Journal articles: 'Basal ganglia model'

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Barker, Roger. "Model for basal ganglia disorders." Trends in Neurosciences 13, no. 3 (March 1990): 93. http://dx.doi.org/10.1016/0166-2236(90)90181-9.

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Gonzalo, N. "The parafascicular thalamic complex and basal ganglia circuitry: further complexity to the basal ganglia model." Thalamus & Related Systems 1, no. 4 (June 2002): 341–48. http://dx.doi.org/10.1016/s1472-9288(02)00007-9.

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Gonzalo, N., J. L. Lanciego, M. Castle, A. Vázquez, E. Erro, and J. A. Obeso. "The parafascicular thalamic complex and basal ganglia circuitry: further complexity to the basal ganglia model." Thalamus and Related Systems 1, no. 04 (June 2002): 341. http://dx.doi.org/10.1017/s1472928802000079.

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Hallett, Mark. "Physiology of Basal Ganglia Disorders: An Overview." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 20, no. 3 (August 1993): 177–83. http://dx.doi.org/10.1017/s0317167100047909.

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ABSTRACT:The pathophysiology of the movement disorders arising from basal ganglia disorders has been uncertain, in part because of a lack of a good theory of how the basal ganglia contribute to normal voluntary movement. An hypothesis for basal ganglia function is proposed here based on recent advances in anatomy and physiology. Briefly, the model proposes that the purpose of the basal ganglia circuits is to select and inhibit specific motor synergies to carry out a desired action. The direct pathway is to select and the indirect pathway is to inhibit these synergies. The clinical and physiological features of Parkinson's disease, L-DOPA dyskinesias, Huntington's disease, dystonia and tic are reviewed. An explanation of these features is put forward based upon the model.

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Yin, Henry H. "How Basal Ganglia Outputs Generate Behavior." Advances in Neuroscience 2014 (November 18, 2014): 1–28. http://dx.doi.org/10.1155/2014/768313.

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The basal ganglia (BG) are a collection of subcortical nuclei critical for voluntary behavior. According to the standard model, the output projections from the BG tonically inhibit downstream motor centers and prevent behavior. A pause in the BG output opens the gate for behavior, allowing the initiation of actions. Hypokinetic neurological symptoms, such as inability to initiate actions in Parkinson’s disease, are explained by excessively high firing rates of the BG output neurons. This model, widely taught in textbooks, is contradicted by recent electrophysiological results, which are reviewed here. In addition, I also introduce a new model, based on the insight that behavior is a product of closed loop negative feedback control using internal reference signals rather than sensorimotor transformations. The nervous system is shown to be a functional hierarchy comprising independent controllers occupying different levels, each level controlling specific variables derived from its perceptual inputs. The BG represent the level of transition control in this hierarchy, sending reference signals specifying the succession of body orientations and configurations. This new model not only explains the major symptoms in movement disorders but also generates a number of testable predictions.

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FÃ©ger, J. "Updating the functional model of the basal ganglia." Trends in Neurosciences 20, no. 4 (May 13, 1997): 152–53. http://dx.doi.org/10.1016/s0166-2236(96)01016-8.

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Suri, R. E., C. Albani, and A. H. Glattfelder. "A dynamic model of motor basal ganglia functions." Biological Cybernetics 76, no. 6 (July 22, 1997): 451–58. http://dx.doi.org/10.1007/s004220050358.

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Lepora, Nathan F., and Kevin N. Gurney. "The Basal Ganglia Optimize Decision Making over General Perceptual Hypotheses." Neural Computation 24, no. 11 (November 2012): 2924–45. http://dx.doi.org/10.1162/neco_a_00360.

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The basal ganglia are a subcortical group of interconnected nuclei involved in mediating action selection within cortex. A recent proposal is that this selection leads to optimal decision making over multiple alternatives because the basal ganglia anatomy maps onto a network implementation of an optimal statistical method for hypothesis testing, assuming that cortical activity encodes evidence for constrained gaussian-distributed alternatives. This letter demonstrates that this model of the basal ganglia extends naturally to encompass general Bayesian sequential analysis over arbitrary probability distributions, which raises the proposal to a practically realizable theory over generic perceptual hypotheses. We also show that the evidence in this model can represent either log likelihoods, log-likelihood ratios, or log odds, all leading proposals for the cortical processing of sensory data. For these reasons, we claim that the basal ganglia optimize decision making over general perceptual hypotheses represented in cortex. The relation of this theory to cortical encoding, cortico-basal ganglia anatomy, and reinforcement learning is discussed.

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Plotkin, Joshua L., and Joshua A. Goldberg. "Thinking Outside the Box (and Arrow): Current Themes in Striatal Dysfunction in Movement Disorders." Neuroscientist 25, no. 4 (October 31, 2018): 359–79. http://dx.doi.org/10.1177/1073858418807887.

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The basal ganglia are an intricately connected assembly of subcortical nuclei, forming the core of an adaptive network connecting cortical and thalamic circuits. For nearly three decades, researchers and medical practitioners have conceptualized how the basal ganglia circuit works, and how its pathology underlies motor disorders such as Parkinson’s and Huntington’s diseases, using what is often referred to as the “box-and-arrow model”: a circuit diagram showing the broad strokes of basal ganglia connectivity and the pathological increases and decreases in the weights of specific connections that occur in disease. While this model still has great utility and has led to groundbreaking strategies to treat motor disorders, our evolving knowledge of basal ganglia function has made it clear that this classic model has several shortcomings that severely limit its predictive and descriptive abilities. In this review, we will focus on the striatum, the main input nucleus of the basal ganglia. We describe recent advances in our understanding of the rich microcircuitry and plastic capabilities of the striatum, factors not captured by the original box-and-arrow model, and provide examples of how such advances inform our current understanding of the circuit pathologies underlying motor disorders.

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Yin, Henry H. "The Basal Ganglia in Action." Neuroscientist 23, no. 3 (June 15, 2016): 299–313. http://dx.doi.org/10.1177/1073858416654115.

