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  1. Article: Pharmacological properties of BN82451: a novel multitargeting neuroprotective agent.

    Chabrier, Pierre Etienne / Auguet, Michel

    CNS drug reviews

    2006  Volume 13, Issue 3, Page(s) 317–332

    Abstract: BN82451 belongs to a new family of small molecules designated as multitargeting or hybrid molecules. BN82451 is orally active, has good central nervous system penetration, and elicits potent neuronal protection and antiinflammatory properties. Neuronal ... ...

    Abstract BN82451 belongs to a new family of small molecules designated as multitargeting or hybrid molecules. BN82451 is orally active, has good central nervous system penetration, and elicits potent neuronal protection and antiinflammatory properties. Neuronal protection is due to Na+ channel blockade, antioxidant properties, and mitochondria-protecting activity, whereas inhibition of cyclooxygenases is mostly responsible for its antiinflammatory activity. BN82451 has been shown to exert a potent neuroprotective effect in various in vitro and in vivo animal models. BN82451 was found to exert a significant protection in experimental animal models mimicking aspects of cerebral ischemia, Parkinson disease, Huntington disease, and more particularly amyotrophic lateral sclerosis. Collectively, its pharmacological properties designate BN82451 as a promising neuroprotective agent.
    MeSH term(s) Animals ; Disease Models, Animal ; Nervous System Diseases/prevention & control ; Neuroprotective Agents/pharmacology ; Neuroprotective Agents/therapeutic use ; Phenols/chemistry ; Phenols/pharmacology ; Phenols/therapeutic use ; Thiazoles/pharmacology ; Thiazoles/therapeutic use
    Chemical Substances BN82451 ; Neuroprotective Agents ; Phenols ; Thiazoles ; butylphen (O81VMW36CV)
    Language English
    Publishing date 2006-02-02
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1341919-5
    ISSN 1080-563X
    ISSN 1080-563X
    DOI 10.1111/j.1527-3458.2007.00018.x
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  2. Article ; Online: Different antinociceptive effects of botulinum toxin type A in inflammatory and peripheral polyneuropathic rat models.

    Favre-Guilmard, Christine / Auguet, Michel / Chabrier, Pierre-Etienne

    European journal of pharmacology

    2009  Volume 617, Issue 1-3, Page(s) 48–53

    Abstract: In addition to inhibition of acetylcholine release in the neuromuscular junction botulinum toxin type A (BoNT-A) also inhibits the release of mediators involved in pain perception. We have investigated the effect of two types of BoNT-A on mechanical ... ...

