37 results match your criteria bcl2l1 bdnf


Effects of novel brain-penetrating oxime acetylcholinesterase reactivators on sarin surrogate-induced changes in rat brain gene expression.

J Biochem Mol Toxicol 2021 Mar 8:e22755. Epub 2021 Mar 8.

Department of Comparative Biomedical Sciences, Center for Environmental Health Sciences, Mississippi State University, College of Veterinary Medicine, Mississippi State, United States, USA.

Past assassinations and terrorist attacks demonstrate the need for a more effective antidote against nerve agents and other organophosphates (OP) that cause brain damage through inhibition of acetylcholinesterase (AChE). Our lab has invented a platform of phenoxyalkyl pyridinium oximes (US patent 9,277,937) that demonstrate the ability to cross the blood-brain barrier in in vivo rat tests with a sarin surrogate nitrophenyl isopropyl methylphosphonate (NIMP) and provide evidence of brain penetration by reducing cessation time of seizure-like behaviors, accumulation of glial fibrillary acidic protein (GFAP), and hippocampal neuropathology, as opposed to the currently approved oxime, 2-pyridine aldoxime methyl chloride (2-PAM). Using two of the novel oximes (Oximes 1 and 20), this project examined whether gene expression changes might help explain this protection. Read More

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XQ-1H alleviates cerebral ischemia in mice through inhibition of apoptosis and promotion of neurogenesis in a Wnt/β-catenin signaling dependent way.

Life Sci 2019 Oct 6;235:116844. Epub 2019 Sep 6.

State Key Laboratory of Natural Medicines, Department of Physiology, China Pharmaceutical University, Nanjing 210009, PR China. Electronic address:

Aims: 10-O-(N,N-dimethylaminoethyl)-ginkgolide B methanesulfonate (XQ-1H), a new derivative of ginkgolide B, has drawn great attention for its potent bioactivities against ischemia-induced injury. The purpose of this study was to further investigate the effect of XQ-1H against acute ischemic stroke by inducing middle cerebral artery occlusion/reperfusion (MCAO/R) injuries in mice.

Main Methods: Treatment of XQ-1H (78 or 39 mg/kg, i. Read More

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October 2019

Sevoflurane Exacerbates Cognitive Impairment Induced by A in Rats through Initiating Neurotoxicity, Neuroinflammation, and Neuronal Apoptosis in Rat Hippocampus.

Mediators Inflamm 2018 9;2018:3802324. Epub 2018 Oct 9.

Department of Pharmacy, Shengjing Hospital of China Medical University, No. 36, Sanhao Street, Herping District, Shenyang, Liaoning 110004, China.

Objective: This study was aimed at investigating whether sevoflurane inhalation induced cognitive impairment in rats with a possible mechanism involved in the event.

Methods: Thirty-two rats were randomly divided into four groups of normal saline (NS) + O, NS + sevoflurane (sevo), amyloid- peptide (A) + O, and A + sevo. The rats in the four groups received bilateral intrahippocampus injections of NS or A. Read More

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January 2019

Doxycycline Used for Control of Transgene Expression has its Own Effects on Behaviors and Bcl-xL in the Rat Hippocampus.

Cell Mol Neurobiol 2018 Jan 31;38(1):281-288. Epub 2017 Aug 31.

Functional Neurogenomics Laboratory, Institute of Cytology and Genetics, Siberian Branch, Russian Academy of Sciences, Novosibirsk, Russia, 630090.

Doxycycline (Dox)-inducible transgenic approach is used to examine the neural mechanisms of anxiety and depression; however, its own effects on related behaviors are not clear. To address this, in the present study, we tested the anxiety- and depression-like behaviors in rats treated with Dox in drinking water (2 mg/ml) in the elevated plus-maze (EPM; on day 5) and forced swim (FST; on day 8) tests, respectively. In addition, the levels of mRNAs and proteins of brain-derived neurotrophic factor (BDNF) and anti-apoptotic protein Bcl-xL in the hippocampus (HIPP) and frontal cortex (FC) were also analyzed. Read More

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January 2018

Effects of Short-Term Exposure to Lithium on Antiapoptotic Bcl-xL Protein Expression in Cortex and Hippocampus of Rats after Acute Stress.

Biochemistry (Mosc) 2017 Mar;82(3):345-350

Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, Novosibirsk, 630090, Russia.

