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Nature Reviews. Neuroscience Jun 2018The basal ganglia and the cerebellum are considered to be distinct subcortical systems that perform unique functional operations. The outputs of the basal ganglia and... (Review)
Review
The basal ganglia and the cerebellum are considered to be distinct subcortical systems that perform unique functional operations. The outputs of the basal ganglia and the cerebellum influence many of the same cortical areas but do so by projecting to distinct thalamic nuclei. As a consequence, the two subcortical systems were thought to be independent and to communicate only at the level of the cerebral cortex. Here, we review recent data showing that the basal ganglia and the cerebellum are interconnected at the subcortical level. The subthalamic nucleus in the basal ganglia is the source of a dense disynaptic projection to the cerebellar cortex. Similarly, the dentate nucleus in the cerebellum is the source of a dense disynaptic projection to the striatum. These observations lead to a new functional perspective that the basal ganglia, the cerebellum and the cerebral cortex form an integrated network. This network is topographically organized so that the motor, cognitive and affective territories of each node in the network are interconnected. This perspective explains how synaptic modifications or abnormal activity at one node can have network-wide effects. A future challenge is to define how the unique learning mechanisms at each network node interact to improve performance.
Topics: Animals; Basal Ganglia; Cerebellum; Humans; Models, Neurological; Motivation; Nervous System Diseases; Neural Pathways; Reward; Subthalamic Nucleus; Thalamus
PubMed: 29643480
DOI: 10.1038/s41583-018-0002-7 -
Trends in Neurosciences Oct 1989Basal ganglia disorders are a heterogeneous group of clinical syndromes with a common anatomic locus within the basal ganglia. To account for the variety of clinical... (Review)
Review
Basal ganglia disorders are a heterogeneous group of clinical syndromes with a common anatomic locus within the basal ganglia. To account for the variety of clinical manifestations associated with insults to various parts of the basal ganglia we propose a model in which specific types of basal ganglia disorders are associated with changes in the function of subpopulations of striatal projection neurons. This model is based on a synthesis of experimental animal and post-mortem human anatomic and neurochemical data. Hyperkinetic disorders, which are characterized by an excess of abnormal movements, are postulated to result from the selective impairment of striatal neurons projecting to the lateral globus pallidus. Hypokinetic disorders, such as Parkinson's disease, are hypothesized to result from a complex series of changes in the activity of striatal projection neuron subpopulations resulting in an increase in basal ganglia output. This model suggests that the activity of subpopulations of striatal projection neurons is differentially regulated by striatal afferents and that different striatal projection neuron subpopulations may mediate different aspects of motor control.
Topics: Basal Ganglia; Basal Ganglia Diseases; Humans; Movement Disorders
PubMed: 2479133
DOI: 10.1016/0166-2236(89)90074-x -
Neuron Nov 2008The dorsal striatum, which consists of the caudate and putamen, is the gateway to the basal ganglia. It receives convergent excitatory afferents from cortex and thalamus... (Review)
Review
The dorsal striatum, which consists of the caudate and putamen, is the gateway to the basal ganglia. It receives convergent excitatory afferents from cortex and thalamus and forms the origin of the direct and indirect pathways, which are distinct basal ganglia circuits involved in motor control. It is also a major site of activity-dependent synaptic plasticity. Striatal plasticity alters the transfer of information throughout basal ganglia circuits and may represent a key neural substrate for adaptive motor control and procedural memory. Here, we review current understanding of synaptic plasticity in the striatum and its role in the physiology and pathophysiology of basal ganglia function.