    Abstract In addition to inhibition of acetylcholine release in the neuromuscular junction botulinum toxin type A (BoNT-A) also inhibits the release of mediators involved in pain perception. We have investigated the effect of two types of BoNT-A on mechanical hyperalgesia in the rat models of carrageenan-induced hyperalgesia and of paclitaxel-induced peripheral neuropathy. A subplantar (s.p.) injection of BoNT-A in the ipsilateral hindpaw 3 days before carrageenan administration reduced hypersensitivity. Dysport and Botox elicited comparable antihyperalgesic effects. Dysport up to 30 U/kg and Botox up to 20 U/kg did not impair the rat withdrawal nociceptive reflex or the locomotor performance as assessed by the rotarod test. Intraperitoneal administration of the skeletal muscle relaxant dantrolene produced, in contrast to BoNT-A, more motor impairment than analgesia. Paclitaxel treatment resulted in a peripheral neuropathy that affected the two hindpaws. Injection of 20 U/kg (s.p.) Dysport produced a significant antihyperalgesic effect in the injected paw of neuropathic animals 3 days after administration. Unexpectedly, a similar analgesic effect was observed in the contralateral paw. The same results were also observed when Botox was used instead of Dysport. In contrast, a contralateral administration of Dysport in the carrageenan test was ineffective. We conclude that BoNT-A elicits antinociceptive effects independent of the effects on muscular relaxation. Our results suggest that different mechanisms of action are responsible for the effect of BoNT-A in inflammatory and peripheral polyneuropathic rat models.
    MeSH term(s) Analgesics/administration & dosage ; Analgesics/pharmacology ; Analgesics/therapeutic use ; Animals ; Botulinum Toxins, Type A/administration & dosage ; Botulinum Toxins, Type A/pharmacology ; Botulinum Toxins, Type A/therapeutic use ; Carrageenan ; Dantrolene/administration & dosage ; Dantrolene/pharmacology ; Dantrolene/therapeutic use ; Disease Models, Animal ; Edema/chemically induced ; Edema/drug therapy ; Hyperalgesia/chemically induced ; Hyperalgesia/drug therapy ; Hyperalgesia/physiopathology ; Inflammation/chemically induced ; Inflammation/drug therapy ; Inflammation/physiopathology ; Injections ; Male ; Motor Activity/drug effects ; Paclitaxel ; Polyneuropathies/chemically induced ; Polyneuropathies/drug therapy ; Polyneuropathies/physiopathology ; Rats ; Rats, Sprague-Dawley
    Chemical Substances Analgesics ; Carrageenan (9000-07-1) ; Botulinum Toxins, Type A (EC 3.4.24.69) ; Dantrolene (F64QU97QCR) ; Paclitaxel (P88XT4IS4D)
    Language English
    Publishing date 2009-09-01
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 80121-5
    ISSN 1879-0712 ; 0014-2999
    ISSN (online) 1879-0712
    ISSN 0014-2999
    DOI 10.1016/j.ejphar.2009.06.047
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  3. Article ; Online: Engineered botulinum neurotoxin B with improved efficacy for targeting human receptors

    Liang Tao / Lisheng Peng / Ronnie P.-A. Berntsson / Sai Man Liu / SunHyun Park / Feifan Yu / Christopher Boone / Shilpa Palan / Matthew Beard / Pierre-Etienne Chabrier / Pål Stenmark / Johannes Krupp / Min Dong

    Nature Communications, Vol 8, Iss 1, Pp 1-

    2017  Volume 10

    Abstract: Humans are less sensitive to the therapeutic effects of botulinum neurotoxin B (BoNT/B) than the animal models it is tested on due to differences between the human and the mouse receptors. Here, the authors engineer BoNT/B to improve its affinity to ... ...

    Abstract Humans are less sensitive to the therapeutic effects of botulinum neurotoxin B (BoNT/B) than the animal models it is tested on due to differences between the human and the mouse receptors. Here, the authors engineer BoNT/B to improve its affinity to human receptors and enhance its therapeutic efficacy.
    Keywords Science ; Q
    Language English
    Publishing date 2017-07-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
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  4. Article ; Online: Engineered botulinum neurotoxin B with improved efficacy for targeting human receptors.

    Tao, Liang / Peng, Lisheng / Berntsson, Ronnie P-A / Liu, Sai Man / Park, SunHyun / Yu, Feifan / Boone, Christopher / Palan, Shilpa / Beard, Matthew / Chabrier, Pierre-Etienne / Stenmark, Pål / Krupp, Johannes / Dong, Min

    Nature communications

    2017  Volume 8, Issue 1, Page(s) 53

    Abstract: Botulinum neurotoxin B is a Food and Drug Administration-approved therapeutic toxin. However, it has lower binding affinity toward the human version of its major receptor, synaptotagmin II (h-Syt II), compared to mouse Syt II, because of a residue ... ...

