Neuroprotective effects of erythropoietin in the rat hippocampus after pilocarpine-induced status epilepticus.


:Neuroprotective functions of erythropoietin (Epo) are thought to involve a heteroreceptor composed of both Epo receptor (Epo-R) and common beta chain (betac). Here, we measured the response of hippocampal Epo system components (Epo, Epo-R and betac) during neurodegenerative processes following pilocarpine-induced status epilepticus (SE), and examined whether recombinant human Epo (rHuEpo) could support neuronal survival. We evidence that Epo is induced in astroglia following SE, in particular within areas displaying delayed neuronal death. In addition, we demonstrate for the first time that rHuEpo reduces considerably hippocampal neurodegeneration following SE. rHuEpo may thus supplement astroglial induction of Epo to promote enhanced hippocampal neuronal survival following SE. We also show that Epo-R is expressed by neurons and astrocytes mainly, while betac is barely detectable in basal conditions and induced in reactive microglia exclusively following SE. Altogether, our results suggest that Epo/rHuEpo exerts neuroprotection, through Epo-R signaling and independently of betac, and, therefore, may be anti-epileptogenic.


Neurobiol Dis


Neurobiology of disease


Nadam J,Navarro F,Sanchez P,Moulin C,Georges B,Laglaine A,Pequignot JM,Morales A,Ryvlin P,Bezin L




Has Abstract


2007-02-01 00:00:00














  • Environmental risk factors and Parkinson's disease: selective degeneration of nigral dopaminergic neurons caused by the herbicide paraquat.

    abstract::Environmental toxicants and, in particular, pesticides have been implicated as risk factors in Parkinson's disease (PD). The purpose of this study was to determine if selective nigrostriatal degeneration could be reproduced by systemic exposure of mice to the widely used herbicide paraquat. Repeated intraperitoneal pa...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章


    authors: McCormack AL,Thiruchelvam M,Manning-Bog AB,Thiffault C,Langston JW,Cory-Slechta DA,Di Monte DA

    更新日期:2002-07-01 00:00:00

  • TDP-43 knockdown causes innate immune activation via protein kinase R in astrocytes.

    abstract::TAR-DNA binding protein 43 (TDP-43) is a multifunctional RNA binding protein directly implicated in the etiology of amyotrophic lateral sclerosis (ALS). Previous studies have demonstrated that loss of TDP-43 function leads to intracellular accumulation of non-coding repetitive element transcripts and double-stranded R...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章


    authors: LaRocca TJ,Mariani A,Watkins LR,Link CD

    更新日期:2019-12-01 00:00:00

  • Impaired cognitive discrimination and discoordination of coupled theta-gamma oscillations in Fmr1 knockout mice.

    abstract::Fragile X syndrome (FXS) patients do not make the fragile X mental retardation protein (FMRP). The absence of FMRP causes dysregulated translation, abnormal synaptic plasticity and the most common form of inherited intellectual disability. But FMRP loss has minimal effects on memory itself, making it difficult to unde...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章


    authors: Radwan B,Dvorak D,Fenton AA

    更新日期:2016-04-01 00:00:00

  • Identification of candidate proteins binding to prion protein.

    abstract::Prion diseases are disorders of protein conformation that produce neurodegeneration in humans and animals. Studies of transgenic (Tg) mice indicate that a factor designated protein X is involved in the conversion of the normal cellular prion protein (PrPC) into the scrapie isoform (PrPSc); protein X appears to interac...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章


    authors: Yehiely F,Bamborough P,Da Costa M,Perry BJ,Thinakaran G,Cohen FE,Carlson GA,Prusiner SB

    更新日期:1997-01-01 00:00:00

  • BDNF regulates BIM expression levels in 3-nitropropionic acid-treated cortical neurons.

    abstract::3-Nitropropionic acid (3-NP) is an irreversible inhibitor of succinate dehydrogenase that has been used to explore the primary mechanisms of cell death associated with mitochondrial dysfunction and neurodegeneration in Huntington's disease. In this study we investigated the ability of brain-derived neurotrophic factor...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章


    authors: Almeida S,Laço M,Cunha-Oliveira T,Oliveira CR,Rego AC

    更新日期:2009-09-01 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


    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

  • Polyglutamine-expanded ataxin-3 causes cerebellar dysfunction of SCA3 transgenic mice by inducing transcriptional dysregulation.

