Organization of the Globus Pallidus

Kita, Hitoshi; Jaeger, Dieter

doi:10.1016/b978-0-12-802206-1.00013-1

Cited by 19 publications

(14 citation statements)

References 154 publications

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“…1). The globus pallidus external segment (GPe) receives its two major inputs from STN and striatal iSPNs (Kita and Jaeger 2016). Interesting, however, all dSPNs projecting to the GPi appear to send axon collaterals to the GPe (Wu et al 2000).…”

Section: The Pallidal–subthalamic Networkmentioning

confidence: 99%

“…The majority of GPe neurons are GABAergic projection neurons whose main targets are other basal ganglia nuclei (Kita and Jaeger 2016). The output from GPe involves distinct cell groups, that is, prototypical neurons with strong projections to the STN, and the so-called arkypallidal neurons projecting to both SPNs and striatal fast-spiking interneurons (Gittis et al 2014).…”

Section: The Pallidal–subthalamic Networkmentioning

confidence: 99%

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On the neuronal circuitry mediating l-DOPA-induced dyskinesia

2018

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With the advent of rodent models of l-DOPA-induced dyskinesia (LID), a growing literature has linked molecular changes in the striatum to the development and expression of abnormal involuntary movements. Changes in information processing at the striatal level are assumed to impact on the activity of downstream basal ganglia nuclei, which in turn influence brain-wide networks, but very little is actually known about systems-level mechanisms of dyskinesia. As an aid to approach this topic, we here review the anatomical and physiological organisation of cortico-basal ganglia-thalamocortical circuits, and the changes affecting these circuits in animal models of parkinsonism and LID. We then review recent findings indicating that an abnormal cerebellar compensation plays a causal role in LID, and that structures outside of the classical motor circuits are implicated too. In summarizing the available data, we also propose hypotheses and identify important knowledge gaps worthy of further investigation. In addition to informing novel therapeutic approaches, the study of LID can provide new clues about the interplay between different brain circuits in the control of movement.

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Section: The Pallidal–subthalamic Networkmentioning

confidence: 99%

Section: The Pallidal–subthalamic Networkmentioning

confidence: 99%

On the neuronal circuitry mediating l-DOPA-induced dyskinesia

2018

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“…The BLeG parcellation instead divides the globus pallidus into three regions. But recent work suggests that the globus pallidus does, in fact, divide into three regions: the external segment, the lateral internal segment, and the medial internal segment (Kita, 2010). Gordon et al (2014) also previously showed increased within-parcel homogeneity of functional connectivity patterns for their parcellation compared to spatially randomized variants of it.…”

Section: Discussionmentioning

confidence: 99%

A sub+ cortical fMRI-based surface parcellation

Lewis

Bezgin

Fonov

et al. 2019

Preprint

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Both the cortex and the subcortical structures are organized into a large number of distinct areas reflecting functional and cytoarchitectonic differences. Mapping these areas is of fundamental importance to neuroscience.A central obstacle to this task is the inaccuracy associated with mapping results from individuals into a common space. The vast individual differences in morphology pose a serious problem for volumetric registration. Surfacebased approaches fare substantially better, but have thus far been used only for cortical parcellation. We extend this surface-based approach to include also the subcortical deep gray-matter structures. Using the life-span data from the Enhanced Nathan Klein Institute -Rockland Sample, comprised of data from 590 individuals from 6 to 85 years of age, we generate a functional parcellation of both the cortical and subcortical surfaces. To assess this extended parcellation, we show that our extended functional parcellation provides greater homogeneity of functional connectivity patterns than * These two authors contributed equally.do arbitrary parcellations matching in the number and size of parcels. We also show that our subcortical parcels align with known subnuclei. Further, we show that this parcellation is appropriate for use with data from other modalities; we generate cortical and subcortical white/gray contrast measures for this same dataset, and draw on the fact that areal differences are evident in the relation of white/gray contrast to age, to sex, to brain volume, and to interactions of these terms; we show that our extended functional parcellation provides an improved fit to the complexity of the life-span changes in the white/gray contrast data compared to arbitrary parcellations matching in the number and size of parcels. We provide our extended functional parcellation for the use of the neuroimaging community.