    Abstract Botulinum neurotoxin B is a Food and Drug Administration-approved therapeutic toxin. However, it has lower binding affinity toward the human version of its major receptor, synaptotagmin II (h-Syt II), compared to mouse Syt II, because of a residue difference. Increasing the binding affinity to h-Syt II may improve botulinum neurotoxin B's therapeutic efficacy and reduce adverse effects. Here we utilized the bacterial adenylate cyclase two-hybrid method and carried out a saturation mutagenesis screen in the Syt II-binding pocket of botulinum neurotoxin B. The screen identifies E1191 as a key residue: replacing it with M/C/V/Q enhances botulinum neurotoxin B binding to human synaptotagmin II. Adding S1199Y/W or W1178Q as a secondary mutation further increases binding affinity. Mutant botulinum neurotoxin B containing E1191M/S1199Y exhibits ~11-fold higher efficacy in blocking neurotransmission than wild-type botulinum neurotoxin B in neurons expressing human synaptotagmin II, demonstrating that enhancing receptor binding increases the overall efficacy at functional levels. The engineered botulinum neurotoxin B provides a platform to develop therapeutic toxins with improved efficacy.Humans are less sensitive to the therapeutic effects of botulinum neurotoxin B (BoNT/B) than the animal models it is tested on due to differences between the human and the mouse receptors. Here, the authors engineer BoNT/B to improve its affinity to human receptors and enhance its therapeutic efficacy.
    MeSH term(s) Acetylcholine Release Inhibitors/pharmacology ; Animals ; Botulinum Toxins, Type A/genetics ; Botulinum Toxins, Type A/metabolism ; Botulinum Toxins, Type A/pharmacology ; Humans ; Mutagenesis, Site-Directed ; Neurons/drug effects ; Neurons/metabolism ; Patch-Clamp Techniques ; Protein Binding/genetics ; Rats ; Recombinant Proteins ; Synaptotagmin II/metabolism ; Two-Hybrid System Techniques
    Chemical Substances Acetylcholine Release Inhibitors ; Recombinant Proteins ; SYT2 protein, human ; Synaptotagmin II ; rimabotulinumtoxinB (0Y70779M1F) ; Botulinum Toxins, Type A (EC 3.4.24.69)
    Language English
    Publishing date 2017-07-03
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2041-1723
    ISSN (online) 2041-1723
    DOI 10.1038/s41467-017-00064-y
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  5. Article ; Online: An improved model to investigate the efficacy of antidyskinetic agents in hemiparkinsonian rats.

    Spinnewyn, Brigitte / Charnet, Christelle / Cornet, Sylvie / Roubert, Véronique / Chabrier, Pierre-Etienne / Auguet, Michel

    Fundamental & clinical pharmacology

    2011  Volume 25, Issue 5, Page(s) 608–618

    Abstract: A number of experimental models of L-DOPA-induced dyskinesia have been proposed, but these models result in a low to medium rate of dyskinetic animals with mild to severe symptoms. The objective of this study was to combine a model of 6-OHDA-induced ... ...