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The basal ganglia (BG) are the major subcortical nuclei in the brain. Disorders implicating the BG are characterized by diverse symptoms, but it remains unclear what these symptoms have in common or how they can be explained by changes in the BG circuits. This review summarizes recent findings that not only question traditional assumptions about the role of the BG in movement but also elucidate general computations performed by these circuits. To explain these findings, a new conceptual framework is introduced for understanding the role of the BG in behavior. According to this framework, the cortico-BG networks implement transition control in an extended hierarchy of closed loop negative feedback control systems. The transition control model provides a solution to the posture/movement problem, by postulating that BG outputs send descending signals to alter the reference states of downstream position control systems for orientation and body configuration. It also explains major neurological symptoms associated with BG pathology as a result of changes in system parameters such as multiplicative gain and damping.

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Crossley, Matthew J., Jon C. Horvitz, Peter D. Balsam, and F. Gregory Ashby. "Expanding the role of striatal cholinergic interneurons and the midbrain dopamine system in appetitive instrumental conditioning." Journal of Neurophysiology 115, no. 1 (January 1, 2016): 240–54. http://dx.doi.org/10.1152/jn.00473.2015.

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The basal ganglia are a collection of subcortical nuclei thought to underlie a wide variety of vertebrate behavior. Although a great deal is known about the functional and physiological properties of the basal ganglia, relatively few models have been formally developed that have been tested against both behavioral and physiological data. Our previous work (Ashby FG, Crossley MJ. J Cogn Neurosci 23: 1549–1566, 2011) showed that a model grounded in the neurobiology of the basal ganglia could account for basic single-neuron recording data, as well as behavioral phenomena such as fast reacquisition that constrain models of conditioning. In this article we show that this same model accounts for a variety of appetitive instrumental conditioning phenomena, including the partial reinforcement extinction (PRE) effect, rapid and slowed reacquisition following extinction, and renewal of previously extinguished instrumental responses by environmental context cues.

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Moustafa, Ahmed A., and Mark A. Gluck. "A Neurocomputational Model of Dopamine and Prefrontal–Striatal Interactions during Multicue Category Learning by Parkinson Patients." Journal of Cognitive Neuroscience 23, no. 1 (January 2011): 151–67. http://dx.doi.org/10.1162/jocn.2010.21420.

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Most existing models of dopamine and learning in Parkinson disease (PD) focus on simulating the role of basal ganglia dopamine in reinforcement learning. Much data argue, however, for a critical role for prefrontal cortex (PFC) dopamine in stimulus selection in attentional learning. Here, we present a new computational model that simulates performance in multicue category learning, such as the “weather prediction” task. The model addresses how PD and dopamine medications affect stimulus selection processes, which mediate reinforcement learning. In this model, PFC dopamine is key for attentional learning, whereas basal ganglia dopamine, consistent with other models, is key for reinforcement and motor learning. The model assumes that competitive dynamics among PFC neurons is the neural mechanism underlying stimulus selection with limited attentional resources, whereas competitive dynamics among striatal neurons is the neural mechanism underlying action selection. According to our model, PD is associated with decreased phasic and tonic dopamine levels in both PFC and basal ganglia. We assume that dopamine medications increase dopamine levels in both the basal ganglia and PFC, which, in turn, increase tonic dopamine levels but decrease the magnitude of phasic dopamine signaling in these brain structures. Increase of tonic dopamine levels in the simulated PFC enhances attentional shifting performance. The model provides a mechanistic account for several phenomena, including (a) medicated PD patients are more impaired at multicue probabilistic category learning than unmedicated patients and (b) medicated PD patients opt out of reversal when there are alternative and redundant cue dimensions.

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Bogacz, Rafal, and Tobias Larsen. "Integration of Reinforcement Learning and Optimal Decision-Making Theories of the Basal Ganglia." Neural Computation 23, no. 4 (April 2011): 817–51. http://dx.doi.org/10.1162/neco_a_00103.

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This article seeks to integrate two sets of theories describing action selection in the basal ganglia: reinforcement learning theories describing learning which actions to select to maximize reward and decision-making theories proposing that the basal ganglia selects actions on the basis of sensory evidence accumulated in the cortex. In particular, we present a model that integrates the actor-critic model of reinforcement learning and a model assuming that the cortico-basal-ganglia circuit implements a statistically optimal decision-making procedure. The values of corico-striatal weights required for optimal decision making in our model differ from those provided by standard reinforcement learning models. Nevertheless, we show that an actor-critic model converges to the weights required for optimal decision making when biologically realistic limits on synaptic weights are introduced. We also describe the model's predictions concerning reaction times and neural responses during learning, and we discuss directions required for further integration of reinforcement learning and optimal decision-making theories.

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Tan, Xiaolong, Hudong Zhang, Yan Xie, and Yuan Chai. "Electromagnetic radiation and electrical stimulation controls of absence seizures in a coupled reduced corticothalamic model." Electronic Research Archive 31, no. 1 (2022): 58–74. http://dx.doi.org/10.3934/era.2023004.

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<abstract> <p>The important role of basal ganglia in corticothalamic loops has received widespread attention. However, its connection between coupled reduced corticothalamic networks is rarely researched, particularly the regulatory mechanism about electromagnetic radiation and electrical stimulation has not been comprehensively investigated. In this paper, we establish a model simplified the basal-ganglia as a connector connecting two corticothalamic loops. Four kinds of treatment methods are applied to the coupled reduced corticothalamic model, for instance deep brain stimulation (DBS), 1:0 coordinate reset stimulation (CRS) and 3:2 CRS to stimulate thalamic reticular nucleus (TRN) and electromagnetic radiation to stimulate the pyramidal neuronal population (PY). One of the important results is that the epileptic area can be significantly reduced in varying degrees by changing the strength of the basal-ganglia connector. Another one is that electromagnetic radiation, DBS and CRS have preferable inhibitory effects on absence seizure. The results show that DBS has a more significant inhibitory effect than 1:0 CRS and 3:2 CRS. The results might contribute to understanding the role of basal ganglia in coupled model and providing a reference for inhibiting epileptic seizures.</p> </abstract>

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Caiola, Michael, and Mark H. Holmes. "Model and Analysis for the Onset of Parkinsonian Firing Patterns in a Simplified Basal Ganglia." International Journal of Neural Systems 29, no. 01 (January 10, 2019): 1850021. http://dx.doi.org/10.1142/s0129065718500211.

