Memantine

Memantine questions and answers

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Q: how can i get Memantine and gabapentin for nystagmus eye condition?
i read on a google search the Memantine and gabapentin can help with nystagmus, can my doctor prescribe this? or how should i go about getting it... any help is great! thanks!

A: First, confirm that your primary care physician has diagnosed the underlying cause of your nystagmus. Nystagmus is a clinical finding, not a disease. There are several different potential causes and underlying diseases, some very serious. You don't want to treat a symptom and ignore the cause. Once the diagnosis and treatment have been addressed, if the nystagmus continues, ask your physician for a referral to a neurologist. They are best qualified to recommend treatment... and, yes, nerve modifies like Neurontin (gabapentin) may help. There are many other options. Namenda (memantine) is still in trials for this use. It is unproven.

Q: What are the structures and events that are involved at the site where glutamate causes transmission...?
What are the structures and events that are involved at the site where glutamate causes transmission of an impulse between two neurons in the brain? HOw can MK801 and memantine slow the growth of glioma? Please help me with these questions and tell me any useful websites where I can find information because I really don't get it, and can' seem to find find anything on it in my textbook or on the internet. Also some technologies taht could be used to study glial cancer Also some technologies thatt could be used to study glial cancer

A: This is a tough one. I'll do my best. What are the structures and events that are involved at the site where glutamate causes transmission of an impulse between two neurons in the brain? Glutamate is a neurotransmitter which is released from the axon terminal and binds with a surface receptor on an effector cell (such as another neuron). Astrocytes function to absorb glutamate and process by converting it to glutamine then delivering it back to the pre-synaptic cell. Not sure the level of detail you need, but hopefully this gives you a starting point. HOw can MK801 and memantine slow the growth of glioma? MK801 and memantine are known glutamate antagonists, which bind with the glutamate receptor. Tumor cells in the brain (gliomas) have been found to release an excessive amount of glutamate into the brain extra-cellular matrix leading to neuronal cell death. These drugs apparently help to prevent neuronal death and possibly inhibit tumor growth by preventing glutamate release. Here is an excellent article, that I think answers your question directly and will probably be a better source for you than me: http://www.nature.com/nm/journal/v7/n9/full/nm0901-1010.html Addition: Also some technologies thatt could be used to study glial cancer I would guess the most effective would be conventional methods like genetics, various imaging methods (CT scans, PET scans, MRIs).

Q: NMDA receptor antagonists?
Why is it that activation of the NMDA receptor by glutamate is responsible for neuronal plasticity, memory and learning but NMDA receptor antagonists (such as memantine) are used in the treatment of Alzheimer's disease? It seems that a perceived side effect of the NMDAR antagonist would be memory and learning deficits? Also, since NMDARs are responsible for excitotoxicity would it stand to reason that antagonists such as dexomethorphan dosed regularly might be effective in treating stroke victims, or those predisposed to schizophrenia? I have read an exhausting 16 hours about all of this and the potential for use of NMDAR antagonists in antinociception, potentiating opioids and mitigating withdrawal - plus antidepressant effects? Does glutamate play a role in depression and pain? Too many questions, I know, who is really, really smart- :-) (note, this originally was errantly placed in biology section_

A: Memantine (sold in the USA as Namenda) is a moderate affinity antagonist of the NMDA receptor. The primary goal of this treatment is to limit excitotoxic injury due to calcium flux through the NMDA-R, which has some of the highest calcium permeabilities of any channel desribed. The compound also has a relatively rapid off-rate and it allows for the NMDA-R to still respond if glutamate concentrations are high enough. Given the relatively modest effects of anticholinergic drugs in treating AD symptoms this was viewed as a way to mitigate the worsening of symptoms in later stage disease where it is felt that excitotoxicity may be playing a more important role. Interstingly, memantine also has an impact at both cholinergic and serotonergic synapses which may likely confuse the issue somewhat.