    Abstract A number of experimental models of L-DOPA-induced dyskinesia have been proposed, but these models result in a low to medium rate of dyskinetic animals with mild to severe symptoms. The objective of this study was to combine a model of 6-OHDA-induced parkinsonism and of L-DOPA-induced dyskinesia in rats to establish a reliable preclinical model. Two stereotaxic injections of 6-OHDA were administered in the left striatum. This model led to 90-100% of rats with a marked contralateral circling behaviour, significant limb use asymmetry (20%), a decrease in ipsilateral striatal dopamine content (70%) and degeneration of dopamine neurons in the substantia nigra (70%). Chronic treatment with L-DOPA was administered for 35 days and consisted of three phases with incremental daily doses. The third phase resulted in 83-90% of rats developing severe abnormal involuntary movements (AIMs) which included limb and locomotive dyskinesia, axial dystonia and orolingual dyskinesia. Reproducibility of the model, criteria of strict blinding, placebo-controlled design, randomization of study subjects and pretrial determination of sample size were used to measure efficacy of amantadine and istradefylline and to validate the protocol design. Acute or subchronic post-treatment with amantadine reduced the severity of dyskinesia while istradefylline punctually attenuated AIMs. Our experimental conditions using gradual development of dyskinesia induced by increasing doses of L-DOPA resulted in a reliable model of L-DOPA-induced dyskinesia with a high rate of dyskinetic rats.
    MeSH term(s) Adenosine A2 Receptor Antagonists/pharmacology ; Adenosine A2 Receptor Antagonists/toxicity ; Amantadine/pharmacology ; Amantadine/therapeutic use ; Amantadine/toxicity ; Animals ; Antiparkinson Agents/adverse effects ; Antiparkinson Agents/pharmacology ; Antiparkinson Agents/therapeutic use ; Behavior, Animal ; Benserazide/pharmacology ; Biological Assay ; Corpus Striatum ; Disease Models, Animal ; Dopamine/physiology ; Dopamine Agents/pharmacology ; Dopamine Agents/toxicity ; Drug Administration Schedule ; Drug Evaluation, Preclinical ; Dyskinesia, Drug-Induced/drug therapy ; Enzyme Inhibitors/pharmacology ; Levodopa/adverse effects ; Levodopa/pharmacology ; Levodopa/toxicity ; Male ; Oxidopamine/toxicity ; Parkinsonian Disorders/chemically induced ; Parkinsonian Disorders/drug therapy ; Placebos ; Purines/pharmacology ; Purines/therapeutic use ; Purines/toxicity ; Random Allocation ; Rats ; Reproducibility of Results ; Rotation ; Sample Size ; Single-Blind Method ; Sympatholytics/toxicity
    Chemical Substances Adenosine A2 Receptor Antagonists ; Antiparkinson Agents ; Dopamine Agents ; Enzyme Inhibitors ; Placebos ; Purines ; Sympatholytics ; istradefylline (2GZ0LIK7T4) ; Levodopa (46627O600J) ; Benserazide (762OS3ZEJU) ; Oxidopamine (8HW4YBZ748) ; Amantadine (BF4C9Z1J53) ; Dopamine (VTD58H1Z2X)
    Language English
    Publishing date 2011-10
    Publishing country England
    Document type Journal Article
    ZDB-ID 639134-5
    ISSN 1472-8206 ; 0767-3981
    ISSN (online) 1472-8206
    ISSN 0767-3981
    DOI 10.1111/j.1472-8206.2010.00883.x
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    Zs.A 2247: Show issues Location:
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  6. Article ; Online: Does Reduction of Number of Intradetrusor Injection Sites of aboBoNTA (Dysport®) Impact Efficacy and Safety in a Rat Model of Neurogenic Detrusor Overactivity?

    Huynh Le Maux, Amélie / Pignol, Bernadette / Behr-Roussel, Delphine / Blachon, Jean-Luc / Chabrier, Pierre-Etienne / Compagnie, Sandrine / Picaut, Philippe / Bernabé, Jacques / Giuliano, François / Denys, Pierre

    Toxins

    2015  Volume 7, Issue 12, Page(s) 5462–5471

    Abstract: Intradetrusor injections of Botulinum toxin A-currently onabotulinumtoxinA-is registered as a second-line treatment to treat neurogenic detrusor overactivity (NDO). The common clinical practice is 30 × 1 mL injections in the detrusor; however, protocols ... ...

