scholarly journals How Basal Ganglia Outputs Generate Behavior

2014 ◽  
Vol 2014 ◽  
pp. 1-28 ◽  
Author(s):  
Henry H. Yin
Keyword(s):  
Basal Ganglia ◽  
Internal Reference ◽  
New Model ◽  
Transition Control ◽  
Sensorimotor Transformations ◽  
Reference Signals ◽  
Voluntary Behavior ◽  
Functional Hierarchy ◽  
Subcortical Nuclei ◽  
Output Neurons

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.

scholarly journals The Basal Ganglia in Action

2016 ◽  
Vol 23 (3) ◽  
pp. 299-313 ◽  
Author(s):  
Henry H. Yin
Keyword(s):  
Basal Ganglia ◽  
Control Systems ◽  
Position Control ◽  
Brain Disorders ◽  
Transition Control ◽  
Feedback Control Systems ◽  
Subcortical Nuclei ◽  
Negative Feedback Control ◽  
The Brain

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.

scholarly journals Detection of cannabinoid receptors CB1 and CB2 within basal ganglia output neurons in macaques: changes following experimental parkinsonism

2014 ◽  
Vol 220 (5) ◽  
pp. 2721-2738 ◽  
Author(s):  
Salvador Sierra ◽  
Natasha Luquin ◽  
Alberto J. Rico ◽  
Virginia Gómez-Bautista ◽  
Elvira Roda ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Cannabinoid Receptors ◽  
Experimental Parkinsonism ◽  
Output Neurons

scholarly journals Activation of Nigral and Pallidal Dopamine D1-Like Receptors Modulates Basal Ganglia Outflow in Monkeys

2007 ◽  
Vol 98 (3) ◽  
pp. 1489-1500 ◽  
Author(s):  
Michele A. Kliem ◽  
Nigel T. Maidment ◽  
Larry C. Ackerson ◽  
Sugong Chen ◽  
Yoland Smith ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Rhesus Monkeys ◽  
Receptor Agonist ◽  
Gaba Release ◽  
Aminobutyric Acid ◽  
Substantia Nigra Pars Reticulata ◽  
Axon Terminals ◽  
Discharge Rates ◽  
Dopaminergic Tone ◽  
Output Neurons

Studies of the effects of dopamine in the basal ganglia have focused on the striatum, whereas the functions of dopamine released in the internal pallidal segment (GPi) or in the substantia nigra pars reticulata (SNr) have received less attention. Anatomic and biochemical investigations have demonstrated the presence of dopamine D1-like receptors (D1LRs) in GPi and SNr, which are primarily located on axons and axon terminals of the GABAergic striatopallidal and striatonigral afferents. Our experiments assessed the effects of D1LR ligands in GPi and SNr on local γ-aminobutyric acid (GABA) levels and neuronal activity in these nuclei in rhesus monkeys. Microinjections of the D1LR receptor agonist SKF82958 into GPi and SNr significantly reduced discharge rates in GPi and SNr, whereas injections of the D1LR antagonist SCH23390 increased firing in the majority of GPi neurons. D1LR activation also increased bursting and oscillations in neuronal discharge in the 3- to 15-Hz band in both structures, whereas D1LR blockade had the opposite effects in GPi. Microdialysis measurements of GABA concentrations in GPi and SNr showed that the D1LR agonist increased the level of the transmitter. Both findings are compatible with the hypothesis that D1LR activation leads to GABA release from striatopallidal or striatonigral afferents, which may secondarily reduce firing of basal ganglia output neurons. The antagonist experiments suggest that a dopaminergic “tone” exists in GPi. Our results support the finding that D1LR activation may have powerful effects on GPi and SNr neurons and may mediate some of the effects of dopamine replacement therapies in Parkinson's disease.

scholarly journals Action, time and the basal ganglia

2014 ◽  
Vol 369 (1637) ◽  
pp. 20120473 ◽  
Author(s):  
Henry H. Yin
Keyword(s):  
Basal Ganglia ◽  
Neurological Disorders ◽  
Rate Of Change ◽  
Feedback Circuit ◽  
Velocity Control ◽  
Movement Velocity ◽  
Reference Signals ◽  
Action Time ◽  
Recent Experimental Work ◽  
Action Timing

The ability to control the speed of movement is compromised in neurological disorders involving the basal ganglia, a set of subcortical cerebral nuclei that receive prominent dopaminergic projections from the midbrain. For example, bradykinesia, slowness of movement, is a major symptom of Parkinson's disease, whereas rapid tics are observed in patients with Tourette syndrome. Recent experimental work has also implicated dopamine (DA) and the basal ganglia in action timing. Here, I advance the hypothesis that the basal ganglia control the rate of change in kinaesthetic perceptual variables. In particular, the sensorimotor cortico-basal ganglia network implements a feedback circuit for the control of movement velocity. By modulating activity in this network, DA can change the gain of velocity reference signals. The lack of DA thus reduces the output of the velocity control system which specifies the rate of change in body configurations, slowing the transition from one body configuration to another.