    abstract::In the present study, we prepared a SCA3 animal model by generating transgenic mice expressing polyglutamine-expanded ataxin-3-Q79. Ataxin-3-Q79 was expressed in brain areas implicated in SCA3 neurodegeneration, including cerebellum, pontine nucleus and substantia nigra. Ataxin-3-Q79 transgenic mice displayed motor dy...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章


    authors: Chou AH,Yeh TH,Ouyang P,Chen YL,Chen SY,Wang HL

    更新日期:2008-07-01 00:00:00

  • Distinct behavioral and neuropathological abnormalities in transgenic mouse models of HD and DRPLA.

    abstract::Huntington's disease (HD) and Dentatorubral and pallidoluysian atrophy (DRPLA) are autosomal dominant, neurodegenerative disorders caused by the expansion of polyglutamine tracts in their respective proteins, huntingtin and atrophin-1. We have previously generated mouse models of these disorders, using transgenes expr...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章


    authors: Schilling G,Jinnah HA,Gonzales V,Coonfield ML,Kim Y,Wood JD,Price DL,Li XJ,Jenkins N,Copeland N,Moran T,Ross CA,Borchelt DR

    更新日期:2001-06-01 00:00:00

  • Every-other-day feeding exacerbates inflammation and neuronal deficits in 5XFAD mouse model of Alzheimer's disease.

    abstract::Food restriction has been widely associated with beneficial effects on brain aging and age-related neurodegenerative diseases such as Alzheimer's disease. However, previous studies on the effects of food restriction on aging- or pathology-related cognitive decline are controversial, emphasizing the importance of the t...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章


    authors: Lazic D,Tesic V,Jovanovic M,Brkic M,Milanovic D,Zlokovic BV,Kanazir S,Perovic M

    更新日期:2020-03-01 00:00:00

  • Reduced dopamine transporter density in the ventral striatum of patients with Parkinson's disease and pathological gambling.

    abstract::Pathological gambling (PG) represents a behavioral side effect of dopamine replacement therapy in a minority of patients with Parkinson's disease (PD). Using striatal dopamine transporter (DAT) with single photon emission tomography we assessed presynaptic dopaminergic function in 8 PD patients with PG, 21 matched PD ...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章


    authors: Cilia R,Ko JH,Cho SS,van Eimeren T,Marotta G,Pellecchia G,Pezzoli G,Antonini A,Strafella AP

    更新日期:2010-07-01 00:00:00

  • Metabolomics tools for identifying biomarkers for neuropsychiatric diseases.

    abstract::The repertoire of biochemicals (or small molecules) present in cells, tissue, and body fluids is known as the metabolome. Today, clinicians utilize only a very small part of the information contained in the metabolome, as revealed by the quantification of a limited set of analytes to gain information on human health. ...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章,评审


    authors: Quinones MP,Kaddurah-Daouk R

    更新日期:2009-08-01 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


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

    更新日期:2013-06-01 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


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

    更新日期:1996-04-01 00:00:00

  • Hyperphosphorylated tau and paired helical filament-like structures in the brains of mice carrying mutant amyloid precursor protein and mutant presenilin-1 transgenes.

    abstract::Senile plaques composed mainly of beta-amyloid (Abeta) and neurofibrillary tangles principally composed of hyperphosphorylated tau are the major pathological features of Alzheimer's disease (AD). Despite the fact that increased expression of amyloid precursor protein (APP) and presenilin-1 (PS1) transgenes in mice lea...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章


    authors: Kurt MA,Davies DC,Kidd M,Duff K,Howlett DR

    更新日期:2003-10-01 00:00:00

  • Beta burst coupling across the motor circuit in Parkinson's disease.

    abstract::Exaggerated activity in the beta band (13-35 Hz) is a hallmark of basal ganglia signals in patients with Parkinson's disease (PD). Beta activity however is not constantly elevated, but comes in bursts. In previous work we showed that the longer beta bursts are maintained, the more the oscillatory synchronisation withi...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章


    authors: Tinkhauser G,Torrecillos F,Duclos Y,Tan H,Pogosyan A,Fischer P,Carron R,Welter ML,Karachi C,Vandenberghe W,Nuttin B,Witjas T,Régis J,Azulay JP,Eusebio A,Brown P

    更新日期:2018-09-01 00:00:00

  • Hippocampal subregion-specific microRNA expression during epileptogenesis in experimental temporal lobe epilepsy.

    abstract::Since aberrant miRNA expression has been implicated in numerous brain diseases, we studied miRNA expression and miRNA regulation of important signaling pathways during temporal lobe epileptogenesis in order to identify possible targets for epilepsy therapy. The temporal profile of miRNA expression was analyzed in thre...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章


    authors: Gorter JA,Iyer A,White I,Colzi A,van Vliet EA,Sisodiya S,Aronica E

    更新日期:2014-02-01 00:00:00

  • Lack of CCR5 modifies glial phenotypes and population of the nigral dopaminergic neurons, but not MPTP-induced dopaminergic neurodegeneration.

    abstract::Constitutive expression of C-C chemokine receptor (CCR) 5 has been detected in astrocytes, microglia and neurons, but its physiological roles in the central nervous system are obscure. The bidirectional interactions between neuron and glial cells through CCR5 and its ligands were thought to be crucial for maintaining ...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章


    authors: Choi DY,Lee MK,Hong JT

    更新日期:2013-01-01 00:00:00

  • Genetically encoded redox sensor identifies the role of ROS in degenerative and mitochondrial disease pathogenesis.

    abstract::Mitochondrial dysfunction plays an important role in the pathogenesis of neurodegenerative diseases, numerous other disease states and senescence. The ability to monitor reactive oxygen species (ROS) within tissues and over time in animal model systems is of significant research value. Recently, redox-sensitive fluore...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章


    authors: Liu Z,Celotto AM,Romero G,Wipf P,Palladino MJ

    更新日期:2012-01-01 00:00:00

  • Exonic microdeletions of the gephyrin gene impair GABAergic synaptic inhibition in patients with idiopathic generalized epilepsy.

    abstract::Gephyrin is a postsynaptic scaffolding protein, essential for the clustering of glycine and γ-aminobutyric acid type-A receptors (GABAARs) at inhibitory synapses. An impairment of GABAergic synaptic inhibition represents a key pathway of epileptogenesis. Recently, exonic microdeletions in the gephyrin (GPHN) gene have...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章


    authors: Dejanovic B,Lal D,Catarino CB,Arjune S,Belaidi AA,Trucks H,Vollmar C,Surges R,Kunz WS,Motameny S,Altmüller J,Köhler A,Neubauer BA,Epicure Consortium,Nürnberg P,Noachtar S,Schwarz G,Sander T

    更新日期:2014-07-01 00:00:00

  • Matrix metalloproteinase 9 regulates cell death following pilocarpine-induced seizures in the developing brain.

    abstract::Matrix metalloproteinases (MMPs) are involved in tissue repair, cell death and morphogenesis. We investigated the role of the gelatinases MMP-2 and MMP-9 in the pathogenesis of neuronal death induced by prolonged seizures in the developing brain. Seven-day-old rats, MMP-9 knockout mice and transgenic rats overexpressi...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章


    authors: Hoehna Y,Uckermann O,Luksch H,Stefovska V,Marzahn J,Theil M,Gorkiewicz T,Gawlak M,Wilczynski GM,Kaczmarek L,Ikonomidou C

    更新日期:2012-12-01 00:00:00

  • Biology of A beta amyloid in Alzheimer's disease.