    Abstract Intradetrusor injections of Botulinum toxin A-currently onabotulinumtoxinA-is registered as a second-line treatment to treat neurogenic detrusor overactivity (NDO). The common clinical practice is 30 × 1 mL injections in the detrusor; however, protocols remain variable and standardization is warranted. The effect of reducing the number of injection sites of Dysport(®) abobotulinumtoxinA (aboBoNTA) was assessed in the spinal cord-injured rat (SCI). Nineteen days post-spinalization, female rats received intradetrusor injections of saline or aboBoNTA 22.5 U distributed among four or eight sites. Two days after injection, continuous cystometry was performed in conscious rats. Efficacy of aboBoNTA 22.5 U was assessed versus aggregated saline groups on clinically-relevant parameters: maximal pressure, bladder capacity, compliance, voiding efficiency, as well as amplitude, frequency, and volume threshold for nonvoiding contractions (NVC). AboBoNTA 22.5 U significantly decreased maximal pressure, without affecting voiding efficiency. Injected in four sites, aboBoNTA significantly increased bladder capacity and compliance while only the latter when in eight sites. AboBoNTA significantly reduced NVC frequency and amplitude. This preclinical investigation showed similar inhibiting effects of aboBoNTA despite the number of sites reduction. Further studies are warranted to optimize dosing schemes to improve the risk-benefit ratio of BoNTA-based treatment modalities for NDO and further idiopathic overactive bladder.
    MeSH term(s) Animals ; Botulinum Toxins, Type A/administration & dosage ; Botulinum Toxins, Type A/therapeutic use ; Female ; Injections, Intramuscular ; Neuromuscular Agents/administration & dosage ; Neuromuscular Agents/therapeutic use ; Rats, Sprague-Dawley ; Spinal Cord Injuries/drug therapy ; Spinal Cord Injuries/physiopathology ; Treatment Outcome ; Urinary Bladder, Overactive/drug therapy ; Urinary Bladder, Overactive/physiopathology
    Chemical Substances Neuromuscular Agents ; Botulinum Toxins, Type A (EC 3.4.24.69) ; abobotulinumtoxinA (EC 3.4.24.69)
    Language English
    Publishing date 2015-12-17
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2518395-3
    ISSN 2072-6651 ; 2072-6651
    ISSN (online) 2072-6651
    ISSN 2072-6651
    DOI 10.3390/toxins7124896
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  7. Article ; Online: Does Reduction of Number of Intradetrusor Injection Sites of aboBoNTA (Dysport®) Impact Efficacy and Safety in a Rat Model of Neurogenic Detrusor Overactivity?

    Amélie Huynh Le Maux / Bernadette Pignol / Delphine Behr-Roussel / Jean-Luc Blachon / Pierre-Etienne Chabrier / Sandrine Compagnie / Philippe Picaut / Jacques Bernabé / François Giuliano / Pierre Denys

    Toxins, Vol 7, Iss 12, Pp 5462-

    2015  Volume 5471

    Abstract: Intradetrusor injections of Botulinum toxin A—currently onabotulinumtoxinA—is registered as a second-line treatment to treat neurogenic detrusor overactivity (NDO). The common clinical practice is 30 × 1 mL injections in the detrusor; however, protocols ... ...

    Abstract Intradetrusor injections of Botulinum toxin A—currently onabotulinumtoxinA—is registered as a second-line treatment to treat neurogenic detrusor overactivity (NDO). The common clinical practice is 30 × 1 mL injections in the detrusor; however, protocols remain variable and standardization is warranted. The effect of reducing the number of injection sites of Dysport® abobotulinumtoxinA (aboBoNTA) was assessed in the spinal cord-injured rat (SCI). Nineteen days post-spinalization, female rats received intradetrusor injections of saline or aboBoNTA 22.5 U distributed among four or eight sites. Two days after injection, continuous cystometry was performed in conscious rats. Efficacy of aboBoNTA 22.5 U was assessed versus aggregated saline groups on clinically-relevant parameters: maximal pressure, bladder capacity, compliance, voiding efficiency, as well as amplitude, frequency, and volume threshold for nonvoiding contractions (NVC). AboBoNTA 22.5 U significantly decreased maximal pressure, without affecting voiding efficiency. Injected in four sites, aboBoNTA significantly increased bladder capacity and compliance while only the latter when in eight sites. AboBoNTA significantly reduced NVC frequency and amplitude. This preclinical investigation showed similar inhibiting effects of aboBoNTA despite the number of sites reduction. Further studies are warranted to optimize dosing schemes to improve the risk-benefit ratio of BoNTA-based treatment modalities for NDO and further idiopathic overactive bladder.
    Keywords abobotulinumtoxinA ; injection procedure ; injection site number ; neurogenic detrusor overactivity ; spinal-cord injury ; Medicine ; R
    Subject code 630
    Language English
    Publishing date 2015-12-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
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  8. Article ; Online: High-throughput 3D whole-brain quantitative histopathology in rodents.