The antiapoptotic protein Bcl-xL is involved in development of neurobiological resilience to stress; hence, the possibility of use of psychotropic drugs to increase its expression in brain in response to stress is of considerable interest. Lithium is a neurotropic drug widely used in psychiatry. In work, we studied effects of lithium administration (for 2 or 7 days) on the expression of Bcl-xL mRNA and protein in the hippocampi and cortices of rats subjected to stress that induced depression-like behavior in the animals. Read More

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[Influence of chronic alcohol treatment on the expression of the Bdnf, Bax, Bcl-xL, and CASP3 genes in the mouse brain: Role of the C1473G polymorphism in the gene encoding tryptophan hydroxylase 2].

Mol Biol (Mosk) 2016 Mar-Apr;50(2):302-10

Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, Novosibirsk, 630090, Russia.

Tryptophan hydroxylase 2 (Tph-2) is the key enzyme in serotonin biosynthesis. Serotonin is one of the main neurotransmitters involved in the regulation of various physiological functions and behavior patterns. The influence of chronic ethanol consumption on the expression of the Bdnf, Bax, Bcl-xL, and CASP3 genes was studied in the brain structures of B6-1473C (C/C) and B6-1473G (G/G) mice that had been obtained on the base of the C57BL/6 strain. Read More

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The p75 neurotrophin receptor augments survival signaling in the striatum of pre-symptomatic Q175(WT/HD) mice.

Neuroscience 2016 Jun 3;324:297-306. Epub 2016 Mar 3.

Department of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, MI, USA; Neuroscience Graduate Program, University of Michigan School of Medicine, Ann Arbor, MI, USA. Electronic address:

Huntington's disease (HD) is a dominantly inherited neurodegenerative disorder characterized by a constellation of motor, cognitive, and psychiatric features. Striatal medium spiny neurons, one of the most affected populations, are dependent on brain-derived neurotrophic factor (BDNF) anterogradely transported from the cortex for proper function and survival. Recent studies suggest both receptors for BDNF, TrkB and p75 neurotrophin receptor (p75), are improperly regulated in the striata of HD patients and mouse models of HD. Read More

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Sexual Differences in Cell Loss during the Post-Hatch Development of Song Control Nuclei in the Bengalese Finch.

PLoS One 2015 4;10(5):e0125802. Epub 2015 May 4.

Beijing Key Laboratory of Gene Resource and Molecular Development, Beijing Normal University, Beijing, China.

Birdsongs and the regions of their brain that control song exhibit obvious sexual differences. However, the mechanisms underlying these sexual dimorphisms remain unknown. To address this issue, we first examined apoptotic cells labeled with caspase-3 or TUNEL in Bengalese finch song control nuclei - the robust nucleus of the archopallium (RA), the lateral magnocellular nucleus of the anterior nidopallium (LMAN), the high vocal center (HVC) and Area X from post-hatch day (P) 15 to 120. Read More

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Effect of actual long-term spaceflight on BDNF, TrkB, p75, BAX and BCL-XL genes expression in mouse brain regions.

Neuroscience 2015 Jan 4;284:730-736. Epub 2014 Nov 4.

Institute of Cytology and Genetics, Lavrentyeva Avenue, 10, 633090 Novosibirsk, Russia.

Mice of C57BL/6J strain were exposed to 1-month spaceflight on Russian biosatellite Bion-M1 to determine the effect of long-term actual spaceflight on the expression of genes involved in the processes of neurogenesis and apoptosis. Specifically, we focused on the genes encoding proapoptotic factor BAX, antiapoptotic factor BCL-XL, brain-derived neurotrophic factor (BDNF) and BDNF receptors TrkB and p75. Spaceflight reduced the expression of the antiapoptotic BCL-XL gene in the striatum and hypothalamus, but increased it in the hippocampus. Read More

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January 2015

The neuroprotective and neurogenic effects of neuropeptide Y administration in an animal model of hippocampal neurodegeneration and temporal lobe epilepsy induced by trimethyltin.

J Neurochem 2012 Jul 21;122(2):415-26. Epub 2012 May 21.

Institute of Anatomy and Cell Biology, Università Cattolica del Sacro Cuore, Rome, Italy.

