当前位置： SCI文献检索 > NEUROBIOLOGY OF DISEASE期刊下所有文献 > 200-300Hz movement modulated oscillations in the internal globus pallidus of patients with Parkinson's Disease.

200-300Hz movement modulated oscillations in the internal globus pallidus of patients with Parkinson's Disease.

Abstract：

:Symptoms in Parkinson's Disease (PD) have been linked to oscillatory activity within the basal ganglia. In humans, such activity has been detected mainly in the local field potentials (LFPs) recorded from electrode contacts used for deep brain stimulation. Although most studies have focused on activity within the subthalamic nucleus (STN), the internal part of the globus pallidus (GPi) is considered an equally efficacious site for therapeutic neuromodulation. Moreover, while most investigations have evaluated changes in oscillatory activity in the beta (12-35Hz) and gamma (35-100Hz) bands, our preliminary spectral analysis of LFP signals in the GPi suggested distinct activity at higher frequencies as well. We hypothesized there is a unique LFP signature in the GPi that consists of movement modulated spectral power increases above 100Hz. Using invasive recordings from the GPi of patients undergoing DBS, in addition to confirming increased beta band activity within the GPi of patients with PD, we have identified and characterized a previously undescribed peak between 200 and 300Hz centered at approximately 235Hz, whose height and width but not center frequency are movement modulated. An increase in peak height is not transient, but rather persists for the duration of movement. The 200-300Hz rhythms in the GPi could have a functional role in the basal ganglia reentrant circuits by encoding output information entering the thalamo-cortical network or by organizing downstream activity for the successful execution of tasks.

journal_name

Neurobiol Dis

journal_title

Neurobiology of disease

authors

Tsiokos C,Hu X,Pouratian N

doi

10.1016/j.nbd.2013.01.020

subject

Has Abstract

pub_date

2013-06-01 00:00:00

pages

464-74

eissn

0969-9961

issn

1095-953X

pii

S0969-9961(13)00044-2

journal_volume

54

pub_type

杂志文章

相关文献

NEUROBIOLOGY OF DISEASE文献大全
  • Hyperleucinemia causes hippocampal retromer deficiency linking diabetes to Alzheimer's disease.

    abstract：:Type 2 diabetes (T2D) is a major risk factor for late-onset Alzheimer's disease (AD). A variety of metabolic changes related to T2D (e.g. hyperinsulinemia, hyperglycemia, and elevated branched-chain amino acids) have been proposed as mechanistic links, but the basis for this association remains unknown. Retromer-depen...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2013.12.017

    authors： Morabito MV,Berman DE,Schneider RT,Zhang Y,Leibel RL,Small SA

    更新日期：2014-05-01 00:00:00

  • Preventing polyglutamine-induced activation of c-Jun delays neuronal dysfunction in a mouse model of SCA7 retinopathy.

    abstract：:We have approached the role of cellular stress in neurodegenerative diseases caused by polyglutamine expansion (polyQ) in the context of Spinocerebellar ataxia type 7 (SCA7) that includes retinal degeneration. Using the R7E mouse, in which polyQ-ataxin-7 is specifically over-expressed in rod photoreceptors, we previou...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2006.11.002

    authors： Merienne K,Friedman J,Akimoto M,Abou-Sleymane G,Weber C,Swaroop A,Trottier Y

    更新日期：2007-03-01 00:00:00

  • Effects of enriched environment on animal models of neurodegenerative diseases and psychiatric disorders.

    abstract：:Environmental stimulation throughout development adjusts the neurobehavioral systems involved in learning, memory and defensive responses. Environment-mediated phenotypic plasticity can be considered from two different, yet complementary, viewpoints. On one hand, the possibility that environmental interventions protec...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章,评审

    doi：10.1016/j.nbd.2008.05.001

    authors： Laviola G,Hannan AJ,Macrì S,Solinas M,Jaber M

    更新日期：2008-08-01 00:00:00

  • Over-expression of tau results in defective synaptic transmission in Drosophila neuromuscular junctions.

    abstract：:We have shown that over-expression of human tau (0N3R) in Drosophila larval motor neurons causes significant morphological and functional disruption to the neuromuscular junctions (NMJs). Tau-expressing NMJs are reduced in size with irregular and abnormal bouton structure. Immunocytochemical analysis shows that the ab...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2005.05.029

    authors： Chee FC,Mudher A,Cuttle MF,Newman TA,MacKay D,Lovestone S,Shepherd D

    更新日期：2005-12-01 00:00:00

  • Unraveling substantia nigra sequential gene expression in a progressive MPTP-lesioned macaque model of Parkinson's disease.

