Electrical Stimulation of the Subthalamic Nucleus in Fully Parkinsonian (MPTP) Monkeys

Hayase, Nobuaki; Filion, Michel; Richard, Hélène; Boraud, Thomas

doi:10.1007/978-1-4899-0194-1_28

Cited by 4 publications

(7 citation statements)

References 31 publications

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“…Based on this hypothesis, a simple reduction in discharge rate in GPi without an associated change in the pattern of neuronal activity would not be associated with the development of dyskinesias. Consistent with this prediction, during STN stimulation Hayase and associates 49 reported improvement in parkinsonian motor signs without the development of dyskinesias that occurred coincident with a reduction in the mean discharge rate and normalization of the pattern of discharge of GPi neurons.…”

Section: Neuronal Activity Changes Inmentioning

confidence: 60%

“…48 Hayase and colleagues also observed that the reduction in mean discharge rate of GPi neurons, which occurred in parkinsonian monkeys receiving dopamine agonists or during deep brain stimulation, was greater in the animals that developed dyskinesias than in those that did not. 49 Thus, there appeared to be a level of neuronal activity in GPi, below which dyskinesias developed and above which parkinsonian motor signs emerged.…”

Section: Model Of Hyperkinetic Movement Disordersmentioning

confidence: 98%

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Pathophysiology of dystonia: A neuronal model

2002

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Dystonia has commonly been thought to represent a disorder of basal ganglia function. Although long considered a hyperkinetic movement disorder, the evidence to support such a classification was based on the presence of excessive involuntary movement, not on physiological data. Only recently, with the return of surgical procedures using microelectrode guidance for the treatment of dystonia, has electrophysiological data demonstrated an alteration in mean discharge rate, somatosensory responsiveness and the pattern of neuronal activity in the basal ganglia thalamocortical motor circuit. Previous models of dystonia suggested that reduced mean discharge rates in the globus pallidus internus (GPi) led to unopposed increases in activity in the thalamocortical circuit that precipitated the development of involuntary movement associated with dystonia. This model has subsequently been modified given the clear improvement in dystonic symptoms following lesions in the GPi, a procedure that is associated with a further reduction in pallidal output. The improvement in dystonia following pallidal lesions is difficult to reconcile with the "rate" hypothesis for hypokinetic and hyperkinetic movement disorders and has led to the development of alternative models that, in addition to rate, incorporate changes in pattern, somatosensory responsiveness and degree of synchronization of neuronal activity. Present models of dystonia, however, must not only take these changes into account but must reconcile these changes with the reported changes in cortical excitability reported with transcranial magnetic stimulation, the changes in metabolic activity in cortical and subcortical structures documented by positron emission tomography (PET), and the alterations in spinal and brainstem reflexes. A model incorporating these changes together with the reported changes in neuronal activity in the basal ganglia and thalamus is presented.

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Section: Neuronal Activity Changes Inmentioning

confidence: 60%

Section: Model Of Hyperkinetic Movement Disordersmentioning

confidence: 98%

Pathophysiology of dystonia: A neuronal model

2002

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“…As the pattern of discharge of STN neurons may play an important role in the physio-pathology of parkinsonism (Bergman et al 1994;Hollerman and Grace 1992), it is tempting to correlate the present effects of in vitro HFS on the spontaneous STN activity, to the beneficial effects of high-frequency deep brain stimulation in the STN of MPTP-treated monkeys (Benazzouz et al 1992;Hayase et al 1996) or parkinsonian patients (Benabid et al 1994;Limousin et al 1998). However, such a direct correlation needs further experiments.…”

Section: Discussionmentioning

confidence: 99%

“…In keeping with this, HFS in the STN has been shown to significantly decrease the frequency of extracellularly recorded STN neurons in rats in vivo (Benazzouz et al 1997). As STN neurons are glutamatergic excitatory output neurons (Hammond et al 1978;Robledo and Féger 1990;Smith and Parent 1988), the immediate consequence of their reduction of activity could be the decrease of activity in target nuclei [substantia nigra pars reticulata (SNr) and entopeduncular nucleus/globus pallidus internal part (EP/GPi)] as observed in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated monkeys and naive rats (Benazzouz et al 1995;Burbaud et al 1994;Hayase et al 1996). It has also been suggested that the consequence of clinical HFS will be to somehow counteract the abnormal bursting pattern recorded in the STN in animal models of Parkinson disease (Bergman et al 1994;Hassani et al 1996;Hollerman and Grace 1992;Vila et al 2000).…”