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Parkinson’s disease (PD) is a degenerative neurological disease that disrupts the movement cycle in the basal ganglia. As the disease progresses, dopamine depletion leads to changes to how the basal ganglia functions as well as the appearance of abnormal beta oscillations. There is much debate on just exactly how these connection strengths change and just how the oscillations emerge. One leading hypothesis claims that the oscillations develop in the globus pallidus external, subthalamic nucleus, and globus pallidus internal loop. We introduce a mathematical model that calculates the average firing rates of this loop while still accounting for the larger closed loop of the entire basal ganglia system. This model is constructed such that physiologically realistic results can be obtained while not sacrificing the use of analytic methods. Because of this, it is possible to determine how the change in the connection strengths can drive the necessary changes in firing rates seen in recordings and account for the generation of trademark beta oscillations of PD without relying on highly specific time delays, stochastic approaches, or numerical approximations. Additionally, we find that the entire cortico-basal ganglia-thalamo-cortical loop is essential for abnormal oscillations to originate.

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Lipski, Witold J., Thomas A. Wozny, Ahmad Alhourani, Efstathios D. Kondylis, Robert S. Turner, Donald J. Crammond, and Robert Mark Richardson. "Dynamics of human subthalamic neuron phase-locking to motor and sensory cortical oscillations during movement." Journal of Neurophysiology 118, no. 3 (September 1, 2017): 1472–87. http://dx.doi.org/10.1152/jn.00964.2016.

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Coupled oscillatory activity recorded between sensorimotor regions of the basal ganglia-thalamocortical loop is thought to reflect information transfer relevant to movement. A neuronal firing-rate model of basal ganglia-thalamocortical circuitry, however, has dominated thinking about basal ganglia function for the past three decades, without knowledge of the relationship between basal ganglia single neuron firing and cortical population activity during movement itself. We recorded activity from 34 subthalamic nucleus (STN) neurons, simultaneously with cortical local field potentials and motor output, in 11 subjects with Parkinson's disease (PD) undergoing awake deep brain stimulator lead placement. STN firing demonstrated phase synchronization to both low- and high-beta-frequency cortical oscillations, and to the amplitude envelope of gamma oscillations, in motor cortex. We found that during movement, the magnitude of this synchronization was dynamically modulated in a phase-frequency-specific manner. Importantly, we found that phase synchronization was not correlated with changes in neuronal firing rate. Furthermore, we found that these relationships were not exclusive to motor cortex, because STN firing also demonstrated phase synchronization to both premotor and sensory cortex. The data indicate that models of basal ganglia function ultimately will need to account for the activity of populations of STN neurons that are bound in distinct functional networks with both motor and sensory cortices and code for movement parameters independent of changes in firing rate. NEW & NOTEWORTHY Current models of basal ganglia-thalamocortical networks do not adequately explain simple motor functions, let alone dysfunction in movement disorders. Our findings provide data that inform models of human basal ganglia function by demonstrating how movement is encoded by networks of subthalamic nucleus (STN) neurons via dynamic phase synchronization with cortex. The data also demonstrate, for the first time in humans, a mechanism through which the premotor and sensory cortices are functionally connected to the STN.

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Dorval, Alan D., Alexis M. Kuncel, Merrill J. Birdno, Dennis A. Turner, and Warren M. Grill. "Deep Brain Stimulation Alleviates Parkinsonian Bradykinesia by Regularizing Pallidal Activity." Journal of Neurophysiology 104, no. 2 (August 2010): 911–21. http://dx.doi.org/10.1152/jn.00103.2010.

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Deep brain stimulation (DBS) of the basal ganglia can alleviate the motor symptoms of Parkinson's disease although the therapeutic mechanisms are unclear. We hypothesize that DBS relieves symptoms by minimizing pathologically disordered neuronal activity in the basal ganglia. In human participants with parkinsonism and clinically effective deep brain leads, regular (i.e., periodic) high-frequency stimulation was replaced with irregular (i.e., aperiodic) stimulation at the same mean frequency (130 Hz). Bradykinesia, a symptomatic slowness of movement, was quantified via an objective finger tapping protocol in the absence and presence of regular and irregular DBS. Regular DBS relieved bradykinesia more effectively than irregular DBS. A computational model of the relevant neural structures revealed that output from the globus pallidus internus was more disordered and thalamic neurons made more transmission errors in the parkinsonian condition compared with the healthy condition. Clinically therapeutic, regular DBS reduced firing pattern disorder in the computational basal ganglia and minimized model thalamic transmission errors, consistent with symptom alleviation by clinical DBS. However, nontherapeutic, irregular DBS neither reduced disorder in the computational basal ganglia nor lowered model thalamic transmission errors. Thus we show that clinically useful DBS alleviates motor symptoms by regularizing basal ganglia activity and thereby improving thalamic relay fidelity. This work demonstrates that high-frequency stimulation alone is insufficient to alleviate motor symptoms: DBS must be highly regular. Descriptive models of pathophysiology that ignore the fine temporal resolution of neuronal spiking in favor of average neural activity cannot explain the mechanisms of DBS-induced symptom alleviation.

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Parent, André, and Francesca Cicchetti. "The current model of basal ganglia organization under scrutiny." Movement Disorders 13, no. 2 (March 1998): 199–202. http://dx.doi.org/10.1002/mds.870130202.

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Hanssen, Henrike, Jannik Prasuhn, Marcus Heldmann, Cid C. Diesta, Aloysius Domingo, Martin Göttlich, Anne J. Blood, et al. "Imaging gradual neurodegeneration in a basal ganglia model disease." Annals of Neurology 86, no. 4 (August 23, 2019): 517–26. http://dx.doi.org/10.1002/ana.25566.

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Darbin, Olivier, Daniel Dees, Anthony Martino, Elizabeth Adams, and Dean Naritoku. "An Entropy-Based Model for Basal Ganglia Dysfunctions in Movement Disorders." BioMed Research International 2013 (2013): 1–5. http://dx.doi.org/10.1155/2013/742671.