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“…The 662 instantaneous phase of each population was estimated by applying the Hilbert transform 663 to the average somatic membrane voltage of cells in the population, after band-pass 664 filtering using a neutral-phase filter (Butterworth filter, 4th order, command sosfiltfilt) 665 in an 8 Hz wide frequency band centered on the dominant oscillation frequency. For 666 populations that were modeled as surrogate spike trains (cortex and striatum), artificial 667 membrane voltage signals were first constructed by convolving the spike trains with a [46,47] proximal [15] GPe 57 [93] 883 [94] proximal [95] depression [93] 4 ms [96] strengthened [92] prolonged decay [74] GPe GPe proximal,somatic [49,97] depression [82] strengthened [82] STN 135 [98] dendritic,distal [99] facilitation, 2 ms [100] strengthened [78] depression [51] MSN 10622 [98] dendritic, distal [49] facilitation [82] 5 ms [100] Table 2. STN model intrinsic current equations from Gillies and Willshaw [43].…”

Section: Signal Analysis 657mentioning

confidence: 99%

“…1-4.3). Cortical patterning of neural activity in the STN-GPe network via the 97 hyperdirect pathway was then investigated by modeling cortical input to the STN 98 inputs as periodically bursting spike trains. To investigate whether changing the 99 excitation-inhibition balance in STN and GPe contributed to changes in spontaneous 100 synchronization and functional coupling between nuclei, we shifted the ratio of 101 excitation and inhibition by systematically altering the strength of individual 102 projections between nuclei.…”

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confidence: 99%

Autonomous oscillations and phase-locking in a biophysically detailed model of the STN-GPe network

Koelman

Lowery

2019

Preprint

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The aim of this study was to understand the relative role of autonomous oscillations and patterning by exogenous oscillatory inputs in the generation of pathological oscillatory activity within the subthalamic nucleus (STN) -external globus pallidus (GPe) network in Parkinson's disease. A biophysically detailed model that accounts for the integration of synaptic currents and their interaction with intrinsic membrane currents in dendritic structures within the STN and GPe was developed. The model was used to investigate the development of beta-band synchrony and bursting within the STN-GPe network by changing the balance of excitation and inhibition in both nuclei, and by adding exogenous oscillatory inputs with varying phase relationships through the hyperdirect cortico-subthalamic and indirect striato-pallidal pathways. The model showed an intrinsic susceptibility to beta-band oscillations that was manifest in weak autonomously generated oscillations within the STN-GPe network and in selective amplification of exogenous beta-band synaptic inputs near the network's endogenous oscillation frequency. The resonant oscillation frequency was determined by the net level of excitatory drive in the loop. Intrinsically generated oscillations were too weak to support a pacemaker role for the STN-GPe network, however, they were considerably amplified by sparse cortical beta inputs when their frequency range overlapped and were further amplified by striatal beta inputs that promoted anti-phase firing of the cortex and GPe, resulting in maximum transient inhibition of STN neurons. The model elucidates a mechanism of cortical patterning of the STN-GPe network through feedback inhibition whereby intrinsic susceptibility to beta-band oscillations can lead to phase locked spiking under parkinsonian conditions. These results point to resonance of endogenous oscillations with exogenous patterning of the STN-GPe network as a mechanism of pathological synchronization, and a role for the pallido-striatal feedback loop in amplifying beta oscillations. Author summaryExaggerated beta-frequency neuronal synchrony is observed throughout the basal ganglia in Parkinson's disease and is reduced with medication and during deep brain stimulation. The power of beta-band oscillations is increasingly used as a biomarker to guide antiparkinsonian therapies. Despite their importance as a clinical target, the mechanisms by which pathological beta-band oscillations are generated are not yet clearly understood. In vitro electrophysiological recordings support a theory of enhanced phase locking of the reciprocally connected subthalamo-pallidal network to beta-band April 11, 2019 1/33 cortical inputs but this has not yet been clearly demonstrated in a model. We present a new model of the subthalamo-pallidal network consisting of biophysically detailed cell models that captures the interaction between synaptic and intrinsic currents in dendritic structures. The model shows how phase locking of subthalamic and pallidal neurons and exaggerated bursting in s...

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Organization of the Globus Pallidus

Cited by 19 publications

References 154 publications

On the neuronal circuitry mediating l-DOPA-induced dyskinesia

On the neuronal circuitry mediating l-DOPA-induced dyskinesia

A sub+ cortical fMRI-based surface parcellation

Autonomous oscillations and phase-locking in a biophysically detailed model of the STN-GPe network

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