Introduction: Generally, NMDA receptor antagonists inhibit learning and long-term potentiation (LTP). However, it has been suggested that direct tonic activation of NMDA receptors, in contrast to learning, may lead to an increase in synaptic “noise”. Uncompetitive NMDA receptor antagonist Memantine can paradoxically reverse deficits in learning and synaptic plasticity, and restore LTP impaired by tonic NMDA receptor activation.  Material and Methods: Adult rats weighed 200 to 250 g were used in this in vivo study. Stimulating Schaffer collaterals field excitatory postsynaptic potentials (fEPSPs) were evoked in neurons of the CA1 area of the hippocampus. For induction of LTP, high frequency stimulation was applied to the path. Pre- and post-tetanic fEPSPs were recorded extracellularly in the anesthetized rats. Test groups were administered intraperitoneally with Memantine (10 mg/kg or 20 mg/kg) and the control animals received equal volumes of saline. Results: Our results express that the drug has no effect on the baseline EPSPs. The tetanic stimulation induced a pronounced LTP in the control group lasting at least 2 hours. The animals treated with 10 mg/kg of Memantine also displayed a significant LTP; however, the potentiation was lower than the controls. The high frequency stimulation under administration of 20 mg/kg of Memantine failed to induce LTP in the fEPSPs. Conclusion: These findings point out a dose dependent attenuation of LTP by Memantine. Comparison of the present data and those indicating the ability of Memantine to restore LTP led us to conclude that, due to the activation level of the recording path, this moderate affinity NMDA receptor antagonist displays different effects on potentiation of hippocampal recordings.

Background and Aim: Vascular dementia is one of the most common form of dementia. There is no treatment available to cure vascular dementia or to alter clinical course. The aim of this study was to evaluate the effects of donepezil, Memantine, rivastigmine and galantamine on mean flow velocity (MFV) and Mini-Mental State Examination (MMSE). Materials and Methods: This double-blind clinical trial was conducted on 44 patients with vascular dementia. Vascular dementia was diagnosed based on the DSM-V criteria. According to the order of entry into the study, the participants were treated with one of the drugs (donepezil (10 mg/d), Memantine 10 mg/d ), galantamine (8 mg/d) and rivastigmine6 mg/d. The sampling finished whenever 11 patients in each group completed the three-month trial. The MMSE and color Doppler ultrasound was performed for all participants before and three months after the intervention. Results: Our findings showed that Memantine and donepezil significantly increased MMSE score (P = 0. 009 and P = 0. 001 respectively). Since there was no significant difference between the groups in the frequency of variables and the mean MMSE scores before the intervention, the administration of Memantine and donepezil increased the MMSE scores. The findings also demonstrated that rivastigmine, galantamin and donepezil significantly increased MFV in some arteries. Conclusion: Memantine and donepazil improve cognitive function in patients with vascular dementia. Rivastigmine, galantamin and donepezil increase MFV in some arteries although this effect seems limited.

Purpose: Evaluation of efficacy of Memantine (N-Methyl-D-Aspartate Receptor Antagonist) on visual function of patients with acute non-arteritic ischemic optic neuropathy (NAION).Methods: The study was conducted as interventional case series from November 2005 through November 2006 in Farabi Eye Hospital. Twenty-two patients with acute NAION of less than 8 weeks duration entered the study. Memantine was prescribed with a dose of 5 mg per day for the first week and 10 mg per day for the following two weeks. Baseline best corrected visual acuity (BCVA); visual evoked potential (VEP) and visual field was done for all patients. BCVA recording repeated 3 weeks, 3 and 6 months later. VEP and perimetry repeated 3 months after treatment.Results: After 3 weeks, 3 and 6 months, BCVA improved -0.32±0.40 LogMAR, -0.51±0.49 and -0.51±0.49, respectively (P=0.005, P=0.001 and P=0.001, respectively). VEP recordings after 3 months, demonstrated -8.61±14.51 db mean decrease in implicit time (P=0.019). Amplitude of voltage did not show significant difference with baseline (P=0.10). Perimetry results after 3 months showed that mean deviation (MD) improved 2.77±3.94 db (P=0.016).Conclusion: Memantine resulted in significant improvement of BCVA 3 weeks, 3 and 6 months after treatment of acute NAION. Memantine also resulted in significant decrease of implicit time and significant improvement of mean deviation in VEP and perimetry after 3 months.

Stuttering is a complex speech disorder. There are two forms of stuttering: developmental stuttering and acquired stuttering. Developmental stuttering is a disorder of early childhood but acquired stuttering can develop at any age. Some medications can induce or deteriorate stuttering as an adverse effect. There are several reports of stuttering due to psychotropic drugs. Memantine, a glutamate antagonist used in the treatment of Alzheimer’s disease, has also been studied for the treatment of autism spectrum disorders. This report presents deterioration of stuttering and speech problemin two children with autistic disorder who were receiving Memantine. Based on our knowledge, this is the first time these adverse drug reactions have been attributed to Memantine. In conclusion clinicians should consider that speech problems including stuttering may be due to the consumption of Memantine, especially, in children may be a side effect of Memantine especially in children.