Move to the rhythm: oscillations in the subthalamic nucleus–external globus pallidus network

Bevan, Mark D.; Magill, Peter J.; Terman, David; Bolam, J. Paul; Wilson, Charles J.

doi:10.1016/s0166-2236(02)02235-x

Cited by 602 publications

(458 citation statements)

References 71 publications

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“…Loss of direct dopaminergic control of the microcircuity network formed by the STN-GPe/GPi interconnections could play a part in this regard. 68 Second, the neuronal network underlying tremor might not primarily lie in the basal ganglia. This possibility is supported by the high association between the Vim and cerebellar activation and tremor and by the exquisite sensitivity of Vim manipulations to cessation of tremor.…”

Section: Tremormentioning

confidence: 99%

Initial clinical manifestations of Parkinson's disease: features and pathophysiological mechanisms

Rodriguez-Oroz

Jahanshahi

Krack

et al. 2009

The Lancet Neurology

742

500

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A dopaminergic defi ciency in patients with Parkinson's disease (PD) causes abnormalities of movement, behaviour, learning, and emotions. The main motor features (ie, tremor, rigidity, and akinesia) are associated with a defi ciency of dopamine in the posterior putamen and the motor circuit. Hypokinesia and bradykinesia might have a dual anatomo-functional basis: hypokinesia mediated by brainstem mechanisms and bradykinesia by cortical mechanisms. The classic pathophysiological model for PD (ie, hyperactivity in the globus pallidus pars interna and substantia nigra pars reticulata) does not explain rigidity and tremor, which might be caused by changes in primary motor cortex activity. Executive functions (ie, planning and problem solving) are also impaired in early PD, but are usually not clinically noticed. These impairments are associated with dopamine defi ciency in the caudate nucleus and with dysfunction of the associative and other non-motor circuits. Apathy, anxiety, and depression are the main psychiatric manifestations in untreated PD, which might be caused by ventral striatum dopaminergic defi cit and depletion of serotonin and norepinephrine. In this Review we discuss the motor, cognitive, and psychiatric manifestations associated with the dopaminergic defi ciency in the early phase of the parkinsonian state and the diff erent circuits implicated, and we propose distinct mechanisms to explain the wide clinical range of PD symptoms at the time of diagnosis.

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Section: Tremormentioning

confidence: 99%

Initial clinical manifestations of Parkinson's disease: features and pathophysiological mechanisms

Rodriguez-Oroz

Jahanshahi

Krack

et al. 2009

The Lancet Neurology

742

500

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“…Finally, a highly important parkinsonismrelated change in spontaneous discharge is the abnormal level of synchrony between neighboring neurons [144,152]. It is not specifically known how changes such as burst discharges, oscillatory discharge, or abnormal synchrony develop in parkinsonism, although altered striatal output to the extrastriatal basal ganglia, changes in collateral inhibition in the external pallidum [156], or changes in the strength and morphology of synapses within the subthalamopallidal network of connections (see below and [157,158]) may contribute to correlated oscillatory activity in the output nuclei of the basal ganglia [152,159,160] .…”

Section: Pathophysiology Of Parkinsonism and Dystoniamentioning

confidence: 99%

“…Although it is tempting to attribute signs and symptoms to specific abnormalities in neuronal activity or LFPs in PD, the (causal) importance of any of the multiple changes in basal ganglia activity for the development of parkinsonism remains uncertain because they are not always found in animal models of parkinsonism, or in humans with PD, and, if they occur, tend to occur late in the development of parkinsonian signs in animal models, well after their onset [158][159][160][161].…”

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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“…Glutamatergic inputs have been demonstrated to greatly modulate the spontaneous (Bevan et al, 2002) GP activity through the activation of both AMPA/kainate and NMDA receptors , aside with metabotropic glutamate receptors (mGluRs) (Conn et al, 2005;Rouse et al, 2000). The glutamatergic drive to the GP neuronal activity has been shown to be differently modulated by classical neurotransmitters and neuromodulators (Chen et al, 2006;Hernandez et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Nitric oxide-active compounds modulate the intensity of glutamate-evoked responses in the globus pallidus of the rat

et al. 2011

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Aim: The effects of local applied NO-active compounds on glutamate (GLU)-evoked responses were investigated in globus pallidus (GP) neurons. Main methods: Extracellularly recorded single units from anesthetized rats were treated with GLU before and during the microiontophoretic application of S-nitrosoglutathione (SNOG), a NO donor, and Nω-nitro-Larginine methyl ester (L-NAME), a NOS inhibitor. Key findings: Most GP cells were excited by SNOG whereas administration of L-NAME induced decrease of GP neurons activity. Nearly all neurons responding to SNOG and/or L-NAME showed significant modulation of their excitatory responses to the administration of iontophoretic GLU. In these cells, the changes induced by NO-active drugs in the magnitude of GLU-evoked responses were used as indicators of NO modulation. In fact, when a NO-active drug was co-iontophoresed with GLU, significant changes in GLU-induced responses were observed: generally, increased magnitudes of GLU-evoked responses were observed during SNOG ejection, whereas the administration of L-NAME decreased responses to GLU. Significance: The results suggest that the NO-active drugs modulate the response of GP neurons to glutamatergic transmission. Nitrergic modulation of glutamatergic transmission could play an important role in the control of GP bioelectric activity, considered a fundamental key in the BG function.

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Move to the rhythm: oscillations in the subthalamic nucleus–external globus pallidus network

Cited by 602 publications

References 71 publications

Initial clinical manifestations of Parkinson's disease: features and pathophysiological mechanisms

Initial clinical manifestations of Parkinson's disease: features and pathophysiological mechanisms

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

Nitric oxide-active compounds modulate the intensity of glutamate-evoked responses in the globus pallidus of the rat

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