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pubmed:abstractText |
The effects of D-cycloserine (DCS), a N-methyl-D-aspartate receptor-associated glycine site agonist, and milacemide (MIL), a glycine prodrug, were examined on learning impairments induced by administration of beta 25-35-amyloid peptide (3 nmol i.c.v.). Mice were examined for spontaneous alternation and step-down passive avoidance, 7 and 14 days after beta 25-35, respectively. The beta 25-35-induced deficits were reversed by DCS, 1-30 mg/kg i.p., or MIL, 3-100 mg/kg i.p., each drug being ineffective on control mice behaviours. These observations strengthen the therapeutic potential of glycine site agonists against the memory impairments induced by beta-amyloid peptides.
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pubmed:affiliation |
INSERM U. 336, Développement, Plasticité et Vieillissement du Système Nerveux, Ecole Nationale Supérieure de Chimie, Montpellier, France. maurice@cit.enscm.fr
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