Section: Introductionmentioning

confidence: 99%

High-Frequency Stimulation Produces a Transient Blockade of Voltage-Gated Currents in Subthalamic Neurons

Beurrier

Bioulac

Audin

et al. 2001

Journal of Neurophysiology

473

316

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Beurrier, Corinne, Bernard Bioulac, Jacques Audin, and Constance Hammond. High-frequency stimulation produces a transient blockade of voltage-gated currents in subthalamic neurons. J Neurophysiol 85: 1351Neurophysiol 85: -1356Neurophysiol 85: , 2001. The effect of high-frequency stimulation (HFS) of the subthalamic nucleus (STN) was analyzed with patch-clamp techniques (whole cell configuration, current-and voltage-clamp modes) in rat STN slices in vitro. A brief tetanus, consisting of 100-s bipolar stimuli at a frequency of 100 -250 Hz during 1 min, produced a full blockade of ongoing STN activity whether it was in the tonic or bursting mode. This HFS-induced silence lasted around 6 min after the end of stimulation, was frequency dependent, could be repeated without alteration, and was not synaptically induced as it was still observed in the presence of blockers of ionotropic GABA and glutamate receptors or in the presence of cobalt at a concentration (2 mM) that blocks voltage-gated Ca 2ϩ channels and synaptic transmission. During HFS-induced silence, the following alterations were observed: the persistent Na ϩ current (I NaP ) was totally blocked (by 99%), the Ca 2ϩ -mediated responses were strongly reduced including the posthyperpolarization rebound (Ϫ62% in amplitude) and the plateau potential (Ϫ76% in duration), suggesting that T-and L-type Ca 2ϩ currents are transiently depressed by HFS, whereas the Cs ϩ -sensitive, hyperpolarization-activated cationic current (I h ) was little affected. Thus a high-frequency tetanus produces a blockade of the spontaneous activities of STN neurons as a result of a strong depression of intrinsic voltage-gated currents underlying single-spike and bursting modes of discharge. These effects of HFS, which are completely independent of synaptic transmission, provide a mechanism for interrupting ongoing activities of STN neurons.

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“…Although DBS mimics the effects of ablation (Guridi et al, 1993; Gill and Heywood, 1997; Guridi and Obeso, 2001), its precise mechanism of action is still unknown. Because HFS appears to have the same clinical effect as a lesion, stimulations are assumed to “block” STN neurons (Benazzouz et al, 1995; Hayase et al, 1996). This was recently supported from in vitro experiments demonstrating that 1 min of extracellular stimulation at 100–250 Hz produced blockade of ongoing activity in STN neurons for 6 min (Beurrier et al, 2001).…”

mentioning

confidence: 99%

Influence of the frequency parameter on extracellular glutamate and γ‐aminobutyric acid in substantia nigra and globus pallidus during electrical stimulation of subthalamic nucleus in rats

Windels

Bruet

Poupard

et al. 2003

J of Neuroscience Research

158

105

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High-frequency stimulation (HFS) of the subthalamic nucleus (STN) proves to be an efficient treatment for alleviating motor symptoms in Parkinson's disease (PD). However, the mechanisms of HFS underlying these clinical effects remain unknown. Using intracerebral microdialysis, we previously reported that HFS induces, in normal rats, a significant increase of extracellular glutamate (Glu) in the globus pallidus (GP in rats or GPe in primates) and the substantia nigra pars reticulata (SNr), whereas gamma-aminobutyric acid (GABA) was increased only in the SNr. Bradykinesia can be improved by STN stimulation in a frequency-dependent manner, a plateau being reached around 130 Hz. The aim of the present study was to determine whether neurochemical changes are also frequency dependent. Electrical STN stimulation was applied at various frequencies (10, 60, 130, and 350 Hz) in normal rats. The results show that, for Glu, the amplitude of increase detected in GP and SNr is maximal at 130 Hz and is maintained at 350 Hz. No modifications of GABA were observed in GP whatever the frequency applied, whereas, in SNr, GABA increased from 60 to 350 Hz. Our results provide new neurochemical data implicating STN target structures in deep-brain-stimulation mechanisms.

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Electrical Stimulation of the Subthalamic Nucleus in Fully Parkinsonian (MPTP) Monkeys

Cited by 4 publications

References 31 publications

Pathophysiology of dystonia: A neuronal model

Pathophysiology of dystonia: A neuronal model

High-Frequency Stimulation Produces a Transient Blockade of Voltage-Gated Currents in Subthalamic Neurons

Influence of the frequency parameter on extracellular glutamate and γ‐aminobutyric acid in substantia nigra and globus pallidus during electrical stimulation of subthalamic nucleus in rats

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