当前位置： SCI文献检索 > NEUROBIOLOGY OF DISEASE期刊下所有文献 > Pathological high frequency oscillations associate with increased GABA synaptic activity in pediatric epilepsy surgery patients.

Pathological high frequency oscillations associate with increased GABA synaptic activity in pediatric epilepsy surgery patients.

Abstract：

:Pathological high-frequency oscillations (HFOs), specifically fast ripples (FRs, >250 Hz), are pathognomonic of an active epileptogenic zone. However, the origin of FRs remains unknown. Here we explored the correlation between FRs recorded with intraoperative pre-resection electrocorticography (ECoG) and spontaneous synaptic activity recorded ex vivo from cortical tissue samples resected for the treatment of pharmacoresistant epilepsy. The cohort included 47 children (ages 0.22-9.99 yr) with focal cortical dysplasias (CD types I and II), tuberous sclerosis complex (TSC) and non-CD pathologies. Whole-cell patch clamp recordings were obtained from pyramidal neurons and interneurons in cortical regions that were positive or negative for pathological HFOs, defined as FR band oscillations (250-500 Hz) at ECoG. The frequency of spontaneous excitatory and inhibitory postsynaptic currents (sEPSCs and IPSCs, respectively) was compared between HFO+ and HFO- regions. Regardless of pathological substrate, regions positive for FRs displayed significantly increased frequencies of sIPSCs compared with regions negative for FRs. In contrast, the frequency of sEPSCs was similar in both regions. In about one third of cases (n = 17), pacemaker GABA synaptic activity (PGA) was observed. In the vast majority (n = 15), PGA occurred in HFO+ areas. Further, fast-spiking interneurons displayed signs of hyperexcitability exclusively in HFO+ areas. These results indicate that, in pediatric epilepsy patients, increased GABA synaptic activity is associated with interictal FRs in the epileptogenic zone and suggest an active role of GABAergic interneurons in the generation of pathological HFOs. Increased GABA synaptic activity could serve to dampen excessive excitability of cortical pyramidal neurons in the epileptogenic zone, but it could also promote neuronal network synchrony.

journal_name

Neurobiol Dis

journal_title

Neurobiology of disease

authors

Cepeda C,Levinson S,Nariai H,Yazon VW,Tran C,Barry J,Oikonomou KD,Vinters HV,Fallah A,Mathern GW,Wu JY

doi

10.1016/j.nbd.2019.104618

subject

Has Abstract

pub_date

2020-02-01 00:00:00

pages

104618

eissn

0969-9961

issn

1095-953X

pii

S0969-9961(19)30293-1

journal_volume

134

pub_type

杂志文章

相关文献

NEUROBIOLOGY OF DISEASE文献大全
  • 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

  • Glial overexpression of Dube3a causes seizures and synaptic impairments in Drosophila concomitant with down regulation of the Na+/K+ pump ATPα.

    abstract：:Duplication 15q syndrome (Dup15q) is an autism-associated disorder co-incident with high rates of pediatric epilepsy. Additional copies of the E3 ubiquitin ligase UBE3A are thought to cause Dup15q phenotypes, yet models overexpressing UBE3A in neurons have not recapitulated the epilepsy phenotype. We show that Drosoph...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2017.09.003

    authors： Hope KA,LeDoux MS,Reiter LT

    更新日期：2017-12-01 00:00:00

  • Degenerative and regenerative mechanisms governing spinal cord injury.

    abstract：:Spinal cord injury (SCI) is a major cause of disability, and at present, there is no universally accepted treatment. The functional decline following SCI is contributed to both direct mechanical injury and secondary pathophysiological mechanisms that are induced by the initial trauma. These mechanisms initially involv...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章,评审

    doi：10.1016/j.nbd.2003.11.015

    authors： Profyris C,Cheema SS,Zang D,Azari MF,Boyle K,Petratos S

    更新日期：2004-04-01 00:00:00

  • Alzheimer's brains show inter-related changes in RNA and lipid metabolism.