The effects of intracerebroventricular administration of neuropeptide Y (NPY), which is believed to play an important role in neuroprotection against excitotoxicity and in the modulation of adult neurogenesis, were evaluated in an animal model of hippocampal neurodegeneration and temporal lobe epilepsy represented by trimethyltin (TMT) intoxication. A single TMT injection (8 mg/kg) causes, in the rat brain, massive neuronal death, selectively involving pyramidal neurons, accompanied by glial activation and enhanced hippocampal neurogenesis. Our data indicate that intracerebroventricular administration of exogenous NPY (at the dose of 2 μg/2 μL, 4 days after TMT-administration), in adult rats, exerts a protective role in regard to TMT-induced hippocampal damage and a proliferative effect on the hippocampal neurogenic niche through the up-regulation of Bcl-2, Bcl2l1, Bdnf, Sox-2, NeuroD1, Noggin and Doublecortin genes, contributing to delineate more clearly the role of NPY in in vivo neurodegenerative processes. Read More

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[Behavior in the forced-swimming test and expression of BDNF and Bcl-xl genes in the rat brain].

Zh Vyssh Nerv Deiat Im I P Pavlova 2011 May-Jun;61(3):332-9

A single exposure of rats to the forced-swimming stress decreased BDNF mRNA levels in the cortex and increased Bcl-xl gene expression in the hippocampus and amygdala 24 h after the stress. The animals demonstrated a depressive-like behavior and elevated blood corticosterone level. There was a significant negative correlation between BDNF mRNA level in the cortex and immobility time during swimming. Read More

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September 2011

Stress-induced activation of the brainstem Bcl-xL gene expression in rats treated with fluoxetine: correlations with serotonin metabolism and depressive-like behavior.

Neuropharmacology 2012 Jan 29;62(1):177-83. Epub 2011 Jun 29.

Functional Neurogenomics Laboratory, Institute of Cytology and Genetics, Novosibirsk 630090, Russia.

Mechanisms underlying stress-induced depression and antidepressant drug action were shown to involve alterations in serotonergic (5-HT) neurotransmission and expression of genes coding for proteins associated with neurotrophic signaling pathways and cell-survival in the hippocampus and cortex. Expression of these genes in the brainstem containing 5-HT neurons may also be related to vulnerability or resilience to stress-related psychopathology. Here we investigated 5-HT markers and expression of genes for Brain-Derived Neurotrophic Factor (BDNF) and apoptotic proteins in the brainstem in relation to swim stress-induced behavioral despair. Read More

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January 2012

[Effect of acupuncture on the expression of Bcl-xl and BDNF of retina in rabbits with chronic intraocular hypertension].

Zhongguo Zhen Jiu 2010 Aug;30(8):661-4

The First Hospital Affiliated to Heilongjiang University of TCM, Harbin 150040, China.

Objective: To explore the protection effects of acupuncture on glaucomatous optic nerve damage and its mechanism.

Methods: Experimental glaucoma model was induced by intracameral injection of compound Carbomer solution in rabbits. After 28 days, ocular tension returned to normal by filtration surgery. Read More

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Brain-derived neurotrophic factor enhances Bcl-xL expression through protein kinase casein kinase 2-activated and nuclear factor kappa B-mediated pathway in rat hippocampus.

Brain Pathol 2011 Mar;21(2):150-62

Institute of Neuroscience, National Chengchi University, Taipei, Taiwan. Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.

Brain-derived neurotrophic factor (BDNF) was shown to produce its neuroprotective effect through extracellular signal-regulated kinase 1/2 (ERK1/2) and phosphatidylinositol-3 kinase (PI3-K) signaling. But whether other pathways also mediate the neuroprotective effect of BDNF is less known. In this study, we found that direct administration of BDNF to rat hippocampal CA1 area dose-dependently increased the mRNA and protein levels of Bcl-xL. Read More

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Resistance to the development of stress-induced behavioral despair in the forced swim test associated with elevated hippocampal Bcl-xl expression.

Behav Brain Res 2010 Dec 8;213(2):218-24. Epub 2010 May 8.

Functional Neurogenomics Laboratory, Institute of Cytology and Genetics, Lavrentjev Av. 10, Novosibirsk, Russia.

Stress may predispose individuals toward depression through down-regulation of neurogenesis and increase in apoptosis in the brain. However, many subjects show high resistance to stress in relation to psychopathology. In the present study, we assessed the possibility that individual-specific patterns of gene expression associated with cell survival and proliferation may be among the molecular factors underlying stress resilience. Read More

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December 2010

Brain-derived neurotrophic factor protects cementoblasts from serum starvation-induced cell death.

