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The galanin receptor 2/3 agonist Gal2‐11 protects the SN56 cells against β‐amyloid 25–35 toxicity
Author(s) -
Pirondi S.,
Giuliani A.,
Del Vecchio G.,
Giardino L.,
Hökfelt T.,
Calzà L.
Publication year - 2010
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.22278
Subject(s) - galanin , agonist , medicine , cholinergic , endocrinology , galanin receptor , chemistry , cholinergic neuron , receptor , amyloid (mycology) , neuropeptide , biology , inorganic chemistry
The neuropeptide galanin is a modulator of cholinergic function and may play a role in Aβ peptide‐induced degeneration of cholinergic forebrain neurons. We have studied the effect of galanin and its galanin receptor subtype 2/3 agonist Gal2‐11on toxicity induced by freshly‐prepared β‐amyloid 25–35 in the cholinergic cell line SN56. Both nuclear fragmentation and caspase‐3 expression were analysed. β‐amyloid 25–35 ‐exposure induced a significant increase in caspase‐3 mRNA expression after 30, 60, 90 or 150 min of β‐amyloid 25–35 exposure. These effects were abolished in the presence of Gal2‐11 (10 nM). Similarly, β‐amyloid 25–35 ‐induced nuclear fragmentation was prevented by the galanin agonist at all time points studied. These findings indicate that the galanin 2/3 agonist Gal2‐11 protects SN56 cholinergic cells from β‐amyloid 25–35 ‐induced cell death and that this action is mediated by an early reduction of caspase‐3 expression. © 2009 Wiley‐Liss, Inc.