    abstract::The genetic associations with the pathological features of AD are diverse: A rapidly growing number of mutations in presenilin 1 and 2 on chromosomes 14 and 1, respectively, are found in many early-onset FAD patients (Lendon et al., 1997). In addition, beta PP mutations are found in a small percentage of early-onset F...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章,评审


    authors: Wisniewski T,Ghiso J,Frangione B

    更新日期:1997-01-01 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


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

    更新日期:2012-03-01 00:00:00

  • Impairments in social novelty recognition and spatial memory in mice with conditional deletion of Scn1a in parvalbumin-expressing cells.

    abstract::Loss of function mutations in the SCN1A gene, which encodes the voltage-gated sodium channel Nav1.1, have been described in the majority of Dravet syndrome patients presenting with epileptic seizures, hyperactivity, autistic traits, and cognitive decline. We previously reported predominant Nav1.1 expression in parvalb...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章


    authors: Tatsukawa T,Ogiwara I,Mazaki E,Shimohata A,Yamakawa K

    更新日期:2018-04-01 00:00:00

  • Imaging biomarkers of epileptogenecity after traumatic brain injury - Preclinical frontiers.

    abstract::Posttraumatic epilepsy (PTE) is a major neurodegenerative disease accounting for 20% of symptomatic epilepsy cases. A long latent phase offers a potential window for prophylactic treatment strategies to prevent epilepsy onset, provided that the patients at risk can be identified. Some promising imaging biomarker candi...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章,评审


    authors: Immonen R,Harris NG,Wright D,Johnston L,Manninen E,Smith G,Paydar A,Branch C,Grohn O

    更新日期:2019-03-01 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


    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

  • Adeno-associated viral vector-mediated gene transfer of brain-derived neurotrophic factor reverses atrophy of rubrospinal neurons following both acute and chronic spinal cord injury.

    abstract::Rubrospinal neurons (RSNs) undergo marked atrophy after cervical axotomy. This progressive atrophy may impair the regenerative capacity of RSNs in response to repair strategies that are targeted to promote rubrospinal tract regeneration. Here, we investigated whether we could achieve long-term rescue of RSNs from lesi...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章


    authors: Ruitenberg MJ,Blits B,Dijkhuizen PA,te Beek ET,Bakker A,van Heerikhuize JJ,Pool CW,Hermens WT,Boer GJ,Verhaagen J

    更新日期:2004-03-01 00:00:00

  • Hereditary sensory neuropathy type 1-associated deoxysphingolipids cause neurotoxicity, acute calcium handling abnormalities and mitochondrial dysfunction in vitro.

    abstract::Hereditary sensory neuropathy type 1 (HSN-1) is a peripheral neuropathy most frequently caused by mutations in the SPTLC1 or SPTLC2 genes, which code for two subunits of the enzyme serine palmitoyltransferase (SPT). SPT catalyzes the first step of de novo sphingolipid synthesis. Mutations in SPT result in a change in ...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章


    authors: Wilson ER,Kugathasan U,Abramov AY,Clark AJ,Bennett DLH,Reilly MM,Greensmith L,Kalmar B

    更新日期:2018-09-01 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


    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

  • YOD1 attenuates neurogenic proteotoxicity through its deubiquitinating activity.

    abstract::Ubiquitination, a fundamental post-translational modification of intracellular proteins, is enzymatically reversed by deubiquitinase enzymes (deubiquitinases). >90 deubiquitinases have been identified. One of these enzymes, YOD1, possesses deubiquitinase activity and is similar to ovarian tumor domain-containing prote...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章


    authors: Tanji K,Mori F,Miki Y,Utsumi J,Sasaki H,Kakita A,Takahashi H,Wakabayashi K

    更新日期:2018-04-01 00:00:00

  • GluN3A promotes NMDA spiking by enhancing synaptic transmission in Huntington's disease models.

    abstract::Age-inappropriate expression of juvenile NMDA receptors (NMDARs) containing GluN3A subunits has been linked to synapse loss and death of spiny projection neurons of the striatum (SPNs) in Huntington's disease (HD). Here we show that suppressing GluN3A expression prevents a multivariate synaptic transmission phenotype ...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章


    authors: Mahfooz K,Marco S,Martínez-Turrillas R,Raja MK,Pérez-Otaño I,Wesseling JF

    更新日期:2016-09-01 00:00:00