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During this last decade, nonlinear analyses have been used to characterize the irregularity that exists in the neuronal data stream of the basal ganglia. In comparison to linear parameters for disparity (i.e., rate, standard deviation, and oscillatory activities), nonlinear analyses focus on complex patterns that are composed of groups of interspike intervals with matching lengths but not necessarily contiguous in the data stream. In light of recent animal and clinical studies, we present a review and commentary on the basal ganglia neuronal entropy in the context of movement disorders.

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Kahan, Joshua, Laura Mancini, Guillaume Flandin, Mark White, Anastasia Papadaki, John Thornton, Tarek Yousry, et al. "Deep brain stimulation has state-dependent effects on motor connectivity in Parkinson’s disease." Brain 142, no. 8 (June 20, 2019): 2417–31. http://dx.doi.org/10.1093/brain/awz164.

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How DBS affects information flow along basal ganglia pathways is unclear. Kahan et al. model fMRI data, revealing differences in the neuromodulatory effects of DBS during different behavioural states. The results suggest that DBS has both behaviour-independent effects on basal ganglia connectivity as well as behaviour-dependent neuromodulatory effects.

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Parent, André. "The brain in evolution and involution." Biochemistry and Cell Biology 75, no. 6 (December 1, 1997): 651–67. http://dx.doi.org/10.1139/o97-094.

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This paper provides an overview of the phylogenetic evolution and structural organization of the basal ganglia. These large subcortical structures that form the core of the cerebral hemispheres directly participate in the control of psychomotor behavior. Neuroanatomical methods combined with transmitter localization procedures were used to study the chemical organization of the forebrain in each major group of vertebrates. The various components of the basal ganglia appear well developed in amniote vertebrates, but remain rudimentary in anamniote vertebrates. For example, a typical substantia nigra composed of numerous dopaminergic neurons that project to the striatum already exists in the brain of reptiles. Other studies in mammals show that glutamatergic cortical inputs establish distinct functional territories within the basal ganglia, and that neurons in each of these territories act upon other brain neuronal systems principally via a GABAergic disinhibitory output mechanism. The functional status of the various basal ganglia chemospecific systems was examined in animal models of neurodegenerative diseases, as well as in postmortem material from Parkinson's and Huntington's disease patients. The neurodegenerative processes at play in such conditions specifically target the most phylogenetically ancient components of the brain, including the substantia nigra and the striatum, and the marked involution of these brain structures is accompanied by severe motor and cognitive deficits. Studies of neural mechanisms involved in these akinetic and hyperkinetic disorders have led to a complete reevaluation of the current model of the functional organization of the basal ganglia in both health and disease. Key words: brain phylogeny, basal ganglia, neurotransmitters, neurodegenerative disorders.

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Bogacz, Rafal, and Kevin Gurney. "The Basal Ganglia and Cortex Implement Optimal Decision Making Between Alternative Actions." Neural Computation 19, no. 2 (February 2007): 442–77. http://dx.doi.org/10.1162/neco.2007.19.2.442.

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Neurophysiological studies have identified a number of brain regions critically involved in solving the problem of action selection or decision making. In the case of highly practiced tasks, these regions include cortical areas hypothesized to integrate evidence supporting alternative actions and the basal ganglia, hypothesized to act as a central switch in gating behavioral requests. However, despite our relatively detailed knowledge of basal ganglia biology and its connectivity with the cortex and numerical simulation studies demonstrating selective function, no formal theoretical framework exists that supplies an algorithmic description of these circuits. This article shows how many aspects of the anatomy and physiology of the circuit involving the cortex and basal ganglia are exactly those required to implement the computation defined by an asymptotically optimal statistical test for decision making: the multihypothesis sequential probability ratio test (MSPRT). The resulting model of basal ganglia provides a new framework for understanding the computation in the basal ganglia during decision making in highly practiced tasks. The predictions of the theory concerning the properties of particular neuronal populations are validated in existing experimental data. Further, we show that this neurobiologically grounded implementation of MSPRT outperforms other candidates for neural decision making, that it is structurally and parametrically robust, and that it can accommodate cortical mechanisms for decision making in a way that complements those in basal ganglia.

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Magdoom, K. N., D. Subramanian, V. S. Chakravarthy, B. Ravindran, Shun-ichi Amari, and N. Meenakshisundaram. "Modeling Basal Ganglia for Understanding Parkinsonian Reaching Movements." Neural Computation 23, no. 2 (February 2011): 477–516. http://dx.doi.org/10.1162/neco_a_00073.

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We present a computational model that highlights the role of basal ganglia (BG) in generating simple reaching movements. The model is cast within the reinforcement learning (RL) framework with correspondence between RL components and neuroanatomy as follows: dopamine signal of substantia nigra pars compacta as the temporal difference error, striatum as the substrate for the critic, and the motor cortex as the actor. A key feature of this neurobiological interpretation is our hypothesis that the indirect pathway is the explorer. Chaotic activity, originating from the indirect pathway part of the model, drives the wandering, exploratory movements of the arm. Thus, the direct pathway subserves exploitation, while the indirect pathway subserves exploration. The motor cortex becomes more and more independent of the corrective influence of BG as training progresses. Reaching trajectories show diminishing variability with training. Reaching movements associated with Parkinson's disease (PD) are simulated by reducing dopamine and degrading the complexity of indirect pathway dynamics by switching it from chaotic to periodic behavior. Under the simulated PD conditions, the arm exhibits PD motor symptoms like tremor, bradykinesia and undershooting. The model echoes the notion that PD is a dynamical disease.

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Yamamoto, Kazumi, Toshiki Yoshimine, and Takehiko Yanagihara. "Cerebral Ischemia in Rabbit: A New Experimental Model with Immunohistochemical Investigation." Journal of Cerebral Blood Flow & Metabolism 5, no. 4 (December 1985): 529–36. http://dx.doi.org/10.1038/jcbfm.1985.80.