    Vandenberghe, Michel E / Hérard, Anne-Sophie / Souedet, Nicolas / Sadouni, Elmahdi / Santin, Mathieu D / Briet, Dominique / Carré, Denis / Schulz, Jocelyne / Hantraye, Philippe / Chabrier, Pierre-Etienne / Rooney, Thomas / Debeir, Thomas / Blanchard, Véronique / Pradier, Laurent / Dhenain, Marc / Delzescaux, Thierry

    Scientific reports

    2016  Volume 6, Page(s) 20958

    Abstract: Histology is the gold standard to unveil microscopic brain structures and pathological alterations in humans and animal models of disease. However, due to tedious manual interventions, quantification of histopathological markers is classically performed ... ...

    Abstract Histology is the gold standard to unveil microscopic brain structures and pathological alterations in humans and animal models of disease. However, due to tedious manual interventions, quantification of histopathological markers is classically performed on a few tissue sections, thus restricting measurements to limited portions of the brain. Recently developed 3D microscopic imaging techniques have allowed in-depth study of neuroanatomy. However, quantitative methods are still lacking for whole-brain analysis of cellular and pathological markers. Here, we propose a ready-to-use, automated, and scalable method to thoroughly quantify histopathological markers in 3D in rodent whole brains. It relies on block-face photography, serial histology and 3D-HAPi (Three Dimensional Histology Analysis Pipeline), an open source image analysis software. We illustrate our method in studies involving mouse models of Alzheimer's disease and show that it can be broadly applied to characterize animal models of brain diseases, to evaluate therapeutic interventions, to anatomically correlate cellular and pathological markers throughout the entire brain and to validate in vivo imaging techniques.
    MeSH term(s) Alzheimer Disease/diagnostic imaging ; Alzheimer Disease/pathology ; Animals ; Brain/diagnostic imaging ; Brain/pathology ; Brain/ultrastructure ; Brain Mapping ; Disease Models, Animal ; Humans ; Image Processing, Computer-Assisted ; Imaging, Three-Dimensional ; Mice ; Software
    Language English
    Publishing date 2016-02-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/srep20958
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  9. Article ; Online: Long-term treatment with standardized Ginkgo biloba extract (EGb 761) attenuates cognitive deficits and hippocampal neuron loss in a gerbil model of vascular dementia.

    Rocher, Marie-Noelle / Carré, Denis / Spinnewyn, Brigitte / Schulz, Jocelyne / Delaflotte, Sylvie / Pignol, Bernadette / Chabrier, Pierre-Etienne / Auguet, Michel

    Fitoterapia

    2011  Volume 82, Issue 7, Page(s) 1075–1080

    Abstract: The standardized extract of Ginkgo biloba EGb 761 has been used to reduce cognitive dysfunction. The present study was designed to evaluate the effect of postischemic oral treatment with EGb 761 in a model of vascular dementia in gerbils. Daily oral ... ...

    Abstract The standardized extract of Ginkgo biloba EGb 761 has been used to reduce cognitive dysfunction. The present study was designed to evaluate the effect of postischemic oral treatment with EGb 761 in a model of vascular dementia in gerbils. Daily oral posttreatment with EGb 761 led to a significant recovery of spatial memory assessed by the object location test, inhibited the decrease in plasma SOD activity and protected the hippocampal CA1 neurons, even when administered after the insult. These data provide further evidence for the therapeutic potential of EGb 761 in the treatment of vascular dementia.
    MeSH term(s) Animals ; Brain Ischemia/blood ; Brain Ischemia/complications ; Brain Ischemia/drug therapy ; Dementia, Vascular/blood ; Dementia, Vascular/drug therapy ; Dementia, Vascular/pathology ; Disease Models, Animal ; Gerbillinae ; Ginkgo biloba ; Hippocampus/drug effects ; Hippocampus/pathology ; Memory/drug effects ; Memory Disorders/blood ; Memory Disorders/drug therapy ; Nerve Degeneration/blood ; Nerve Degeneration/drug therapy ; Neuroprotective Agents/pharmacology ; Neuroprotective Agents/therapeutic use ; Phytotherapy ; Plant Extracts/pharmacology ; Plant Extracts/therapeutic use ; Superoxide Dismutase/blood
    Chemical Substances Neuroprotective Agents ; Plant Extracts ; Ginkgo biloba extract (19FUJ2C58T) ; Superoxide Dismutase (EC 1.15.1.1)
    Language English
    Publishing date 2011-10
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 412385-2
    ISSN 1873-6971 ; 0367-326X
    ISSN (online) 1873-6971
    ISSN 0367-326X
    DOI 10.1016/j.fitote.2011.07.001
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  10. Article ; Online: BN82451 attenuates L-dopa-induced dyskinesia in 6-OHDA-lesioned rat model of Parkinson's disease.