    abstract：:Taking advantage of a progressive nonhuman primate model mimicking Parkinson's disease (PD) evolution, we monitored transcriptional fluctuations in the substantia nigra using Affymetrix microarrays in control (normal), saline-treated (normal), 6 days-treated (asymptomatic with 20% cell loss), 12 days-treated (asymptom...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2005.02.005

    authors： Bassilana F,Mace N,Li Q,Stutzmann JM,Gross CE,Pradier L,Benavides J,Ménager J,Bezard E

    更新日期：2005-10-01 00:00:00

  • Early glial activation, synaptic changes and axonal pathology in the thalamocortical system of Niemann-Pick type C1 mice.

    abstract：:Niemann-Pick disease type C (NPC) is an inherited lysosomal storage disease characterised by accumulation of cholesterol and glycosphingolipids. NPC patients suffer a progressive neurodegenerative phenotype presenting with motor dysfunction, mental retardation and cognitive decline. To examine the onset and progressio...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2011.12.027

    authors： Pressey SN,Smith DA,Wong AM,Platt FM,Cooper JD

    更新日期：2012-03-01 00:00:00

  • Amyloid-beta peptide is toxic to neurons in vivo via indirect mechanisms.

    abstract：:We have studied the neurotoxicity of amyloid-beta (Abeta) after a single unilateral intravitreal injection. Within the retina apoptotic cells were seen throughout the photoreceptor layer and the inner nuclear layer but not in the ganglion cell layer at 48 h after injection of Abeta(1-42) compared to vehicle control an...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1006/nbdi.2002.0485

    authors： Walsh DT,Montero RM,Bresciani LG,Jen AY,Leclercq PD,Saunders D,EL-Amir AN,Gbadamoshi L,Gentleman SM,Jen LS

    更新日期：2002-06-01 00:00:00

  • Divergent brain changes in two audiogenic rat strains: A voxel-based morphometry and diffusion tensor imaging comparison of the genetically epilepsy prone rat (GEPR-3) and the Wistar Audiogenic Rat (WAR).

    abstract：:Acoustically evoked seizures (e.g., audiogenic seizures or AGS) are common in models of inherited epilepsy and occur in a variety of species including rat, mouse, and hamster. Two models that have been particularly well studied are the genetically epilepsy prone rat (GEPR-3) and the Wistar Audiogenic Rat (WAR) strains...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2017.12.014

    authors： Lee Y,Rodriguez OC,Albanese C,Santos VR,Cortes de Oliveira JA,Donatti ALF,Fernandes A,Garcia-Cairasco N,N'Gouemo P,Forcelli PA

    更新日期：2018-03-01 00:00:00

  • Differential effect of amyloid beta peptides on mitochondrial axonal trafficking depends on their state of aggregation and binding to the plasma membrane.

    abstract：:Inhibition of mitochondrial axonal trafficking by amyloid beta (Aβ) peptides has been implicated in early pathophysiology of Alzheimer's Disease (AD). Yet, it remains unclear whether the loss of motility inevitably induces the loss of mitochondrial function, and whether restoration of axonal trafficking represents a v...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2018.02.003

    authors： Zhang L,Trushin S,Christensen TA,Tripathi U,Hong C,Geroux RE,Howell KG,Poduslo JF,Trushina E

    更新日期：2018-06-01 00:00:00

  • Neurophysiology of the pedunculopontine tegmental nucleus.

    abstract：:The interest in the pedunculopontine tegmental nucleus (PPTg), a structure located in the brainstem at the level of the pontomesencephalic junction, has greatly increased in recent years because it is involved in the regulation of physiological functions that fail in Parkinson's disease and because it is a promising t...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章,评审

    doi：10.1016/j.nbd.2018.03.004

    authors： Vitale F,Capozzo A,Mazzone P,Scarnati E

    更新日期：2019-08-01 00:00:00

  • Lack of nigral pathology in transgenic mice expressing human alpha-synuclein driven by the tyrosine hydroxylase promoter.

