Movement-Related Discharge in the Macaque Globus Pallidus during High-Frequency Stimulation of the Subthalamic Nucleus

Zimnik, Andrew; Nora, Gerald J.; Desmurget, Michel; Turner, Robert S.

doi:10.1523/jneurosci.4899-14.2015

Cited by 27 publications

(27 citation statements)

References 82 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…During locomotion, we found that Ca 2+ transients reliably occurred approximately 100 ms before the onset of movement and then persisted throughout the whole process of each movement. This activity was similar to a previously defined activity in the monkey motor cortex, referred to as perimovement activity (Churchland et al, 2006, 2010; Kemere et al, 2008; Zimnik et al, 2015). Perimovement activity is defined as neuronal activity occurring approximately 100 ms before, during and just after the movement and was initially found using electrophysiological recordings.…”

Section: Discussionsupporting

confidence: 87%

Locomotion-Related Population Cortical Ca2+ Transients in Freely Behaving Mice

Zhang

Yao

et al. 2017

Front. Neural Circuits

View full text Add to dashboard Cite

Locomotion involves complex neural activity throughout different cortical and subcortical networks. The primary motor cortex (M1) receives a variety of projections from different brain regions and is responsible for executing movements. The primary visual cortex (V1) receives external visual stimuli and plays an important role in guiding locomotion. Understanding how exactly the M1 and the V1 are involved in locomotion requires recording the neural activities in these areas in freely moving animals. Here, we used an optical fiber-based method for the real-time monitoring of neuronal population activities in freely moving mice. We combined the bulk loading of a synthetic Ca2+ indicator and the optical fiber-based Ca2+ recordings of neuronal activities. An optical fiber 200 μm in diameter can detect the coherent activity of a subpopulation of neurons. In layer 5 of the M1 and V1, we showed that population Ca2+ transients reliably occurred preceding the impending locomotion. Interestingly, the M1 Ca2+ transients started ~100 ms earlier than that in V1. Furthermore, the population Ca2+ transients were robustly correlated with head movements. Thus, our work provides a simple but efficient approach for monitoring the cortical Ca2+ activity of a local cluster of neurons during locomotion in freely moving animals.

show abstract

Section: Discussionsupporting

confidence: 87%

Locomotion-Related Population Cortical Ca2+ Transients in Freely Behaving Mice

Zhang

Yao

et al. 2017

Front. Neural Circuits

View full text Add to dashboard Cite

show abstract

“…However, recent work in the NHP demonstrated that pallidal information about motor activity may be reduced by symptom-alleviating DBS [30], and that the eliminated information may relate exclusively to parkinsonian symptoms and not to intentioned motor commands [33]. Excess pallidal information reflecting a loss of motor selectivity may convey the very instructions that dictate motor symptoms.…”

Section: Discussionmentioning

confidence: 99%

Information in pallidal neurons increases with parkinsonian severity

Dorval

Muralidharan

Jensen

et al. 2015

Parkinsonism & Related Disorders

View full text Add to dashboard Cite

Introduction The motor symptoms of Parkinson's disease (PD) present with pathological neuronal activity in the basal ganglia. Although neuronal firing rate changes in the globus pallidus internus (GPi) and externus (GPe) are reported to underlie the development of PD motor signs, firing rates change inconsistently, vary confoundingly with some therapies, and are poor indicators of symptom severity. Methods We explored the relationship between parkinsonian symptom severity and the effectiveness with which pallidal neurons transmit information. We quantify neuronal entropy and information – alternatives to firing rate and correlations respectively – in and between GPe and GPi neurons using a progressive, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, non-human primate model of PD. Results Neuronal entropy and symptom severity were not linearly correlated: in both pallidal segments, entropy increased from naive to moderate parkinsonism, but decreased with further progression to the severely parkinsonian condition. In contrast, information transmitted from GPe to GPi increased consistently with symptom severity. Furthermore, antidromic information from GPi to GPe increased substantially with symptom severity. Together, these findings suggest that as parkinsonian severity increases, more and more information enters GPe and GPi from common sources, diminishing the relative importance of the orthodromic GPe to GPi connection. Conclusions With parkinsonian progression, the direct and indirect pathways lose their independence and start to convey redundant information. We hypothesize that a loss of parallel processing impairs the ability of the network to select and implement motor commands, thus promoting the hypokinetic symptoms of PD.

show abstract

“…Recent studies in awake behaving primates, however, have provided some evidence that physiologic sensorimotor-related discharge in the basal ganglia output nucleus (GPi) may be at least partially maintained during STN or pallidal DBS [266,287]. These studies have suggested that DBS may act as a Bselective filter^that permits some sensorimotor-related modulation of the activity of neurons in the stimulated area, while eliminating transmission of pathological low-frequency neuronal activity patterns.…”

Section: Dbs Mechanism Of Actionmentioning

confidence: 99%

Deep Brain Stimulation for Movement Disorders of Basal Ganglia Origin: Restoring Function or Functionality?

2016

View full text Add to dashboard Cite

Deep brain stimulation (DBS) is highly effective for both hypo-and hyperkinetic movement disorders of basal ganglia origin. The clinical use of DBS is, in part, empiric, based on the experience with prior surgical ablative therapies for these disorders, and, in part, driven by scientific discoveries made decades ago. In this review, we consider anatomical and functional concepts of the basal ganglia relevant to our understanding of DBS mechanisms, as well as our current understanding of the pathophysiology of two of the most commonly DBS-treated conditions, Parkinson's disease and dystonia. Finally, we discuss the proposed mechanism(s) of action of DBS in restoring function in patients with movement disorders. The signs and symptoms of the various disorders appear to result from signature disordered activity in the basal ganglia output, which disrupts the activity in thalamocortical and brainstem networks. The available evidence suggests that the effects of DBS are strongly dependent on targeting sensorimotor portions of specific nodes of the basal gangliathalamocortical motor circuit, that is, the subthalamic nucleus and the internal segment of the globus pallidus. There is little evidence to suggest that DBS in patients with movement disorders restores normal basal ganglia functions (e.g., their role in movement or reinforcement learning). Instead, it appears that high-frequency DBS replaces the abnormal basal ganglia output with a more tolerable pattern, which helps to restore the functionality of downstream networks.

show abstract

Movement-Related Discharge in the Macaque Globus Pallidus during High-Frequency Stimulation of the Subthalamic Nucleus

Cited by 27 publications

References 82 publications

Locomotion-Related Population Cortical Ca2+ Transients in Freely Behaving Mice

Locomotion-Related Population Cortical Ca2+ Transients in Freely Behaving Mice

Information in pallidal neurons increases with parkinsonian severity

Deep Brain Stimulation for Movement Disorders of Basal Ganglia Origin: Restoring Function or Functionality?

Contact Info

Product

Resources

About