    abstract：:Alzheimer's disease (AD) involves changes in both lipid and RNA metabolism, but it remained unknown if these differences associate with AD's cognition and/or post-mortem neuropathology indices. Here, we report RNA-sequencing evidence of inter-related associations between lipid processing, cognition level, and AD neuro...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2017.06.008

    authors： Barbash S,Garfinkel BP,Maoz R,Simchovitz A,Nadorp B,Guffanti A,Bennett ER,Nadeau C,Türk A,Paul L,Reda T,Li Y,Buchman AS,Greenberg DS,Seitz A,Bennett DA,Giavalisco P,Soreq H

    更新日期：2017-10-01 00:00:00

  • Effects of environmental manipulations in genetically targeted animal models of affective disorders.

    abstract：:Mental illness is the leading cause of disability worldwide. We are only just beginning to reveal and comprehend the complex interaction that exists between the genetic makeup of an organism and the potential modifying effect of the environment in which it lives, and how this translates into mediating susceptibility t...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章,评审

    doi：10.1016/j.nbd.2012.04.003

    authors： Renoir T,Pang TY,Hannan AJ

    更新日期：2013-09-01 00:00:00

  • Acute exposure to GSM 900-MHz electromagnetic fields induces glial reactivity and biochemical modifications in the rat brain.

    abstract：:The worldwide proliferation of mobile phones raises the question of the effects of 900-MHz electromagnetic fields (EMF) on the brain. Using a head-only exposure device in the rat, we showed that a 15-min exposure to 900-MHz pulsed microwaves at a high brain-averaged power of 6 W/kg induced a strong glial reaction in t...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2004.07.004

    authors： Mausset-Bonnefont AL,Hirbec H,Bonnefont X,Privat A,Vignon J,de Sèze R

    更新日期：2004-12-01 00:00:00

  • Expression analysis of genes responsible for serotonin signaling in the brain.

    abstract：:To thoroughly understand the function and regulation of neurotransmitter systems in the brain, as well as the underlying disease mechanisms, it is important to comprehensively analyze the expression patterns of genes participating in such systems. Using functional annotated cDNA clones (FANTOM), we examined the gene e...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2005.01.021

    authors： Ichikawa M,Okamura-Oho Y,Okunishi R,Kanamori M,Suzuki H,Ritani A,Nitta H,Eguchi N,Urade Y,Hayashizaki Y

    更新日期：2005-08-01 00:00:00

  • Leucine-rich repeat kinase 2 functionally interacts with microtubules and kinase-dependently modulates cell migration.

    abstract：:Recent studies indicate that the Parkinson's disease-linked leucine-rich repeat kinase 2 (LRRK2) modulates cytoskeletal functions by regulating actin and tubulin dynamics, thereby affecting neurite outgrowth. By interactome analysis we demonstrate that the binding of LRRK2 to tubulins is significantly enhanced by phar...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2012.12.019

    authors： Caesar M,Zach S,Carlson CB,Brockmann K,Gasser T,Gillardon F

    更新日期：2013-06-01 00:00:00

  • Worsening of Huntington disease phenotype in CB1 receptor knockout mice.

    abstract：:Huntington's disease (HD) is a progressive neurodegenerative genetic disorder which leads to motor, cognitive and psychiatric disturbances. The primary neuropathological hallmark is atrophy of the striatum. Cannabinoid CB1 receptors (CB1Rs) are particularly enriched in the striatum and previous works indicate their ea...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2011.03.006

    authors： Mievis S,Blum D,Ledent C

    更新日期：2011-06-01 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

  • TRIM9, a novel brain-specific E3 ubiquitin ligase, is repressed in the brain of Parkinson's disease and dementia with Lewy bodies.

    abstract：:TRIM family proteins are involved in a broad range of biological processes, and their alteration results in many diverse pathological conditions found in genetic diseases, viral infections, and cancers. However, the spatial and temporal expression and function of TRIM9, one of TRIM family proteins, remain obscure. Our...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2010.01.007

    authors： Tanji K,Kamitani T,Mori F,Kakita A,Takahashi H,Wakabayashi K

    更新日期：2010-05-01 00:00:00

  • Modulation of inhibitory plasticity in basal ganglia output nuclei of patients with Parkinson's disease.