    abstract：:alpha-Synuclein has been identified as a major component of Lewy body inclusions, which are one of the pathologic hallmarks of idiopathic Parkinson's disease. Mutations in alpha-synuclein have been found to be responsible for rare familial cases of Parkinsonism. To test whether overexpression of human alpha-synuclein ...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1006/nbdi.2001.0392

    authors： Matsuoka Y,Vila M,Lincoln S,McCormack A,Picciano M,LaFrancois J,Yu X,Dickson D,Langston WJ,McGowan E,Farrer M,Hardy J,Duff K,Przedborski S,Di Monte DA

    更新日期：2001-06-01 00:00:00

  • Role of endothelial nitric oxide synthase in cerebral blood flow changes during kainate seizures: a genetic approach using knockout mice.

    abstract：:The role of endothelial nitric oxide (NO) in the cerebrovascular response to partial seizures was investigated in mice deleted for the endothelial NO synthase gene (eNOS-/-) and in their paired wild-type (WT) congeners. Local cerebral blood flow (LCBF, quantitative [14C]iodoantipyrine method) was measured 3-6 h after ...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2006.03.002

    authors： Pereira de Vasconcelos A,Riban V,Wasterlain C,Nehlig A

    更新日期：2006-07-01 00:00:00

  • Functional MAPT haplotypes: bridging the gap between genotype and neuropathology.

    abstract：:The microtubule-associated protein tau (MAPT) locus has long been associated with sporadic neurodegenerative disease, notably progressive supranuclear palsy and corticobasal degeneration, and more recently with Alzheimer's disease and Parkinson's disease. However, the functional biological mechanisms behind the geneti...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章,评审

    doi：10.1016/j.nbd.2007.04.006

    authors： Caffrey TM,Wade-Martins R

    更新日期：2007-07-01 00:00:00

  • Mouse model of rare TOR1A variant found in sporadic focal dystonia impairs domains affected in DYT1 dystonia patients and animal models.

    abstract：:Rare de novo mutations in genes associated with inherited Mendelian disorders are potential contributors to sporadic disease. DYT1 dystonia is an autosomal dominant, early-onset, generalized dystonia associated with an in-frame, trinucleotide deletion (n. delGAG, p. ΔE 302/303) in the Tor1a gene. Here we examine the s...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2016.05.003

    authors： Bhagat SL,Qiu S,Caffall ZF,Wan Y,Pan Y,Rodriguiz RM,Wetsel WC,Badea A,Hochgeschwender U,Calakos N

    更新日期：2016-09-01 00:00:00

  • Genome-wide alterations in hippocampal 5-hydroxymethylcytosine links plasticity genes to acute stress.

    abstract：:Environmental stress is among the most important contributors to increased susceptibility to develop psychiatric disorders, including anxiety and post-traumatic stress disorder. While even acute stress alters gene expression, the molecular mechanisms underlying these changes remain largely unknown. 5-hydroxymethylcyto...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2015.11.010

    authors： Li S,Papale LA,Zhang Q,Madrid A,Chen L,Chopra P,Keleş S,Jin P,Alisch RS

    更新日期：2016-02-01 00:00:00

  • Cytokine profiling in the prefrontal cortex of Parkinson's Disease and Multiple System Atrophy patients.

    abstract：:Parkinson's Disease (PD) and Multiple System Atrophy (MSA) are neurodegenerative diseases characterized neuropathologically by alpha-synuclein accumulation in brain cells. This accumulation is hypothesized to contribute to constitutive neuroinflammation, and to participate in the neurodegeneration. Cytokines, which ar...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2017.07.014

    authors： Rydbirk R,Elfving B,Andersen MD,Langbøl MA,Folke J,Winge K,Pakkenberg B,Brudek T,Aznar S

    更新日期：2017-10-01 00:00:00

  • Human Rab7 mutation mimics features of Charcot-Marie-Tooth neuropathy type 2B in Drosophila.

    abstract：:Charcot-Marie-Tooth disease type 2B (CMT2B) is an inherited axonal peripheral neuropathy. It is characterised by prominent sensory loss, often complicated by severe ulcero-mutilations of toes or feet, and variable motor involvement. Missense mutations in RAB7A, the gene encoding the small GTPase Rab7, cause CMT2B and ...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2014.01.021

    authors： Janssens K,Goethals S,Atkinson D,Ermanoska B,Fransen E,Jordanova A,Auer-Grumbach M,Asselbergh B,Timmerman V