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Regional cerebral ischemia was produced in the rabbit by unilateral transorbital occlusion of the middle cerebral artery (procedure I); the middle cerebral and azygos anterior cerebral or anterior communicating artery (procedure II); or the middle cerebral, azygos anterior cerebral or anterior communicating, and internal carotid artery (procedure III). Evolution of ischemic lesions was examined with the immunohistochemical reaction for tubulin. With procedure I, ischemic lesions did not become constantly visible for 6 h in the basal ganglia and for 8 h in the frontoparietal region of the cerebral cortex. With procedure II, it was shortened to 3 h in the basal ganglia and to 6 h in the cerebral cortex. With procedure III, the ischemic lesions were observed in 1 h both in the basal ganglia and in the cerebral cortex as loss of the reaction for tubulin in the neuropil, nerve cell bodies, and dendrites. The evidence of neuronal damage became apparent in the same areas later by staining with hematoxylin–eosin. The experimental model presented here may be suitable for investigation of the mechanism that shifts reversible ischemia to cerebral infarction and for evaluation of the effectiveness of pharmacological intervention.

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Berns, Gregory S., and Terrence J. Sejnowski. "A Computational Model of How the Basal Ganglia Produce Sequences." Journal of Cognitive Neuroscience 10, no. 1 (January 1998): 108–21. http://dx.doi.org/10.1162/089892998563815.

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We propose a systems-level computational model of the basal ganglia based closely on known anatomy and physiology. First, we assume that the thalamic targets, which relay ascending information to cortical action and planning areas, are tonically inhibited by the basal ganglia. Second, we assume that the output stage of the basal ganglia, the internal segment of the globus pallidus (GPi), selects a single action from several competing actions via lateral interactions. Third, we propose that a form of local working memory exists in the form of reciprocal connections between the external globus pallidus (GPe) and the subthalamic nucleus (STN). As a test of the model, the system was trained to learn a sequence of states that required the context of previous actions. The striatum, which was assumed to represent a conjunction of cortical states, directly selected the action in the GP during training. The STN-to-GP connection strengths were modified by an associative learning rule and came to encode the sequence after 20 to 40 iterations through the sequence. Subsequently, the system automatically reproduced the sequence when cued to the first action. The behavior of the model was found to be sensitive to the ratio of the striatal-nigral learning rate to the STN-GP learning rate. Additionally, the degree of striatal inhibition of the globus pallidus had a significant influence on both learning and the ability to select an action. Low learning rates, which would be hypothesized to reflect low levels of dopamine, as in Parkinson's disease, led to slow acquisition of contextual information. However, this could be partially offset by modeling a lesion of the globus pallidus that resulted in an increase in the gain of the STN units. The parameter sensitivity of the model is discussed within the framework of existing behavioral and lesion data.

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Lieberman, Philip. "Why we can talk, debate, and change our minds: Neural circuits, basal ganglia operations, and transcriptional factors." Behavioral and Brain Sciences 37, no. 6 (December 2014): 561–62. http://dx.doi.org/10.1017/s0140525x13004093.

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AbstractAckermann et al. disregard attested knowledge concerning aphasia, Parkinson disease, cortical-to-striatal circuits, basal ganglia, laryngeal phonation, and other matters. Their dual-pathway model cannot account for “what is special about the human brain.” Their human cortical-to-laryngeal neural circuit does not exist. Basal ganglia operations, enhanced by mutations on FOXP2, confer human motor-control, linguistic, and cognitive capabilities.

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Jing, Chen, and Li Zongshuai. "Basal Ganglia Behaviour Cognitive Model Based on Operant Conditioning Reflex." Open Automation and Control Systems Journal 6, no. 1 (December 31, 2014): 1570–77. http://dx.doi.org/10.2174/1874444301406011570.

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Tortolero, Ivan Carmona, Deepak Kumbhare, Jayasimha Atulasimha, Mark Baron, and Ravi Hadimani. "A computational basal ganglia-thalamocortical circuitry model for Parkinson’s disease." Brain Stimulation 14, no. 6 (November 2021): 1617. http://dx.doi.org/10.1016/j.brs.2021.10.095.

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Yu, Ying, and Qingyun Wang. "Oscillation dynamics in an extended model of thalamic-basal ganglia." Nonlinear Dynamics 98, no. 2 (September 19, 2019): 1065–80. http://dx.doi.org/10.1007/s11071-019-05249-2.

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Porenta, Gerold. "A computer model of neuronal pathways in the basal ganglia." Computer Methods and Programs in Biomedicine 22, no. 3 (June 1986): 325–31. http://dx.doi.org/10.1016/0169-2607(86)90008-8.

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Gangadhar, Garipelli, Denny Joseph, and V. Srinivasa Chakravarthy. "Understanding Parkinsonian Handwriting Through a Computational Model of Basal Ganglia." Neural Computation 20, no. 10 (October 2008): 2491–525. http://dx.doi.org/10.1162/neco.2008.03-07-498.

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Handwriting in Parkinson's disease (PD) is typically characterized by micrographia, jagged line contour, and unusual fluctuations in pen tip velocity. Although PD handwriting features have been used for diagnostics, they are not based on a signaling model of basal ganglia (BG). In this letter, we present a computational model of handwriting generation that highlights the role of BG. When PD conditions like reduced dopamine and altered dynamics of the subthalamic nucleus and globus pallidus externa subsystems are simulated, the handwriting produced by the model manifested characteristic PD handwriting distortions like micrographia and velocity fluctuations. Our approach to PD modeling is in tune with the perspective that PD is a dynamic disease.

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Avecillas-Chasin, Josué M., Fernando Rascón-Ramírez, and Juan A. Barcia. "Tractographical model of the cortico-basal ganglia and corticothalamic connections." Clinical Anatomy 29, no. 4 (February 13, 2016): 481–92. http://dx.doi.org/10.1002/ca.22689.

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Pena-Casanova, Jordi, and Jorge Sigg-Alonso. "Functional Systems and Brain Functional Units Beyond Luria, With Luria: Anatomical Aspects." Lurian Journal 1, no. 1 (July 16, 2020): 48–76. http://dx.doi.org/10.15826/lurian.2020.1.1.6.