J Cell Physiol 2009 Dec;221(3):696-706

Department of Periodontal Medicine, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima, Japan.

Our previous studies have shown that brain-derived neurotrophic factor (BDNF) enhances bone/cementum-related protein gene expression through the TrkB-c-Raf-ERK1/2-Elk-1 signaling pathway in cementoblasts, which play a critical role in the establishment of a functional periodontal ligament. To clarify how BDNF regulates survival in cementoblasts, we examined its effects on cell death induced by serum starvation in immortalized human cementoblast-like (HCEM) cells. BDNF inhibited the death of HCEM cells. Read More

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December 2009

Conditions for tumor-free and dopamine neuron-enriched grafts after transplanting human ES cell-derived neural precursor cells.

Mol Ther 2009 Oct 14;17(10):1761-70. Epub 2009 Jul 14.

Department of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, Seoul 133-791, Korea.

We have previously demonstrated derivation of neural precursor (NP) cells of a midbrain-type from human embryonic stem (hES) cells to yield an enriched population of dopamine (DA) neurons. These hES-derived NPs can be expanded in vitro through multiple passages without altering their DA neurogenic potential. Here, we studied two aspects of these hES-NP cells that are critical issues in cell therapeutic approaches for Parkinson's disease (PD): cell survival and tumorigenic potential. Read More

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October 2009

Overexpression of Bcl-XL in human neural stem cells promotes graft survival and functional recovery following transplantation in spinal cord injury.

J Neurosci Res 2009 Nov;87(14):3186-97

Brain Disease Research Center, Institute for Medical Sciences, Ajou University School of Medicine, Suwon, Korea.

Transplantation of neural stem cells (NSCs) has shown promise for improving functional recovery after spinal cord injury (SCI). The inhospitable milieu of injured spinal cord, however, does not support survival of grafted NSCs, reducing therapeutic efficacy of transplantation. The present study sought to examine whether overexpression of antiapoptotic gene Bcl-X(L) in NSCs could promote graft survival and functional recovery following transplantation in rat contusive SCI model. Read More

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November 2009

Death receptors and caspases but not mitochondria are activated in the GDNF- or BDNF-deprived dopaminergic neurons.

J Neurosci 2008 Jul;28(30):7467-75

Institute of Biotechnology, University of Helsinki, FIN-00014 Helsinki, Finland.

Neurotrophic factors, including glial cell line-derived neurotrophic factor (GDNF) and brain-derived neurotrophic factor (BDNF), promote survival of midbrain dopaminergic neurons, but the death pathways activated in the dopaminergic neurons by deprivation of these factors are poorly studied. We show here that deprivation of GDNF or BDNF triggers a novel mitochondria-independent death pathway in the cultured embryonic dopaminergic neurons: cytochrome c was not released from the mitochondria to cytosol, proapoptotic protein Bax was not activated, and overexpressed Bcl-xL did not block the death. Caspases were critically required, because the death was completely blocked by caspase inhibitor BAF [boc-aspartyl(OMe)-fluoromethylketone] and overexpression of dominant-negative mutants of caspase-9, -3, and -7 significantly blocked the death. Read More

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Suppression of anoikis by the neurotrophic receptor TrkB in human ovarian cancer.

Cancer Sci 2008 Mar 14;99(3):543-52. Epub 2008 Jan 14.

Department of Obstetrics and Gynecology, Shanghai Jiao Tong University Affiliated First People's Hospital, No. 85 Wujin Road, Shanghai 200080, China.

TrkB is a neurotrophic tyrosine kinase receptor (Trk). To investigate its role in anoikis suppression in human ovarian cancer, we used reverse transcription-polymerase chain reaction and real-time polymerase chain reaction, immunohistochemistry, and western blotting to compare the expression levels of TrkB and its ligand brain-derived neurotrophic factor between (i) 20 epithelial ovarian cancers, their multicellular spheroids in ascites or great omentum metastatic lesions, and eight borderline or benign ovarian tumors, as well as four normal ovarian tissues; and (ii) three ovarian cancer cell lines cultured under different conditions: monolayer adhesive culture (adhesive cells), anchorage-independent culture (cell spheroids), and trypsinized cell spheroids placed in monolayer adhesive dishes (cell spheroids replaced). TrkB and brain-derived neurotrophic factor were overexpressed in epithelial ovarian cancers, and full-length TrkB was more often overexpressed in high-grade carcinomas and multicellular spheroids in ascites. Read More

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Lead-induced alterations of apoptosis and neurotrophic factor mRNA in the developing rat cortex, hippocampus, and cerebellum.