    abstract：:Deep brain stimulation of certain target structures within the basal ganglia is an effective therapy for the management of the motor symptoms of Parkinson's disease. However, its mechanisms, as well as the pathophysiology of Parkinson's disease, are varied and complex. The classical model of Parkinson's disease states...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2018.10.020

    authors： Milosevic L,Gramer R,Kim TH,Algarni M,Fasano A,Kalia SK,Hodaie M,Lozano AM,Popovic MR,Hutchison WD

    更新日期：2019-04-01 00:00:00

  • Role of the pituitary–adrenal axis in granulocyte-colony stimulating factor-induced neuroprotection against hypoxia–ischemia in neonatal rats.

    abstract：:Several reports indicate that the activity of the hypothalamic–pituitary–adrenal axis (HPA) is increased after a brain insult and that its down-regulation can improve detrimental outcomes associated with ischemic brain injuries.Granulocyte-colony stimulating factor (G-CSF) is a neuroprotective drug shown in the naïve ...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2012.03.021

    authors： Charles MS,Ostrowski RP,Manaenko A,Duris K,Zhang JH,Tang J

    更新日期：2012-07-01 00:00:00

  • Quantitative ultrasound and apoptotic death in the neonatal primate brain.

    abstract：:Apoptosis is triggered in the developing mammalian brain by sedative, anesthetic or antiepileptic drugs during late gestation and early life. Whether human children are vulnerable to this toxicity mechanism remains unknown, as there are no imaging techniques to capture it. Apoptosis is characterized by distinct struct...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2019.03.032

    authors： Rosado-Mendez IM,Noguchi KK,Castañeda-Martinez L,Kirvassilis G,Wang SH,Manzella F,Swiney BS,Masuoka K,Capuano S III2,Brunner KG,Crosno K,Guerrero QW,Whitson H,Brambrink A,Simmons HS,Mejia AF,Zagzebski JA,Hall TJ,Ikono

    更新日期：2019-07-01 00:00:00

  • Interictal spikes, seizures and ictal cell death are not necessary for post-traumatic epileptogenesis in vitro.

    abstract：:Clinical studies indicate that phenytoin prevents acute post-traumatic seizures but not subsequent post-traumatic epilepsy. We explored this phenomenon using organotypic hippocampal slice cultures as a model of severe traumatic brain injury. Hippocampal slices were cultured for up to eight weeks, during which acute an...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2011.11.001

    authors： Berdichevsky Y,Dzhala V,Mail M,Staley KJ

    更新日期：2012-02-01 00:00:00

  • Progressive neuroanatomical changes caused by Grin1 loss-of-function mutation.

    abstract：:NMDA receptor dysfunction is central to the encephalopathies caused by missense mutations in the NMDA receptor subunit genes. Missense variants of GRIN1, GRIN2A, and GRIN2B cause similar syndromes with varying severity of intellectual impairment, autism, epilepsy, and motor dysfunction. To gain insight into possible b...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2019.104527

    authors： Intson K,van Eede MC,Islam R,Milenkovic M,Yan Y,Salahpour A,Henkelman RM,Ramsey AJ

    更新日期：2019-12-01 00:00:00

  • Approaches to transport therapeutic drugs across the blood-brain barrier to treat brain diseases.

    abstract：:The central nervous system is protected by barriers which control the entry of compounds into the brain, thereby regulating brain homeostasis. The blood-brain barrier, formed by the endothelial cells of the brain capillaries, restricts access to brain cells of blood-borne compounds and facilitates nutrients essential ...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章,评审

    doi：10.1016/j.nbd.2009.07.028

    authors： Gabathuler R

    更新日期：2010-01-01 00:00:00

  • GSK3 inhibitors show benefits in an Alzheimer's disease (AD) model of neurodegeneration but adverse effects in control animals.

