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Books on the topic 'Basal ganglia model'

Author: Grafiati

Published: 10 March 2023

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1

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

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2

Chakravarthy, V. Srinivasa, and 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.

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3

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

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4

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

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5

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

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6

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

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7

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

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8

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

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9

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

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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.

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10

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

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11

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

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12

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

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13

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

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14

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

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15

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

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16

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

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17

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

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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.

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18

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

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19

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

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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.

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20

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

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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.

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21

Vallar, Giuseppe, and Nadia Bolognini. Unilateral Spatial Neglect. Edited by Anna C. (Kia) Nobre and Sabine Kastner. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199675111.013.012.

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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.

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