J Biochem Mol Toxicol 2007 ;21(5):265-72

Department of Natural Sciences, Fayetteville State University, Fayetteville, NC 28301, USA.

Previous reports have recently shown the prototypic neurotoxicant, lead, to induce apoptosis in the brains of developing organisms. In the current study, timed-pregnant rats were exposed to lead acetate (0.2% in the drinking water) 24 h following birth at postnatal day 1 (PND 1). Read More

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February 2008

BH3-only proteins Bid and Bim(EL) are differentially involved in neuronal dysfunction in mouse models of Huntington's disease.

J Neurosci Res 2007 Sep;85(12):2756-69

Departament de Biologia Cellular i Anatomia Patològica, Facultat de Medicina, Universitat de Barcelona, IDIBAPS, Barcelona, Spain.

Apoptosis, a cell death mechanism regulated by Bcl-2 family members, has been proposed as one of the mechanisms leading to neuronal loss in Huntington's disease (HD). Here we examined the regulation of Bcl-2 family proteins in three different mouse models of HD with exon 1 mutant huntingtin: the R6/1, the R6/1:BDNF+/-, and the Tet/HD94 in which the huntingtin transgene is controlled by the tetracycline-inducible system. Our results disclosed an increase in the levels of the BH3-only proteins Bid and Bim(EL) in the striatum of HD mouse models that was different depending on the stage of the disease. Read More

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September 2007

Developmental cell death is enhanced in the cerebral cortex of mice lacking the brain vesicular monoamine transporter.

J Neurosci 2007 Feb;27(6):1315-24

Institut National de la Santé et de la Recherche Médicale, Unité 616, Institut Fédératif de Recherche Neurosciences, Hôpital de la Pitié-Salpêtrière, 75651 Paris, France.

Neurotransmitters have emerged as important players in the control of programmed cell death in the cerebral cortex. We report that genetic depletion of serotonin, dopamine, and norepinephrine in mice lacking the vesicular monoamine transporter (VMAT2 KO mice) causes an increase in cell death in the superficial layers of the cingulate and retrosplenial cortices during early postnatal life (postnatal days 0-4). Electron microscopy and terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling indicated that this represents a form of apoptosis. Read More

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February 2007

Verification of functional AAV-mediated neurotrophic and anti-apoptotic factor expression.

J Neurosci Methods 2007 Apr 18;161(2):291-300. Epub 2006 Dec 18.

Neural Repair and Neurogenesis Laboratory, Department of Pharmacology and Clinical Pharmacology, The University of Auckland, Auckland, New Zealand.

The use of viral vectors for gene delivery offer many advantages for both basic research and therapeutic application through the continuous expression of a gene product within a target region. It is vital however that any gene product is correctly expressed in a biologically active form, and this should be confirmed prior to large scale in vivo studies. Using adeno-associated viral (AAV) vectors to direct the expression of either a neurotrophic factor or an anti-apoptotic protein, we have developed a range of in vitro assays to verify functional transgenic protein expression. Read More

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Cerebral resuscitation: state of the art, experimental approaches and clinical perspectives.

Neurol Clin 2006 Feb;24(1):73-87, vi

Department of Anesthesiology, University of Heidelberg, Im Neuenheimer Feld 110, D-69120, Heidelberg, Germany.

Neuronal injury following global cerebral ischemia continues to bea central problem of patients in the postresuscitation phase following cardiocirculatory arrest. In addition to measures focusing on rapid restoration of spontaneous circulation, the most effective treatment after cardiac arrest, as shown by large randomized trials,is the use of therapeutic mild hypothermia. Current guidelines of the International Liaison Committee on Resuscitation (ILCOR)are recommending the use of therapeutic mild hypothermia for all unconscious patients after cardiac arrest. Read More

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February 2006

Novel neuroprotective mechanism of action of rasagiline is associated with its propargyl moiety: interaction of Bcl-2 family members with PKC pathway.

