Journal article
Soluble beta amyloid evokes alteration in brain norepinephrine levels: role of nitric oxide and interleukin-1.
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Morgese MG
Department of Clinical and Experimental Medicine, University of Foggia Foggia, Italy.
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Colaianna M
Department of Clinical and Experimental Medicine, University of Foggia Foggia, Italy ; Department of Pathology and Immunology, University of Geneva Geneva, Switzerland.
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Mhillaj E
Department of Clinical and Experimental Medicine, University of Foggia Foggia, Italy ; Department of Physiology and Pharmacology, La Sapienza, University of Rome Rome, Italy.
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Zotti M
Department of Clinical and Experimental Medicine, University of Foggia Foggia, Italy.
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Schiavone S
Department of Clinical and Experimental Medicine, University of Foggia Foggia, Italy.
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D'Antonio P
Department of Clinical and Experimental Medicine, University of Foggia Foggia, Italy.
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Harkin A
Neuropsychopharmacology Research Group, School of Pharmacy and Pharmaceutical Sciences and Trinity College Institute of Neuroscience, Trinity College Dublin Dublin, Ireland.
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Gigliucci V
Neuropsychopharmacology Research Group, School of Pharmacy and Pharmaceutical Sciences and Trinity College Institute of Neuroscience, Trinity College Dublin Dublin, Ireland.
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Campolongo P
Department of Physiology and Pharmacology, La Sapienza, University of Rome Rome, Italy.
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Trezza V
Section of Biomedical Sciences and Technologies, Department of Science, University "Roma Tre," Rome, Italy.
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De Stradis A
Department of Bio Agro-Food Sciences, The Institute of Sustainable Plant Protection, National Research Council Bari, Italy.
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Tucci P
Department of Clinical and Experimental Medicine, University of Foggia Foggia, Italy.
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Cuomo V
Department of Physiology and Pharmacology, La Sapienza, University of Rome Rome, Italy.
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Trabace L
Department of Clinical and Experimental Medicine, University of Foggia Foggia, Italy.
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Published in:
- Frontiers in neuroscience. - 2015
English
Strong evidence showed neurotoxic properties of beta amyloid (Aβ) and its pivotal role in the Alzheimer's disease (AD) pathogenesis. Beside, experimental data suggest that Aβ may have physiological roles considering that such soluble peptide is produced and secreted during normal cellular activity. There is now suggestive evidence that neurodegenerative conditions, like AD, involve nitric oxide (NO) in their pathogenesis. Nitric oxide also possess potent neuromodulatory actions in brain regions, such as prefrontal cortex (PFC), hippocampus (HIPP), and nucleus accumbens (NAC). In the present study, we evaluated the effect of acute Aβ injection on norepinephrine (NE) content before and after pharmacological manipulations of nitrergic system in above mentioned areas. Moreover, effects of the peptide on NOS activity were evaluated. Our data showed that 2 h after i.c.v. soluble Aβ administration, NE concentrations were significantly increased in the considered areas along with increased iNOS activity. Pre-treatment with NOS inhibitors, 7-Nitroindazole (7-NI), and N6-(1-iminoethyl)-L-lysine-dihydrochloride (L-NIL), reversed Aβ-induced changes. Ultimately, pharmacological block of interleukin1 (IL-1) receptors prevented NE increase in all brain regions. Taken together our findings suggest that NO and IL-1 are critically involved in regional noradrenergic alterations induced by soluble Aβ injection.
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Language
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Open access status
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gold
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Identifiers
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Persistent URL
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https://sonar.ch/global/documents/46616
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