Topics: Animals; Basal Ganglia; Basal Ganglia Diseases; Cerebral Cortex; Humans; Memory; Movement; Neostriatum; Neural Pathways; Neuronal Plasticity; Synaptic Transmission; Thalamus
PubMed: 19038213
DOI: 10.1016/j.neuron.2008.11.005 -
Seminars in Pediatric Neurology Apr 2018Movement disorders typically arise from dysfunction of the basal ganglia (BG), cerebellum, or both. The BG-a group of deep, subcortical structures-form complex circuits... (Review)
Review
Movement disorders typically arise from dysfunction of the basal ganglia (BG), cerebellum, or both. The BG-a group of deep, subcortical structures-form complex circuits that shape motor control and motor learning, as well as limbic and associative functions. In this article, we summarize the anatomy and physiology of the BG and cerebellum, and briefly highlight the clinical syndromes that may arise in the context of their injury or dysfunction.
Topics: Animals; Basal Ganglia; Humans; Movement Disorders; Neural Pathways; Syndrome
PubMed: 29735113
DOI: 10.1016/j.spen.2017.12.005 -
Cold Spring Harbor Perspectives in... Dec 2012The "basal ganglia" refers to a group of subcortical nuclei responsible primarily for motor control, as well as other roles such as motor learning, executive functions...
The "basal ganglia" refers to a group of subcortical nuclei responsible primarily for motor control, as well as other roles such as motor learning, executive functions and behaviors, and emotions. Proposed more than two decades ago, the classical basal ganglia model shows how information flows through the basal ganglia back to the cortex through two pathways with opposing effects for the proper execution of movement. Although much of the model has remained, the model has been modified and amplified with the emergence of new data. Furthermore, parallel circuits subserve the other functions of the basal ganglia engaging associative and limbic territories. Disruption of the basal ganglia network forms the basis for several movement disorders. This article provides a comprehensive account of basal ganglia functional anatomy and chemistry and the major pathophysiological changes underlying disorders of movement. We try to answer three key questions related to the basal ganglia, as follows: What are the basal ganglia? What are they made of? How do they work? Some insight on the canonical basal ganglia model is provided, together with a selection of paradoxes and some views over the horizon in the field.
Topics: Basal Ganglia; Cerebral Cortex; Emotions; Executive Function; Humans; Lewy Bodies; Neural Pathways; Neurons, Afferent; Neurons, Efferent; Psychomotor Performance; Thalamus
PubMed: 23071379
DOI: 10.1101/cshperspect.a009621 -
Nature Jul 2010Neural circuits of the basal ganglia are critical for motor planning and action selection. Two parallel basal ganglia pathways have been described, and have been...
Neural circuits of the basal ganglia are critical for motor planning and action selection. Two parallel basal ganglia pathways have been described, and have been proposed to exert opposing influences on motor function. According to this classical model, activation of the 'direct' pathway facilitates movement and activation of the 'indirect' pathway inhibits movement. However, more recent anatomical and functional evidence has called into question the validity of this hypothesis. Because this model has never been empirically tested, the specific function of these circuits in behaving animals remains unknown. Here we report direct activation of basal ganglia circuitry in vivo, using optogenetic control of direct- and indirect-pathway medium spiny projection neurons (MSNs), achieved through Cre-dependent viral expression of channelrhodopsin-2 in the striatum of bacterial artificial chromosome transgenic mice expressing Cre recombinase under control of regulatory elements for the dopamine D1 or D2 receptor. Bilateral excitation of indirect-pathway MSNs elicited a parkinsonian state, distinguished by increased freezing, bradykinesia and decreased locomotor initiations. In contrast, activation of direct-pathway MSNs reduced freezing and increased locomotion. In a mouse model of Parkinson's disease, direct-pathway activation completely rescued deficits in freezing, bradykinesia and locomotor initiation. Taken together, our findings establish a critical role for basal ganglia circuitry in the bidirectional regulation of motor behaviour and indicate that modulation of direct-pathway circuitry may represent an effective therapeutic strategy for ameliorating parkinsonian motor deficits.