scholarly journals Dopaminergic modulation of basal ganglia output through coupled excitation–inhibition

2017 ◽  
Vol 114 (22) ◽  
pp. 5713-5718 ◽  
Author(s):  
Agata Budzillo ◽  
Alison Duffy ◽  
Kimberly E. Miller ◽  
Adrienne L. Fairhall ◽  
David J. Perkel
Keyword(s):  
Basal Ganglia ◽  
Dynamic Change ◽  
Vocal Learning ◽  
Synaptic Connections ◽  
Biophysical Mechanism ◽  
Output Neurons ◽  
Neural Variability ◽  
Vocal Variability ◽  
Selection Of

Learning and maintenance of skilled movements require exploration of motor space and selection of appropriate actions. Vocal learning and social context-dependent plasticity in songbirds depend on a basal ganglia circuit, which actively generates vocal variability. Dopamine in the basal ganglia reduces trial-to-trial neural variability when the bird engages in courtship song. Here, we present evidence for a unique, tonically active, excitatory interneuron in the songbird basal ganglia that makes strong synaptic connections onto output pallidal neurons, often linked in time with inhibitory events. Dopamine receptor activity modulates the coupling of these excitatory and inhibitory events in vitro, which results in a dynamic change in the synchrony of a modeled population of basal ganglia output neurons receiving excitatory and inhibitory inputs. The excitatory interneuron thus serves as one biophysical mechanism for the introduction or modulation of neural variability in this circuit.

Dopamine depletion induced up-regulation of HCN3 enhances rebound excitability of basal ganglia output neurons

2009 ◽  
Vol 34 (1) ◽  
pp. 178-188 ◽  
Author(s):  
Bernhard H. Meurers ◽  
Gustavo Dziewczapolski ◽  
Anton Bittner ◽  
Tao Shi ◽  
Fredrik Kamme ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Dopamine Depletion ◽  
Output Neurons

scholarly journals Kv3-Like Potassium Channels Are Required for Sustained High-Frequency Firing in Basal Ganglia Output Neurons

2011 ◽  
Vol 105 (2) ◽  
pp. 554-570 ◽  
Author(s):  
Shengyuan Ding ◽  
Shannon G. Matta ◽  
Fu-Ming Zhou
Keyword(s):  
Basal Ganglia ◽  
High Frequency ◽  
Movement Control ◽  
Dopamine Neurons ◽  
Pcr Analysis ◽  
Delayed Rectifier ◽  
Projection Neurons ◽  
Gaba Neurons ◽  
Fast Spiking ◽  
Output Neurons

The GABA projection neurons in the substantial nigra pars reticulata (SNr) are key output neurons of the basal ganglia motor control circuit. These neurons fire sustained high-frequency, short-duration spikes that provide a tonic inhibition to their targets and are critical to movement control. We hypothesized that a robust voltage-activated K+ conductance that activates quickly and resists inactivation is essential to the remarkable fast-spiking capability in these neurons. Semi-quantitative RT-PCR (qRT-PCR) analysis on laser capture-microdissected nigral neurons indicated that mRNAs for Kv3.1 and Kv3.4, two key subunits for forming high activation threshold, fast-activating, slow-inactivating, 1 mM tetraethylammonium (TEA)-sensitive, fast delayed rectifier ( IDR-fast) type Kv channels, are more abundant in fast-spiking SNr GABA neurons than in slow-spiking nigral dopamine neurons. Nucleated patch clamp recordings showed that SNr GABA neurons have a strong Kv3-like IDR-fast current sensitive to 1 mM TEA that activates quickly at depolarized membrane potentials and is resistant to inactivation. IDR-fast is smaller in nigral dopamine neurons. Pharmacological blockade of IDR-fast by 1 mM TEA impaired the high-frequency firing capability in SNr GABA neurons. Taken together, these results indicate that Kv3-like channels mediating fast-activating, inactivation-resistant IDR-fast current are critical to the sustained high-frequency firing in SNr GABA projection neurons and hence movement control.

scholarly journals Using multi-echo simultaneous multi-slice (SMS) EPI to improve functional MRI of the subcortical nuclei of the basal ganglia at ultra-high field (7T)

NeuroImage ◽  
2018 ◽  
Vol 172 ◽  
pp. 886-895 ◽  
Author(s):  
Alexander M. Puckett ◽  
Saskia Bollmann ◽  
Benedikt A. Poser ◽  
Jake Palmer ◽  
Markus Barth ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Functional Mri ◽  
High Field ◽  
Ultra High Field ◽  
Subcortical Nuclei
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