Ann N Y Acad Sci 2005 Aug;1053:348-55

Eve Topf and USA National Parkinson Foundation Centers of Excellence for Neurodegenerative Diseases Research, Department of Pharmacology, Rappaport Family Research Institute, Technion-Faculty of Medicine, Haifa, Israel.

Our studies have provided new insights into the biological mechanism of neuroprotection of the anti-Parkinson drug, rasagiline [N-propargyl-(1R)-aminoindan], involving the association of Bcl-2 family proteins with protein kinase C (PKC) pathway. In a model of serum withdrawal-induced apoptosis of rat pheochromocytoma PC12 cells, rasagiline and its propargyl moiety, N-propargylamine, decreased cell death via multiple neuroprotective pathways that include the stimulation of PKC phosphorylation; upregulation of PKCepsilon mRNA; induction of Bcl-X(L), Bcl-w, and brain-derived neurotrophic factor (BDNF) mRNAs; and downregulation of PKCgamma, Bad, and Bax mRNAs. Moreover, these drugs inhibited the cleavage and activation of pro-caspase-3 and poly(ADP-ribose) polymerase (PARP), while PKC inhibitor, GF109203X, reversed these actions. Read More

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N-methyl-D-aspartate and TrkB receptors protect neurons against glutamate excitotoxicity through an extracellular signal-regulated kinase pathway.

J Neurosci Res 2005 Apr;80(1):104-13

Department of Neurology and Neuroscience, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, USA.

N-Methyl-D-aspartate (NMDA) at a subtoxic concentration (100 microM) promotes neuronal survival against glutamate-mediated excitotoxicity via a brain-derived neurotrophic factor (BDNF) autocrine loop in cultured cerebellar granule cells. The signal transduction mechanism(s) underlying NMDA neuroprotection, however, remains elusive. The mitogen-activated protein kinase (MAPK) and phosphatidylinositol-3 kinase (PI3-K) pathways alter gene expression and are involved in synaptic plasticity and neuronal survival. Read More

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Brain-derived neurotrophic factor prevents changes in Bcl-2 family members and caspase-3 activation induced by excitotoxicity in the striatum.

J Neurochem 2005 Feb;92(3):678-91

Departament de Biologia Cel-lular i Anatomia Patològica, Facultat de Medicina, Universitat de Barcelona, Institut d'Investigacions Biomédiques August Pi i Sunyer (IDIBAPS), Casanova 143, E-08036 Barcelona, Spain.

Brain-derived neurotrophic factor (BDNF) prevents the loss of striatal neurons caused by excitotoxicity. We examined whether these neuroprotective effects are mediated by changes in the regulation of Bcl-2 family members. We first analyzed the involvement of the phosphatidylinositol 3-kinase/Akt pathway in this regulation, showing a reduction in phosphorylated Akt (p-Akt) levels after both quinolinate (QUIN, an NMDA receptor agonist) and kainate (KA, a non-NMDA receptor agonist) intrastriatal injection. Read More

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February 2005

The generation of dopaminergic neurons by human neural stem cells is enhanced by Bcl-XL, both in vitro and in vivo.

J Neurosci 2004 Dec;24(48):10786-95

Center of Molecular Biology Severo Ochoa, Autonomous University of Madrid, 28049 Madrid, Spain.

Progress in stem cell biology research is enhancing our ability to generate specific neuron types for basic and applied studies and to design new treatments for neurodegenerative diseases. In the case of Parkinson's disease (PD), alternative human dopaminergic (DAergic) neurons other than primary fetal tissue do not yet exist. One possible source could be human neural stem cells (hNSCs), although the yield in DAergic neurons and their survival are very limited. Read More

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December 2004

Chemotherapy-induced cell death in primary cerebellar granule neurons but not in astrocytes: in vitro paradigm of differential neurotoxicity.

J Neurochem 2004 Dec;91(5):1067-74

Laboratory of Molecular Neurodegeneration, Department of General Neurology and Hertie Institute for Clinical Brain Research, University of Tübingen, Germany.

The nervous system is frequently the site of symptomatic toxicity of antineoplastic agents. However, there is limited information about the differential vulnerability of neurons, astrocytes and glioma cells. We have analyzed the effects of four chemotherapeutic drugs (lomustine, cisplatin, topotecan and vincristine) on primary cerebellar granule neurons and astrocytes derived from rats. Read More

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December 2004