    abstract：:The dysregulation of glycogen synthase kinase-3 (GSK3) has been implicated in Alzheimer disease (AD) pathogenesis and in Abeta-induced neurotoxicity, leading us to investigate it as a therapeutic target in an intracerebroventricular Abeta infusion model. Infusion of a specific GSK3 inhibitor SB216763 (SB) reduced a do...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2008.10.007

    authors： Hu S,Begum AN,Jones MR,Oh MS,Beech WK,Beech BH,Yang F,Chen P,Ubeda OJ,Kim PC,Davies P,Ma Q,Cole GM,Frautschy SA

    更新日期：2009-02-01 00:00:00

  • The metabolism of glycosaminoglycans is impaired in prion diseases.

    abstract：:It is well established that the conversion of PrP(C) to PrP(Sc) is the key event in prion disease biology. In addition, several lines of evidence suggest that glycosaminoglycans (GAGs) and in particular heparan sulfate (HS) may play a role in the PrP(C) to PrP(Sc) conversion process. It has been proposed that PrP(Sc) ...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2005.05.009

    authors： Mayer-Sonnenfeld T,Zeigler M,Halimi M,Dayan Y,Herzog C,Lasmezas CI,Gabizon R

    更新日期：2005-12-01 00:00:00

  • Controversies in preterm brain injury.

    abstract：:In this review, we highlight critical unresolved questions in the etiology and mechanisms causing preterm brain injury. Involvement of neurons, glia, endogenous factors and exogenous exposures is considered. The structural and functional correlates of interrupted development and injury in the premature brain are under...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章,评审

    doi：10.1016/j.nbd.2015.10.012

    authors： Penn AA,Gressens P,Fleiss B,Back SA,Gallo V

    更新日期：2016-08-01 00:00:00

  • Proximal movements compensate for distal forelimb movement impairments in a reach-to-eat task in Huntington's disease: new insights into motor impairments in a real-world skill.

    abstract：:Huntington's disease (HD) causes severe motor impairments that are characterized by chorea, dystonia, and impaired fine motor control. The motor deficits include deficits in the control of the forelimb, but as yet there has been no comprehensive assessment of the impairments in arm, hand and digit movements as they ar...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2010.11.002

    authors： Klein A,Sacrey LA,Dunnett SB,Whishaw IQ,Nikkhah G

    更新日期：2011-02-01 00:00:00

  • Activation of caspase-1 dependent interleukins in developmental brain trauma.

    abstract：:Focal mechanical cortical trauma triggers diffuse apoptotic neurodegeneration in the developing rat brain which is associated with invasion of brain tissue with inflammatory mediators. We hypothesized that caspase-1 and the two caspase-1-processed cytokines, interleukin (IL)-1beta and IL-18, are involved in trauma-ind...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2006.11.003

    authors： Sifringer M,Stefovska V,Endesfelder S,Stahel PF,Genz K,Dzietko M,Ikonomidou C,Felderhoff-Mueser U

    更新日期：2007-03-01 00:00:00

  • Targeting 5-HT(1A) receptors in astrocytes to protect dopaminergic neurons in Parkinsonian models.

    abstract：:Astrocytes are abundant neuron-supporting glial cells that harbor a powerful arsenal of neuroprotective antioxidative molecules and neurotrophic factors. Here we examined whether enrichment with healthy striatal astrocytes can provide neuroprotection against progressive dopaminergic neurodegeneration. Serotonin 1A (5-...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2013.08.003

    authors： Miyazaki I,Asanuma M,Murakami S,Takeshima M,Torigoe N,Kitamura Y,Miyoshi K

    更新日期：2013-11-01 00:00:00

  • Delayed calcium dysregulation in neurons requires both the NMDA receptor and the reverse Na+/Ca2+ exchanger.

    abstract：:Glutamate-induced delayed calcium dysregulation (DCD) is a causal factor leading to neuronal death. The mechanism of DCD is not clear but Ca2+ influx via N-methyl-d-aspartate receptors (NMDAR) and/or the reverse plasmalemmal Na+/Ca2+ exchanger (NCXrev) could be involved in DCD. However, the extent to which NMDAR and N...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2011.12.051

    authors： Brittain MK,Brustovetsky T,Sheets PL,Brittain JM,Khanna R,Cummins TR,Brustovetsky N