    Spinnewyn, Brigitte / Mautino, Gisele / Marin, Jean-Gregoire / Rocher, Marie Noëlle / Grandoulier, Anne Sophie / Ferrandis, Eric / Auguet, Michel / Chabrier, Pierre-Etienne

    Neuropharmacology

    2011  Volume 60, Issue 4, Page(s) 692–700

    Abstract: The development of L-dopa-induced dyskinesia (LID) remains a major problem in the long-term treatment of Parkinson's disease (PD). This study aimed to assess the effect of the multitargeting molecule BN82451 on LID and to measure striatal mRNA expression ...

    Abstract The development of L-dopa-induced dyskinesia (LID) remains a major problem in the long-term treatment of Parkinson's disease (PD). This study aimed to assess the effect of the multitargeting molecule BN82451 on LID and to measure striatal mRNA expression of several genes in a rat model of PD. Rats were administered two unilateral injections of 6-OHDA in the striatum. After four weeks, the animals started a chronic daily treatment with increasing doses of L-dopa over a further four-week period. Over the course of L-dopa treatment, the rats developed abnormal involuntary movements (AIMs) classified as locomotive, axial, orolingual and forelimb dyskinesia. In animals rendered dyskinetic by L-dopa, administration of BN82451 at doses ranging from 1 to 10 mg/kg p.o. attenuated the severity of fully-established AIMs in a dose-related manner. This anti-dyskinetic effect could be achieved with lower doses of BN82451 administered sub chronically vs. acute single treatment. The improvement of AIMs is not due to a reduction in the general motor activity of dyskinetic rats. BN82451 treatment significantly reversed the overexpression of c-Fos, FosB and Arc mRNA associated with the dyskinesiogenic action of L-dopa. A significant correlation between the degree of overexpression of c-Fos, FosB and Arc mRNA and the dyskinesiogenic action of L-dopa was observed. The data demonstrate that BN82451 effectively attenuates LID and the associated molecular alterations in an animal model of PD and may represent a treatment option for managing dyskinesia.
    MeSH term(s) Animals ; Area Under Curve ; Behavior, Animal/drug effects ; Chromatography, High Pressure Liquid ; Corpus Striatum/drug effects ; Corpus Striatum/metabolism ; Dose-Response Relationship, Drug ; Dyskinesia, Drug-Induced/drug therapy ; Dyskinesia, Drug-Induced/metabolism ; Gene Expression ; Levodopa/adverse effects ; Male ; Neuroprotective Agents/metabolism ; Neuroprotective Agents/pharmacology ; Neuroprotective Agents/therapeutic use ; Oxidopamine/pharmacology ; Parkinsonian Disorders/drug therapy ; Parkinsonian Disorders/metabolism ; RNA, Messenger/metabolism ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction ; Thiazoles/metabolism ; Thiazoles/pharmacology ; Thiazoles/therapeutic use
    Chemical Substances BN82451 ; Neuroprotective Agents ; RNA, Messenger ; Thiazoles ; Levodopa (46627O600J) ; Oxidopamine (8HW4YBZ748)
    Language English
    Publishing date 2011-03
    Publishing country England
    Document type Journal Article
    ZDB-ID 218272-5
    ISSN 1873-7064 ; 0028-3908
    ISSN (online) 1873-7064
    ISSN 0028-3908
    DOI 10.1016/j.neuropharm.2010.11.019
    Database MEDical Literature Analysis and Retrieval System OnLINE

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