    更新日期：2014-05-01 00:00:00

  • A mouse model of the fragile X premutation: effects on behavior, dendrite morphology, and regional rates of cerebral protein synthesis.

    abstract：:Carriers of FMR1 premutation alleles have 55-200 CGG repeats in the 5' untranslated region of the gene. These individuals are at risk for fragile X associated primary ovarian insufficiency (females) and, in late life, fragile X associated tremor and ataxia syndrome (males, and to a lesser extent, females). Premutation...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2011.01.008

    authors： Qin M,Entezam A,Usdin K,Huang T,Liu ZH,Hoffman GE,Smith CB

    更新日期：2011-04-01 00:00:00

  • Recombinant Adeno Associated Viral (AAV) vector type 9 delivery of Ex1-Q138-mutant huntingtin in the rat striatum as a short-time model for in vivo studies in drug discovery.

    abstract：:Huntington's disease (HD) is an inherited neurodegenerative disorder characterized by dyskinesia, cognitive impairment and emotional disturbances, presenting progressive neurodegeneration in the striatum and intracellular mutant Huntingtin (mHTT) aggregates in various areas of the brain. Recombinant Adeno Associated V...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2015.11.019

    authors： Ceccarelli I,Fiengo P,Remelli R,Miragliotta V,Rossini L,Biotti I,Cappelli A,Petricca L,La Rosa S,Caricasole A,Pollio G,Scali C

    更新日期：2016-02-01 00:00:00

  • Soluble Aβ oligomers impair hippocampal LTP by disrupting glutamatergic/GABAergic balance.

    abstract：:Epileptic activity may be more prevalent in early stage Alzheimer's disease (AD) than previously believed. Several studies report spontaneous seizures and interictal discharges in mouse models of AD undergoing age-related Aβ accumulation. The mechanism by which Aβ-induced neuronal excitability can trigger epileptiform...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2015.10.019

    authors： Lei M,Xu H,Li Z,Wang Z,O'Malley TT,Zhang D,Walsh DM,Xu P,Selkoe DJ,Li S

    更新日期：2016-01-01 00:00:00

  • The role of REST in transcriptional and epigenetic dysregulation in Huntington's disease.

    abstract：:Huntington's disease (HD) is a devastating disorder that affects approximately 1 in 10,000 people and is accompanied by neuronal dysfunction and neurodegeneration. HD manifests as a progressive chorea, a decline in mental abilities accompanied by behavioural, emotional and psychiatric problems followed by, dementia, a...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章,评审

    doi：10.1016/j.nbd.2010.02.003

    authors： Buckley NJ,Johnson R,Zuccato C,Bithell A,Cattaneo E

    更新日期：2010-07-01 00:00:00

  • Prenatal cocaine exposure impairs cognitive function of progeny via insulin growth factor II epigenetic regulation.

    abstract：:Studies have showed that prenatal cocaine exposure (PCOC) can impair cognitive function and social behavior of the offspring; however, the mechanism underlying such effect is poorly understood. Insulin-like growth factor II (Igf-II), an imprinted gene, has a critical role in memory consolidation and enhancement. We hy...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2015.05.014

    authors： Zhao Q,Hou J,Chen B,Shao X,Zhu R,Bu Q,Gu H,Li Y,Zhang B,Du C,Fu D,Kong J,Luo L,Long H,Li H,Deng Y,Zhao Y,Cen X

    更新日期：2015-10-01 00:00:00

  • Coincident thresholds of mutant protein for paralytic disease and protein aggregation caused by restrictively expressed superoxide dismutase cDNA.

    abstract：:Familial amyotrophic lateral sclerosis (FALS) has been modeled in transgenic mice by introducing mutated versions of human genomic DNA encompassing the entire gene for Cu,Zn superoxide dismutase (SOD1). In this setting, the transgene is expressed throughout the body and results in mice that faithfully recapitulate man...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2005.06.005

    authors： Wang J,Xu G,Slunt HH,Gonzales V,Coonfield M,Fromholt D,Copeland NG,Jenkins NA,Borchelt DR

    更新日期：2005-12-01 00:00:00

  • Deletion of exons 9 and 10 of the Presenilin 1 gene in a patient with Early-onset Alzheimer Disease generates longer amyloid seeds.