Topics: Animals; Basal Ganglia; Channelrhodopsins; Chromosomes, Artificial, Bacterial; Disease Models, Animal; Gait; Hypokinesia; Integrases; Mice; Mice, Transgenic; Models, Neurological; Motor Activity; Neostriatum; Neural Pathways; Neurons; Oxidopamine; Parkinson Disease; Psychomotor Performance; Receptors, Dopamine
PubMed: 20613723
DOI: 10.1038/nature09159 -
Proceedings of the Japan Academy.... 2018Involuntary movements and parkinsonism have been interesting and important topics in neurology since the last century. The development of anatomical and physiological... (Review)
Review
Involuntary movements and parkinsonism have been interesting and important topics in neurology since the last century. The development of anatomical and physiological studies of the neural circuitry of motor systems has encouraged the study of movement disorders by means of pathophysiology and brain imaging.Multichannel electromyography from affected muscles has generated objective and analytical data on chorea, ballism, athetosis, and dystonia. Studies using floor reaction forces revealed the pathophysiology of freezing of gait in parkinsonism. Akinesia and bradykinesia are attributable to dysfunctions in the basal ganglia, frontal lobe, and parieto-occipital visual association cortex.Reciprocal innervation is an essential mechanism of smooth voluntary movement. Spinal reflexes on reciprocal innervation has been investigated in awake humans, and the pathophysiology of spasticity and Parkinson's disease were revealed as a result. Clinical applications for the treatment and evaluation of status have been developed.For future studies, detailed neural mechanisms underlying the development of motor disorders in basal ganglia diseases and recovery by interventions including surgery and neurorehabilitation are important.
Topics: Basal Ganglia; Humans; Movement Disorders; Posture
PubMed: 30078828
DOI: 10.2183/pjab.94.019 -
Social Cognitive and Affective... Jul 2020The basal ganglia (BG) and the cerebellum historically have been relegated to a functional role in producing or modulating motor output. Recent research, however, has... (Review)
Review
The basal ganglia (BG) and the cerebellum historically have been relegated to a functional role in producing or modulating motor output. Recent research, however, has emphasized the importance of these subcortical structures in multiple functional domains, including affective processes such as emotion recognition, subjective feeling elicitation and reward valuation. The pathways through the thalamus that connect the BG and cerebellum directly to each other and with extensive regions of the cortex provide a structural basis for their combined influence on limbic function. By regulating cortical oscillations to guide learning and strengthening rewarded behaviors or thought patterns to achieve a desired goal state, these regions can shape the way an individual processes emotional stimuli. This review will discuss the basic structure and function of the BG and cerebellum and propose an updated view of their functional role in human affective processing.
Topics: Basal Ganglia; Cerebellum; Emotions; Humans; Learning; Motivation; Neural Pathways; Neuroimaging
PubMed: 32507876
DOI: 10.1093/scan/nsaa076 -
The Neuroscientist : a Review Journal... Jun 2017The 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... (Review)
Review
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.
Topics: Animals; Basal Ganglia; Humans; Models, Neurological; Movement; Neural Pathways
PubMed: 27306757
DOI: 10.1177/1073858416654115 -
Progress in Brain Research 2007This is the introductory chapter to an edited volume comprising 18 chapters written by 38 specially selected authors covering the anatomy, physiology,... (Review)
Review
This is the introductory chapter to an edited volume comprising 18 chapters written by 38 specially selected authors covering the anatomy, physiology, biochemistry/pharmacology and behavioral aspects of GABA in the basal ganglia. In this chapter the various nuclei of the basal ganglia are defined and their cellular structure, connections and function reviewed in brief in order to provide an orientation for the subsequent 17 chapters.
Topics: Animals; Basal Ganglia; Corpus Striatum; Humans; Neural Inhibition; Neural Pathways; Neurotransmitter Agents; Substantia Nigra; Subthalamic Nucleus; Synaptic Transmission; gamma-Aminobutyric Acid
PubMed: 17499105
DOI: 10.1016/S0079-6123(06)60001-0