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This paper describes the anatomical aspects of a functional brain model that develops A. R. Luria’s ideas. Five functional brain units are described on the basis of ontogenetic, anatomical, histological, functional, and clinical studies: preferential or primordial (unit I), limbic (unit II), cortical (unit III), basal ganglia (unit IV), and cerebellar (unit V). This review allows two large integrated and interrelated functional complexes to be distinguished: a primordial-limbic complex (units I and II) and a supralimbic one (units, III, IV and V). There is consensus that there exists a clear interplay among the cortex, the basal ganglia, and the cerebellum. Three main simplified parallel cortico-basal ganglia systems have been recognized: limbic, associative, and sensorimotor. Certain structures (e. g. neuromodulatory systems, hypothalamus, and paralimbic cortex) form functional links among units. Future studies are required to develop and improve the proposed model.

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NAHVI, ALIREZA, FARIBA BAHRAMI, and SAMIRA HEMMATI. "INVESTIGATING DIFFERENT TARGETS IN DEEP BRAIN STIMULATION ON PARKINSON'S DISEASE USING A MEAN-FIELD MODEL OF THE BASAL GANGLIA-THALAMOCORTICAL SYSTEM." Journal of Mechanics in Medicine and Biology 12, no. 02 (April 2012): 1240004. http://dx.doi.org/10.1142/s0219519412400040.

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In this paper, we investigated effects of deep brain stimulation (DBS) on Parkinson's disease (PD) when different target sites in the basal ganglia are stimulated. The targets which are investigated are subthalamic nucleus (STN), globus pallidus interna (GPi), and globus pallidus externa (GPe). For this purpose we used a computational model of the basal ganglia-thalamocortical system (BGTCS) with parameters calculated for mean field. This model is able to reproduce both the normal and Parkinsonian activities of basal ganglia, thalamus and cortex in a unified structure. In the present study, we used a mean-field model of the BGTCS, allowing a more complete framework to simulate DBS and to interpret its effects in the BGTCS. Our results suggest that DBS in the STN and GPe could restore the thalamus relay activity, while DBS in the GPi could inhibit it. Our results are compatible with the experimental and the clinical outcomes about the effects of DBS of different targets.

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Dorval, Alan D., and Warren M. Grill. "Deep brain stimulation of the subthalamic nucleus reestablishes neuronal information transmission in the 6-OHDA rat model of parkinsonism." Journal of Neurophysiology 111, no. 10 (May 15, 2014): 1949–59. http://dx.doi.org/10.1152/jn.00713.2013.

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Pathophysiological activity of basal ganglia neurons accompanies the motor symptoms of Parkinson's disease. High-frequency (>90 Hz) deep brain stimulation (DBS) reduces parkinsonian symptoms, but the mechanisms remain unclear. We hypothesize that parkinsonism-associated electrophysiological changes constitute an increase in neuronal firing pattern disorder and a concomitant decrease in information transmission through the ventral basal ganglia, and that effective DBS alleviates symptoms by decreasing neuronal disorder while simultaneously increasing information transfer through the same regions. We tested these hypotheses in the freely behaving, 6-hydroxydopamine-lesioned rat model of hemiparkinsonism. Following the onset of parkinsonism, mean neuronal firing rates were unchanged, despite a significant increase in firing pattern disorder (i.e., neuronal entropy), in both the globus pallidus and substantia nigra pars reticulata. This increase in neuronal entropy was reversed by symptom-alleviating DBS. Whereas increases in signal entropy are most commonly indicative of similar increases in information transmission, directed information through both regions was substantially reduced (>70%) following the onset of parkinsonism. Again, this decrease in information transmission was partially reversed by DBS. Together, these results suggest that the parkinsonian basal ganglia are rife with entropic activity and incapable of functional information transmission. Furthermore, they indicate that symptom-alleviating DBS works by lowering the entropic noise floor, enabling more information-rich signal propagation. In this view, the symptoms of parkinsonism may be more a default mode, normally overridden by healthy basal ganglia information. When that information is abolished by parkinsonian pathophysiology, hypokinetic symptoms emerge.

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Scholl, Carolin, Javier Baladron, Julien Vitay, and Fred H. Hamker. "Enhanced habit formation in Tourette patients explained by shortcut modulation in a hierarchical cortico-basal ganglia model." Brain Structure and Function 227, no. 3 (February 3, 2022): 1031–50. http://dx.doi.org/10.1007/s00429-021-02446-x.

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AbstractDevaluation protocols reveal that Tourette patients show an increased propensity to habitual behaviors as they continue to respond to devalued outcomes in a cognitive stimulus-response-outcome association task. We use a neuro-computational model of hierarchically organized cortico-basal ganglia-thalamo-cortical loops to shed more light on habit formation and its alteration in Tourette patients. In our model, habitual behavior emerges from cortico-thalamic shortcut connections, where enhanced habit formation can be linked to faster plasticity in the shortcut or to a stronger feedback from the shortcut to the basal ganglia. We explore two major hypotheses of Tourette pathophysiology—local striatal disinhibition and increased dopaminergic modulation of striatal medium spiny neurons—as causes for altered shortcut activation. Both model changes altered shortcut functioning and resulted in higher rates of responses towards devalued outcomes, similar to what is observed in Tourette patients. We recommend future experimental neuroscientific studies to locate shortcuts between cortico-basal ganglia-thalamo-cortical loops in the human brain and study their potential role in health and disease.

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Houk, J. C., C. Bastianen, D. Fansler, A. Fishbach, D. Fraser, P. J. Reber, S. A. Roy, and L. S. Simo. "Action selection and refinement in subcortical loops through basal ganglia and cerebellum." Philosophical Transactions of the Royal Society B: Biological Sciences 362, no. 1485 (April 11, 2007): 1573–83. http://dx.doi.org/10.1098/rstb.2007.2063.