    更新日期：2012-04-01 00:00:00

  • Progressive phenotype and nuclear accumulation of an amino-terminal cleavage fragment in a transgenic mouse model with inducible expression of full-length mutant huntingtin.

    abstract：:Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder characterized behaviorally by chorea, incoordination, and shortened lifespan and neuropathologically by huntingtin inclusions and neuronal degeneration. In order to facilitate studies of pathogenesis and therapeutics, we have generated a new...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2005.07.014

    authors： Tanaka Y,Igarashi S,Nakamura M,Gafni J,Torcassi C,Schilling G,Crippen D,Wood JD,Sawa A,Jenkins NA,Copeland NG,Borchelt DR,Ross CA,Ellerby LM

    更新日期：2006-02-01 00:00:00

  • Buckminsterfullerenol free radical scavengers reduce excitotoxic and apoptotic death of cultured cortical neurons.

    abstract：:Novel anti-oxidants based on the buckminsterfullerene molecule were explored as neuroprotective agents in cortical cell cultures exposed to excitotoxic and apoptotic injuries. Two polyhydroxylated C60 derivatives, C60(OH)n, n = 12, and C60(OH)nOm, n = 18-20, m = 3-7 hemiketal groups, demonstrated excellent anti-oxidan...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1006/nbdi.1996.0013

    authors： Dugan LL,Gabrielsen JK,Yu SP,Lin TS,Choi DW

    更新日期：1996-04-01 00:00:00

  • Alpha-synuclein deregulates the expression of COL4A2 and impairs ER-Golgi function.

    abstract：:Alpha-synuclein (aSyn) is the major protein component of Lewy bodies and Lewy neurites, the typical pathological hallmarks in Parkinson's disease (PD) and Dementia with Lewy bodies. aSyn is capable of inducing transcriptional deregulation, but the precise effect of specific aSyn mutants associated with familial forms ...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2018.08.001

    authors： Paiva I,Jain G,Lázaro DF,Jerčić KG,Hentrich T,Kerimoglu C,Pinho R,Szegő ÈM,Burkhardt S,Capece V,Halder R,Islam R,Xylaki M,Caldi Gomes LA,Roser AE,Lingor P,Schulze-Hentrich JM,Borovečki F,Fischer A,Outeiro TF

    更新日期：2018-11-01 00:00:00

  • p53 is abnormally elevated and active in the CNS of patients with amyotrophic lateral sclerosis.

    abstract：:Motor neuron degeneration in amyotrophic lateral sclerosis (ALS) is a form of apoptosis, but the mechanisms for this neuronal cell death are not known. We evaluated whether motor neuron degeneration in ALS is associated with changes in the levels and function of the apoptosis regulating protein p53. The protein levels...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1006/nbdi.2000.0314

    authors： Martin LJ

    更新日期：2000-12-01 00:00:00

  • Platform influence on DNA microarray data in postmortem brain research.

    abstract：:In addition to the substantial biological diversity among humans, our limited ability to reliably measure expression changes of small magnitude significantly reduces our capacity to obtain convergent sets of transcriptome data in postmortem brain. In particular, differences in the structure and sensitivity/reproducibi...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2004.10.020

    authors： Hollingshead D,Lewis DA,Mirnics K

    更新日期：2005-04-01 00:00:00

  • Proliferative response of distinct hippocampal progenitor cell populations after cortical infarcts in the adult brain.

    abstract：:Precursor cells in the adult dentate gyrus are a heterogeneous population. Astrocytic cell types with radial glia-like morphology and low proliferative activity have been distinguished from highly dividing subtypes expressing early neuronal properties. Recent evidence indicates that physiological stimuli predominantly...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2005.07.013

    authors： Kunze A,Grass S,Witte OW,Yamaguchi M,Kempermann G,Redecker C

    更新日期：2006-02-01 00:00:00