Protective effect of BDNF against beta-amyloid induced neurotoxicity in vitro and in vivo in rats

Autor: Lucia Tapia-Arancibia, Florent Mouliere, J. Meffre, M. Silhol, Sandor Arancibia, I. Höllinger, T. Maurice
Přispěvatelé: Pathology
Rok vydání: 2008
Předmět:
Male
medicine.medical_specialty
Tropomyosin receptor kinase B
Hippocampal formation
Hippocampus
Neuroprotection
lcsh:RC321-571
Corpus Callosum
Rats
Sprague-Dawley
chemistry.chemical_compound
Alzheimer Disease
In vivo
Internal medicine
mental disorders
medicine
Animals
Receptor
trkB
Receptors
Somatostatin
Axon
Receptor
lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry
Cells
Cultured
β-Amyloid peptides
Amyloid beta-Peptides
Indusium griseum
Dose-Response Relationship
Drug
Chemistry
Push-pull perfusion
Brain-Derived Neurotrophic Factor
Neurotoxicity
Brain
medicine.disease
Peptide Fragments
Rats
Disease Models
Animal
BDNF
Neuroprotective Agents
Treatment Outcome
medicine.anatomical_structure
Endocrinology
nervous system
Neurology
Nerve Degeneration
Dentate gyrus hilus
Female
K252a
Wallerian Degeneration
Zdroj: Arancibia, S, Silhol, M, Moulière, F, Meffre, J, Höllinger, I, Maurice, T & Tapia-Arancibia, L 2008, ' Protective effect of BDNF against beta-amyloid induced neurotoxicity in vitro and in vivo in rats ', Neurobiology of Disease, vol. 31, no. 3, pp. 316-326 . https://doi.org/10.1016/j.nbd.2008.05.012
Neurobiology of Disease, 31(3), 316-326. Academic Press Inc.
Neurobiology of Disease, Vol 31, Iss 3, Pp 316-326 (2008)
ISSN: 0969-9961
Popis: We examined the potential protective effect of BDNF against β-amyloid-induced neurotoxicity in vitro and in vivo in rats. In neuronal cultures, BDNF had specific and dose-response protective effects on neuronal toxicity induced by Aβ1-42 and Aβ25-35. It completely reversed the toxic action induced by Aβ1-42 and partially that induced by Aβ25-35. These effects involved TrkB receptor activation since they were inhibited by K252a. Catalytic BDNF receptors (TrkB.FL) were localized in vitro in cortical neurons (mRNA and protein). In in vivo experiments, Aβ25-35 was administered into the indusium griseum or the third ventricle and several parameters were measured 7 days later to evaluate potential Aβ25-35/BDNF interactions, i.e. local measurement of BDNF release, number of hippocampal hilar cells expressing SRIH mRNA and assessment of the corpus callosum damage (morphological examination, pyknotic nuclei counting and axon labeling with anti-MBP antibody). We conclude that BDNF possesses neuroprotective properties against toxic effects of Aβ peptides.
Databáze: OpenAIRE
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