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Subcortical loops through the basal ganglia and the cerebellum form computationally powerful distributed processing modules (DPMs). This paper relates the computational features of a DPM's loop through the basal ganglia to experimental results for two kinds of natural action selection. First, functional imaging during a serial order recall task was used to study human brain activity during the selection of sequential actions from working memory. Second, microelectrode recordings from monkeys trained in a step-tracking task were used to study the natural selection of corrective submovements. Our DPM-based model assisted in the interpretation of puzzling data from both of these experiments. We come to posit that the many loops through the basal ganglia each regulate the embodiment of pattern formation in a given area of cerebral cortex. This operation serves to instantiate different kinds of action (or thought) mediated by different areas of cerebral cortex. We then use our findings to formulate a model of the aetiology of schizophrenia.

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Baston, Chiara, and Mauro Ursino. "A Biologically Inspired Computational Model of Basal Ganglia in Action Selection." Computational Intelligence and Neuroscience 2015 (2015): 1–24. http://dx.doi.org/10.1155/2015/187417.

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The basal ganglia (BG) are a subcortical structure implicated in action selection. The aim of this work is to present a new cognitive neuroscience model of the BG, which aspires to represent a parsimonious balance between simplicity and completeness. The model includes the 3 main pathways operating in the BG circuitry, that is, the direct (Go), indirect (NoGo), and hyperdirect pathways. The main original aspects, compared with previous models, are the use of a two-term Hebb rule to train synapses in the striatum, based exclusively on neuronal activity changes caused by dopamine peaks or dips, and the role of the cholinergic interneurons (affected by dopamine themselves) during learning. Some examples are displayed, concerning a few paradigmatic cases: action selection in basal conditions, action selection in the presence of a strong conflict (where the role of the hyperdirect pathway emerges), synapse changes induced by phasic dopamine, and learning new actions based on a previous history of rewards and punishments. Finally, some simulations show model working in conditions of altered dopamine levels, to illustrate pathological cases (dopamine depletion in parkinsonian subjects or dopamine hypermedication). Due to its parsimonious approach, the model may represent a straightforward tool to analyze BG functionality in behavioral experiments.

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Lörincz, A. "Static and Dynamic State Feedback Control Model of Basal Ganglia-Thalamocortical Loops." International Journal of Neural Systems 08, no. 03 (June 1997): 339–57. http://dx.doi.org/10.1142/s0129065797000343.

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It is argued that a novel control architecture, the Static and Dynamic State (SDS) feedback scheme, which utilizes speed-field tracking, exhibits global stability, and allows on-line tuning by any adaptation mechanism without canceling stability if certain structural conditions are met, can be viewed as a model of basal ganglia-thalamocortical loops since (1) the SDS scheme predicts the neuronal groups that fit neuronal classification in the supplementary motor area, the motor cortex and the putamen, (2) the structural stability conditions require parallel channels, a feature that these loops provide, and (3) the SDS scheme predicts two major disorders that can be identified as Parkinson's and Huntington's diseases. Simulations suggests that the basal ganglia work outside the realm of the stability condition allowed by the robustness of the scheme and required for increased computation speeds.

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Vitek, Jerrold L., and Luke A. Johnson. "Understanding Parkinson’s disease and deep brain stimulation: Role of monkey models." Proceedings of the National Academy of Sciences 116, no. 52 (December 23, 2019): 26259–65. http://dx.doi.org/10.1073/pnas.1902300116.

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Parkinson’s disease (PD) is a progressive neurodegenerative movement disorder affecting over 10 million people worldwide. In the 1930s and 1940s there was little understanding regarding what caused PD or how to treat it. In a desperate attempt to improve patients’ lives different regions of the neuraxis were ablated. Morbidity and mortality were common, but some patients’ motor signs improved with lesions involving the basal ganglia or thalamus. With the discovery ofl-dopa the advent of medical therapy began and surgical approaches became less frequent. It soon became apparent, however, that medical therapy was associated with side effects in the form of drug-induced dyskinesia and motor fluctuations and surgical therapies reemerged. Fortunately, during this time studies in monkeys had begun to lay the groundwork to understand the functional organization of the basal ganglia, and with the discovery of the neurotoxin MPTP a monkey model of PD had been developed. Using this model scientists were characterizing the physiological changes that occurred in the basal ganglia in PD and models of basal ganglia function and dysfunction were proposed. This work provided the rationale for the return of pallidotomy, and subsequently deep brain stimulation procedures. In this paper we describe the evolution of these monkey studies, how they provided a greater understanding of the pathophysiology underlying the development of PD and provided the rationale for surgical procedures, the search to understand mechanisms of DBS, and how these studies have been instrumental in understanding PD and advancing the development of surgical therapies for its treatment.

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Leasure, Audrey C., Kevin N. Sheth, Mary Comeau, Chad Aldridge, Bradford B. Worrall, Anastasia Vashkevich, Jonathan Rosand, et al. "Identification and Validation of Hematoma Volume Cutoffs in Spontaneous, Supratentorial Deep Intracerebral Hemorrhage." Stroke 50, no. 8 (August 2019): 2044–49. http://dx.doi.org/10.1161/strokeaha.118.023851.

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Background and Purpose— Clinical trials in spontaneous intracerebral hemorrhage (ICH) have used volume cutoffs as inclusion criteria to select populations in which the effects of interventions are likely to be the greatest. However, optimal volume cutoffs for predicting poor outcome in deep locations (thalamus versus basal ganglia) are unknown. Methods— We conducted a 2-phase study to determine ICH volume cutoffs for poor outcome (modified Rankin Scale score of 4–6) in the thalamus and basal ganglia. Cutoffs with optimal sensitivity and specificity for poor outcome were identified in the ERICH ([Ethnic/Racial Variations of ICH] study; derivation cohort) using receiver operating characteristic curves. The cutoffs were then validated in the ATACH-2 trial (Antihypertensive Treatment of Acute Cerebral Hemorrhage-2) by comparing the c-statistic of regression models for outcome (including dichotomized volume) in the validation cohort. Results— Of the 3000 patients enrolled in ERICH, 1564 (52%) had deep ICH, of whom 1305 (84%) had complete neuroimaging and outcome data (660 thalamic and 645 basal ganglia hemorrhages). Receiver operating characteristic curve analysis identified 8 mL in thalamic (area under the curve, 0.79; sensitivity, 73%; specificity, 78%) and 18 mL in basal ganglia ICH (area under the curve, 0.79; sensitivity, 70%; specificity, 83%) as optimal cutoffs for predicting poor outcome. The validation cohort included 834 (84%) patients with deep ICH and complete neuroimaging data enrolled in ATACH-2 (353 thalamic and 431 basal ganglia hemorrhages). In thalamic ICH, the c-statistic of the multivariable outcome model including dichotomized ICH volume was 0.80 (95% CI, 0.75–0.85) in the validation cohort. For basal ganglia ICH, the c-statistic was 0.81 (95% CI, 0.76–0.85) in the validation cohort. Conclusions— Optimal hematoma volume cutoffs for predicting poor outcome in deep ICH vary by the specific deep brain nucleus involved. Utilization of location-specific volume cutoffs may improve clinical trial design by targeting deep ICH patients that will obtain maximal benefit from candidate therapies.

