Doesn't Glutamate/NMDA antagonism cause motor discoordination, memory disruption, and blackouts though?
Because memantine only is a partial antagonist it only causes a temporary decrease in short term memory and memory formation after which you can expect an increase in cognition.
Some ppl report it could take 6 weeks before any decrease in cognition is fully gone.
This mice study also shows a cognitive improving and anxiolotic effect of memantine with chronic
Cognition-enhancing and anxiolytic effects of memantine
Minkeviciene R, Banerjee P, and Tanila H (2008). Neuropharmacology 54(7):1079-85.
Memantine, a moderate-affinity NMDA receptor antagonist, is clinically used for the treatment of Alzheimer's disease (AD). Both clinical and preclinical studies have shown that memantine, at doses producing a steady-state plasma level of 0.5-1muM, is well tolerated and improves cognition. Here we tested the effects of chronic oral administration of memantine (10, 30 and 100mg/kg per day) producing steady state plasma drug levels ranging between approximately 0.5and 6muM on motor, social, emotional and cognitive behavior in normal C57BL/6J mice. Memantine dose-dependently reduced escape latency (hidden platform) and decreased wall swimming tendency in the Morris water maze test, increased time spent in open arms in the elevated plus-maze test, and reduced the number of isolation-induced aggressive attacks, but did not affect exploratory activity in the open field. These data indicate that high, stable doses of memantine improved cognition and exhibited a potential anxiolytic response in normal mice.
Therapeutically relevant plasma concentrations of memantine produce significant NMDA receptor occupancy and do not impair learning in rats
More, L, G N J, Valastro B, Greco S, and Danysz W (2008). Behav Pharmacol 19, 724-734.
Subchronic treatment with memantine using osmotic pumps in male rats was used to verify whether plasma levels significantly blocking L-N-methyl-D-aspartate (NMDA) receptors (and shown previously to be neuroprotective) may impair learning. Treatment with 6.27, 12.5 and 18.8 mg/rat/day provided plasma levels of 1.03+/-0.08, 5.07+/-0.68 and 11.68+/-0.90 micromol/l. Only the lowest plasma level is therapeutically relevant and has previously been shown to be neuroprotective. Significant deficits in a passive avoidance task were only observed at the highest dose. Working memory, tested as spontaneous alternation in the cross maze, was impaired by the middle and highest doses, and these doses also induced hyperlocomotion. Microdialysis experiments with in-vivo recovery (27.4%) showed that infusion of memantine at 6.27 mg/rat/day (ca. 23 mg/kg/day) produced a concentration of 990+/-105 nmol/l in extracellular fluid. In-vivo NMDA receptor occupancy experiments demonstrated significant, dose-dependent receptor occupancy of 32.7 and 65.7% by memantine at the doses producing 1 and 5 micromol/l plasma levels, respectively. Moreover, acute administration (2.5 mg/kg intraperitoneally) of memantine to mature female rats produced approximately two-fold higher plasma levels than in young male rats. In conclusion, a dose of memantine which produces a plasma level (1 micromol/l) within the therapeutic range, reported previously to be neuroprotective, leads to intracellular brain levels similar to the affinity of memantine for NMDA receptors (receptor binding, patch clamp). This has been also extended by the experiments showing that at this plasma concentration, memantine occupies ca. 30% NMDA receptors in the brain and produces no cognitive impairment.
Thats unfortionate it didnt went away for you. Maybe you should have played around with the doses some more (5 or maybe 20mg) some ppl have a differend sweet spot.
Here's an interesting read on memantine: