; the peripheral and central mechanisms of pain and homeostasis; and networks involved in emotion, memory, language, and executive function.

Styles APA, Harvard, Vancouver, ISO, etc.

20

Menon, Vinod. Arithmetic in the Child and Adult Brain. Sous la direction de Roi Cohen Kadosh et Ann Dowker. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199642342.013.041.

Texte intégral

Résumé :

This review examines brain and cognitive processes involved in arithmetic. I take a distinctly developmental perspective because neither the cognitive nor the brain processes involved in arithmetic can be adequately understood outside the framework of how developmental processes unfold. I review four basic neurocognitive processes involved in arithmetic, highlighting (1) the role of core dorsal parietal and ventral temporal-occipital cortex systems that form basic building blocks from which number form and quantity representations are constructed in the brain; (2) procedural and working memory systems anchored in the basal ganglia and frontoparietal circuits, which create short-term representations that allow manipulation of multiple discrete quantities over several seconds; (3) episodic and semantic memory systems anchored in the medial and lateral temporal cortex that play an important role in long-term memory formation and generalization beyond individual problem attributes; and (4) prefrontal cortex control processes that guide allocation of attention resources and retrieval of facts from memory in the service of goal-directed problem solving. Next I examine arithmetic in the developing brain, first focusing on studies comparing arithmetic in children and adults, and then on studies examining development in children during critical stages of skill acquisition. I highlight neurodevelopmental models that go beyond parietal cortex regions involved in number processing, and demonstrate that brain systems and circuits in the developing child brain are clearly not the same as those seen in more mature adult brains sculpted by years of learning. The implications of these findings for a more comprehensive view of the neural basis of arithmetic in both children and adults are discussed.

Styles APA, Harvard, Vancouver, ISO, etc.

21

Vallar, Giuseppe, et Nadia Bolognini. Unilateral Spatial Neglect. Sous la direction de Anna C. (Kia) Nobre et Sabine Kastner. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199675111.013.012.

Texte intégral

Résumé :

Left unilateral spatial neglect is the most frequent and disabling neuropsychological syndrome caused by lesions to the right hemisphere. Over 50% of right-brain-damaged patients show neglect, while right neglect after left-hemispheric damage is less frequent. Neglect patients are unable to orient towards the side contralateral to the lesion, to detect and report sensory events in that portion of space, as well as to explore it by motor action. Neglect is a multicomponent disorder, which may involve the contralesional side of the body or of extra-personal physical or imagined space, different sensory modalities, specific domains (e.g. ‘neglect dyslexia’), and worsen sensorimotor deficits. Neglect is due to higher-order unilateral deficits of spatial attention and representation, so that patients are not aware of contralesional events, which, however, undergo a substantial amount of unconscious processing up to the semantic level. Cross-modal sensory integration is also largely preserved. Neglect is primarily a spatially specific disorder of perceptual consciousness. The responsible lesions involve a network including the fronto-temporo-parietal cortex (particularly the posterior-inferior parietal lobe, at the temporo-parietal junction), their white matter connections, and some subcortical grey nuclei (thalamus, basal ganglia). Damage to primary sensory and motor regions is not associated to neglect. A variety of physiological lateralized and asymmetrical sensory stimulations (vestibular, optokinetic, prism adaptation, motor activation), and transcranial electrical and magnetic stimulations, may temporarily improve or worsen neglect. Different procedures have been successfully developed to rehabilitate neglect, using both ‘top down’ (training the voluntary orientation of attention) and ‘bottom up’ (the above-mentioned stimulations) approaches.

Styles APA, Harvard, Vancouver, ISO, etc.

Nous offrons des réductions sur tous les plans premium pour les auteurs dont les œuvres sont incluses dans des sélections littéraires thématiques. Contactez-nous pour obtenir un code promo unique!