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Chakravarthy, V. Srinivasa. "Do Basal Ganglia Amplify Willed Action by Stochastic Resonance? A Model." PLoS ONE 8, no. 11 (November 26, 2013): e75657. http://dx.doi.org/10.1371/journal.pone.0075657.

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Parent, A., M. Lévesque, and M. Parent. "A re-evaluation of the current model of the basal ganglia." Parkinsonism & Related Disorders 7, no. 3 (July 2001): 193–98. http://dx.doi.org/10.1016/s1353-8020(00)00058-4.

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Prescott, Tony J., Fernando M. Montes González, Kevin Gurney, Mark D. Humphries, and Peter Redgrave. "A robot model of the basal ganglia: Behavior and intrinsic processing." Neural Networks 19, no. 1 (January 2006): 31–61. http://dx.doi.org/10.1016/j.neunet.2005.06.049.

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Humphries, Mark D., and Kevin N. Gurney. "A pulsed neural network model of bursting in the basal ganglia." Neural Networks 14, no. 6-7 (July 2001): 845–63. http://dx.doi.org/10.1016/s0893-6080(01)00060-0.

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Connolly, Christopher I., and J. Brain Burns. "A new striatal model and its relationship to basal ganglia diseases." Neuroscience Research 16, no. 4 (May 1993): 271–74. http://dx.doi.org/10.1016/0168-0102(93)90037-q.

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Njap, Felix, Jens Christian Claussen, Andreas Moser, and Ulrich G. Hofmann. "Modeling effect of GABAergic current in a basal ganglia computational model." Cognitive Neurodynamics 6, no. 4 (May 4, 2012): 333–41. http://dx.doi.org/10.1007/s11571-012-9203-3.

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Federti, Enrica, Alessandro Matte, Veronica Riccardi, Kevin Peikert, Seth L. Alper, Adrian Danek, Ruth H. Walker, et al. "Adaptative Up-Regulation of PRX2 and PRX5 Expression Characterizes Brain from a Mouse Model of Chorea-Acanthocytosis." Antioxidants 11, no. 1 (December 29, 2021): 76. http://dx.doi.org/10.3390/antiox11010076.

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The peroxiredoxins (PRXs) constitute a ubiquitous antioxidant. Growing evidence in neurodegenerative disorders such as Parkinson’s disease (PD) or Alzheimer’s disease (AD) has highlighted a crucial role for PRXs against neuro-oxidation. Chorea-acanthocytosis/Vps13A disease (ChAc) is a devastating, life-shortening disorder characterized by acanthocytosis, neurodegeneration and abnormal proteostasis. We recently developed a Vps13a−/− ChAc-mouse model, showing acanthocytosis, neurodegeneration and neuroinflammation which could be restored by LYN inactivation. Here, we show in our Vps13a−/− mice protein oxidation, NRF2 activation and upregulation of downstream cytoprotective systems NQO1, SRXN1 and TRXR in basal ganglia. This was associated with upregulation of PRX2/5 expression compared to wild-type mice. PRX2 expression was age-dependent in both mouse strains, whereas only Vps13a−/− PRX5 expression was increased independent of age. LYN deficiency or nilotinib-mediated LYN inhibition improved autophagy in Vps13a−/− mice. In Vps13a−/−; Lyn−/− basal ganglia, absence of LYN resulted in reduced NRF2 activation and down-regulated expression of PRX2/5, SRXN1 and TRXR. Nilotinib treatment of Vps13a−/− mice reduced basal ganglia oxidation, and plasma PRX5 levels, suggesting plasma PRX5 as a possible ChAc biomarker. Our data support initiation of therapeutic Lyn inhibition as promptly as possible after ChAc diagnosis to minimize development of irreversible neuronal damage during otherwise inevitable ChAc progression.

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Schmidt, Robert, and Joshua D. Berke. "A Pause-then-Cancel model of stopping: evidence from basal ganglia neurophysiology." Philosophical Transactions of the Royal Society B: Biological Sciences 372, no. 1718 (February 27, 2017): 20160202. http://dx.doi.org/10.1098/rstb.2016.0202.

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Many studies have implicated the basal ganglia in the suppression of action impulses (‘stopping’). Here, we discuss recent neurophysiological evidence that distinct hypothesized processes involved in action preparation and cancellation can be mapped onto distinct basal ganglia cell types and pathways. We examine how movement-related activity in the striatum is related to a ‘Go’ process and how going may be modulated by brief epochs of beta oscillations. We then describe how, rather than a unitary ‘Stop’ process, there appear to be separate, complementary ‘Pause’ and ‘Cancel’ mechanisms. We discuss the implications of these stopping subprocesses for the interpretation of the stop-signal reaction time—in particular, some activity that seems too slow to causally contribute to stopping when assuming a single Stop processes may actually be fast enough under a Pause-then-Cancel model. Finally, we suggest that combining complementary neural mechanisms that emphasize speed or accuracy respectively may serve more generally to optimize speed–accuracy trade-offs. This article is part of the themed issue ‘Movement suppression: brain mechanisms for stopping and stillness’.

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Journal articles on the topic 'Basal ganglia model'

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