In this study the authors tested the hypothesis that treatment with the NMDA receptor antagonist memantine is protective against beta -amyloid neurotoxicity and learning impairment in rats recieving an intra cerebral injection of beta amyloid peptide 1-40 (Abeta 1-40). Sprague–Dawley rats received vehicle or vehicle plus memantine s.c. by osmotic pump for 9 days. After 2 days of treatment, 2 ml of water containing Abeta (1–40) were injected into the hippocampal fissure. After 9 days of further treatment animals were tested for psychomotor activity and spatial discrimination then sacrificed and examined for neuronal degeneration, astrocytic and microglial activation. Abeta(1-40), but not water, injections into hippocampus led to neuronal loss in the CA1 subfield, evidence of widespread apoptosis, and astrocytic and microglial activation and hypertrophy.The memantine treated animals had significant reductions in the amount of neuronal degeneration, pyknotic nuclei, and markers of glial activation as compared with vehicle treated animals. Memantine treatment however did not significantly alter motor activity or spatial learning compared to vehicle. These data suggest that memantine, at therapeutically relevant concentrations, can protect against neuronal degeneration induced by beta-amyloid. The authors concluded that in order to further ascertain the relevance of memantine treatment for neuroprotection against long term Aβ-induced neurodegeneration future studies with longer survival times after amyloid deposition and longer periods of memantine treatment will be required.
In studies using rats, typically the rat weight is reported rather than age. A female Sprague Dawley rat weighing 240-260g is between 10-12 weeks old (https://www.taconic.com/pdfs/sprague-dawley-rat.pdf).