Details

Autor(en) / Beteiligte

• Criscuolo, Chiara
• Fabiani, Carlotta
• Bonadonna, Camilla
• Origlia, Nicola
• Domenici, Luciano

Titel

BDNF prevents amyloid-dependent impairment of LTP in the entorhinal cortex by attenuating p38 MAPK phosphorylation

Ist Teil von

• Neurobiology of aging, 2015-03, Vol.36 (3), p.1303-1309

Ort / Verlag

United States: Elsevier Inc

Erscheinungsjahr

2015

Link zum Volltext

Quelle

MEDLINE

Beschreibungen/Notizen

• Abstract The oligomeric form of the amyloid peptide Aβ1–42 is capable of perturbing synaptic plasticity in different brain areas. Here, we evaluated the protective role of brain-derived neurotrophic factor (BDNF) in beta amyloid (Aβ)-dependent impairment of long-term potentiation in entorhinal cortex (EC) slices. We found that BDNF (1 ng/mL) supplied by perfusion was able to rescue long-term potentiation in Aβ1–42 -treated slices; BDNF protection was mediated by TrkB receptor as assessed by using the tyrosine kinase inhibitor K252a (200 nM). We also investigated the function of endogenous BDNF using a soluble form of TrkB receptor (TrkB IgG). Incubation of slices with TrkB IgG (1 μg/mL) increased the EC vulnerability to Aβ. Finally, we investigated the effect of BDNF on the cell stress-kinase p38 mitogen-activated protein kinase (MAPK) in primary cortical cell cultures exposed to Aβ1–42 . We found that Aβ induces p38 MAPK phosphorylation, although pretreatment with BDNF prevented Aβ-dependent p38 MAPK phosphorylation. This result was confirmed by an immunoassay in tissue extracts from EC slices collected after electrophysiology.