Beschreibung:
<jats:title>Abstract</jats:title><jats:p>Galanin is a neuropeptide involved in a variety of biological functions, including having a strong anticonvulsant activity. To assess a possible role of galanin in modulation of glutamatergic synapses and excitotoxicity, we studied effects of a galanin receptor 2(3) agonist (AR‐M1896) on several molecular events induced by glutamate administration in primary neural hippocampal cells. Exposure of cells, after 5 days <jats:italic>in vitro,</jats:italic> to glutamate 0.5 m<jats:sc>m</jats:sc> for 10 min caused morphological alterations, including disaggregation of β‐tubulin and MAP‐2 cytoskeletal protein assembly, loss of neurites and cell shrinkage. When present in culture medium together with glutamate, 1 and 10 n<jats:sc>m</jats:sc> of AR‐M1896 reduced these alterations. Moreover, AR‐M1896 counteracted glutamate‐induced c‐<jats:italic>fos</jats:italic> mRNA and c‐Fos protein up‐regulation after 30–150 min, and 24 h, respectively. Massive nuclear alterations (Hoechst 33258 staining), observed 24 h after glutamate exposure, were also antagonized by AR‐M1896 (0.1–100 n<jats:sc>m</jats:sc>) in a dose‐dependent manner. These findings indicate that galanin, probably mainly through its type 2 receptor, interferes with events associated with glutamate toxicity.</jats:p>