Effects of L-dopa priming on cortical high beta and high gamma oscillatory activity in a rodent model of Parkinson's disease

Dupre, Kristin B.; Cruz, Ana V.; McCoy, Alex J.; Delaville, Claire; Gerber, Colin M.; Eyring, Katherine W.; Walters, Judith R.

doi:10.1016/j.nbd.2015.11.009

Cited by 65 publications

(70 citation statements)

References 82 publications

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“…By now, the association between high-frequency LFP oscillations and LID has been verified in several independent studies. For example, Judie Walters’ lab has found that the power of cortical 80 Hz oscillations gradually increases as dyskinetic behaviors become more severe during a course of l -DOPA treatment (Dupre et al 2016). The link between narrowband gamma and LID is currently being explored at several levels (Delaville et al 2015; Belic et al 2016; Dupre et al 2016, 2015; Tamte et al 2016).…”

Section: Cortical Dynamicsmentioning

confidence: 99%

“…For example, Judie Walters’ lab has found that the power of cortical 80 Hz oscillations gradually increases as dyskinetic behaviors become more severe during a course of l -DOPA treatment (Dupre et al 2016). The link between narrowband gamma and LID is currently being explored at several levels (Delaville et al 2015; Belic et al 2016; Dupre et al 2016, 2015; Tamte et al 2016). Because cortical activity is under strong control of thalamic input, it is possible that an aberrant thalamic input could be driving fast cortical oscillations in LID (Dupre et al 2015).…”

Section: Cortical Dynamicsmentioning

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: Cortical Dynamicsmentioning

confidence: 99%

Section: Cortical Dynamicsmentioning

confidence: 99%

On the neuronal circuitry mediating l-DOPA-induced dyskinesia

2018

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“…Beta oscillations are viewed as normal for the resting or Bidling^state; their reduction with movement onset may play a role in allowing movement to take place. Conceivably increased or persistent beta-band oscillations could disrupt movement initiation and execution, or may reflect the underlying impairment of movement initiation or even be a compensatory mechanism [164].…”

Section: Pathophysiology Of Parkinsonism and Dystoniamentioning

confidence: 99%

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

2016

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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.

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“…Similar results were obtained for 40 Hz and 80 Hz input frequencies in the case of low (red curve) and high (blue curve) firing rates of FSIs. Previous experimental work [17,39,57] has demonstrated the importance of 80 Hz corticostriatal oscillations for shaping neuronal interactions between cortex and striatum. Recently, it has been found that the FSIs Interplay between periodic stimulation and GABAergic inhibition in striatal network oscillations fire in relation to very high cortical frequencies [43].…”

Section: Propagation Of Cortical Oscillations In the Striatal Networkmentioning

confidence: 99%

Interplay between periodic stimulation and GABAergic inhibition in striatal network oscillations

Belić

Kumar

Kotaleski

2016

Preprint

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Network oscillations are ubiquitous across many brain regions. In the basal ganglia, oscillations are also present at many levels and a wide range of characteristic frequencies have been reported to occur during both health and disease. The striatum, the main input nucleus of the basal ganglia, receives massive glutamatergic inputs from the cortex and is highly susceptible to external oscillations. However, there is limited knowledge about the exact nature of this routing process and therefore, it is of key importance to understand how timedependent, external stimuli propagate through the striatal circuitry. Using a network model of the striatum and corticostriatal projections, we try to elucidate the importance of specific GABAergic neurons and their interactions in shaping striatal oscillatory activity. Here, we propose that fast-spiking interneurons can perform an important role in transferring cortical oscillations to the striatum especially to those medium spiny neurons that are not directly driven by the cortical oscillations. We show how the activity levels of different populations, the strengths of different inhibitory synapses, degree of outgoing projections of striatal cells, ongoing activity and synchronicity of inputs can influence network activity. These results suggest that the propagation of oscillatory inputs into the medium spiny neuron population is most efficient, if conveyed via the fast-spiking interneurons. Therefore, pharmaceuticals that target fast-spiking interneurons may provide a novel treatment for regaining the spectral characteristics of striatal activity that correspond to the healthy state.

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Effects of L-dopa priming on cortical high beta and high gamma oscillatory activity in a rodent model of Parkinson's disease

Cited by 65 publications

References 82 publications

On the neuronal circuitry mediating l-DOPA-induced dyskinesia

On the neuronal circuitry mediating l-DOPA-induced dyskinesia

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

Interplay between periodic stimulation and GABAergic inhibition in striatal network oscillations

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