A Novel peptide prevents death in enriched neuronal cultures
Autor: | Sharon Furman, Illana Gozes, Ilona Zemlyak, Douglas E. Brenneman |
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Rok vydání: | 2000 |
Předmět: |
medicine.medical_specialty
Cell Survival Physiology Clinical Biochemistry Vasoactive intestinal peptide Nerve Tissue Proteins Biology Biochemistry Neuroprotection Incubation period Cellular and Molecular Neuroscience Endocrinology Alzheimer Disease Internal medicine mental disorders medicine Animals Amino Acid Sequence Incubation Cells Cultured Homeodomain Proteins Neurons Amyloid beta-Peptides Cell Death Dose-Response Relationship Drug fungi Neurotoxicity medicine.disease Peptide Fragments Rats Nap Glucose Neuroprotective Agents Animals Newborn Mechanism of action Toxicity medicine.symptom Neuroglia psychological phenomena and processes |
Zdroj: | Regulatory Peptides. 96:39-43 |
ISSN: | 0167-0115 |
DOI: | 10.1016/s0167-0115(00)00198-1 |
Popis: | We have recently cloned a novel protein (activity-dependent neuroprotective protein, ADNP) containing an 8-amino-acid, femtomolar-acting peptide, NAPVSIPQ (NAP). Here we show, for the first time, that NAP exerted a protective effect on glia-depleted neurons in culture. The number of surviving neurons was assessed in cerebral cortical cultures derived from newborn rats. In these cultures, a 24-h treatment with the β-amyloid peptide (the Alzheimer’s disease associated toxin) induced a 30–40% reduction in neuronal survival that was prevented by NAP (10 −13 –10 −11 M). Maximal survival was achieved at NAP concentrations of 10 −12 M. In a second set of experiments, a 5-day incubation period, with NAP added once (at the beginning of the incubation period) exhibited maximal protection at 10 −10 M NAP. In a third set of experiments, a 10-min period of glucose deprivation resulted in a 30–40% neuronal death that was prevented by a 24-h incubation with NAP. Glucose deprivation coupled with β-amyloid treatment did not increase neuronal death, suggesting a common pathway. We thus conclude, that NAP can prevent neurotoxicity associated with direct action of the β-amyloid peptide on neurons, perhaps through protection against impaired glucose metabolism. |
Databáze: | OpenAIRE |
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