    abstract：:Presenilin 1 (PSEN1) mutations are the main cause of autosomal dominant Early-onset Alzheimer Disease (EOAD). Among them, deletions of exon 9 have been reported to be associated with a phenotype of spastic paraparesis. Using exome data from a large sample of 522 EOAD cases and 584 controls to search for genomic copy-n...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2017.04.020

    authors： Le Guennec K,Veugelen S,Quenez O,Szaruga M,Rousseau S,Nicolas G,Wallon D,Fluchere F,Frébourg T,De Strooper B,Campion D,Chávez-Gutiérrez L,Rovelet-Lecrux A

    更新日期：2017-08-01 00:00:00

  • Elevated GDNF levels following viral vector-mediated gene transfer can increase neuronal death after stroke in rats.

    abstract：:Previous studies have indicated that administration of glial cell line-derived neurotrophic factor (GDNF) counteracts neuronal death after stroke. However, in these studies damage was evaluated at most a few days after the insult. Here, we have explored the long-term consequences of two routes of GDNF delivery to the ...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2003.08.002

    authors： Arvidsson A,Kirik D,Lundberg C,Mandel RJ,Andsberg G,Kokaia Z,Lindvall O

    更新日期：2003-12-01 00:00:00

  • Premature stop codons in a facilitating EF-hand splice variant of CaV2.1 cause episodic ataxia type 2.

    abstract：:Premature stop codons in CACNA1A, which encodes the alpha(1A) subunit of neuronal P/Q-type (Ca(V)2.1) Ca(2+) channels, cause episodic ataxia type 2 (EA2). CACNA1A undergoes extensive alternative splicing, which contributes to the pharmacological and kinetic heterogeneity of Ca(V)2.1-mediated Ca(2+) currents. We identi...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2008.06.002

    authors： Graves TD,Imbrici P,Kors EE,Terwindt GM,Eunson LH,Frants RR,Haan J,Ferrari MD,Goadsby PJ,Hanna MG,van den Maagdenberg AM,Kullmann DM

    更新日期：2008-10-01 00:00:00

  • Pituitary adenylate cyclase activating polypeptide (PACAP) and its receptor 1 (PAC1) in the human infant brain and changes in the Sudden Infant Death Syndrome (SIDS).

    abstract：:Pituitary adenylate cyclase activating polypeptide (PACAP) and its complementary receptor, PAC1, are crucial in central respiratory control. PACAP Knockout (KO) mice exhibit a SIDS-like phenotype, with an inability to overcome noxious insults, compression of baseline ventilation, and death in the early post-neonatal p...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2017.04.002

    authors： Huang J,Waters KA,Machaalani R

    更新日期：2017-07-01 00:00:00

  • Bri2-23 is a potential cerebrospinal fluid biomarker in multiple sclerosis.

    abstract：:To identify potential multiple sclerosis (MS)-specific biomarkers, we used a proteomic approach to screen cerebrospinal fluid (CSF) from 40 MS patients and 13 controls. We identified seven proteins (Beta-2-microglobulin, Bri2-23, Fetuin-A, Kallikrein-6, Plasminogen, Ribonuclease-1, and Transferrin) that had significan...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2010.06.007

    authors： Harris VK,Diamanduros A,Good P,Zakin E,Chalivendra V,Sadiq SA

    更新日期：2010-10-01 00:00:00

  • Expression of the methyl-CpG-binding protein MeCP2 in rat brain. An ontogenetic study.

    abstract：:Rett syndrome (RS) is caused by mutations in the gene encoding methyl-CpG-binding protein 2 (MeCP2) and is characterized by arrested postnatal neurodevelopment. We followed the expression of MeCP2 protein in various brain structures of normal rat from birth to 2 years of age. By measuring the amount of protein using t...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2003.10.011

    authors： Cassel S,Revel MO,Kelche C,Zwiller J

    更新日期：2004-03-01 00:00:00

  • IL-6 knockout mice exhibit resistance to stress-induced development of depression-like behaviors.

    abstract：:Cytokine-dependent mechanisms in the CNS have been implicated in the pathogenesis of depression. Interleukin-6 is upregulated in depressed patients and dowregulated by antidepressants. It is, however, unknown whether IL-6 is involved in the pathogenesis of depression. We subjected IL-6-deficient mice (IL-6(-/-)) to de...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2006.05.001

    authors： Chourbaji S,Urani A,Inta I,Sanchis-Segura C,Brandwein C,Zink M,Schwaninger M,Gass P

    更新日期：2006-09-01 00:00:00