Glutamate Blockers

I just posted this info for an FYI, it's interesting.  Most of this data is not from benzo research since benzo withdrawal research is non-existent.

 

Memantine: An anti-glutamate drug

 

"Memantine is an anti-glutamate and energy-buffering drug. As an NMDA antagonist, memantine prevents the neurotransmitter glutamate from leading to nerve cell degeneration by inhibiting glutamate´s binding to the receptor. Memantine has been clinically used to treat dementia and Alzheimer´s disease. Current research on its effects in other diseases of the central nervous system (CNS), including HD, looks promising because memantine appears to be well-tolerated as well as beneficial in terms of learning facilitation. It is possible that memantine may even be able to disrupt the progression of HD.

 

"According to a theory known as the excitotoxicity theory, lower energy levels in the nerve cells of people with HD cause them to be overly sensitive to glutamate. Consequently, even normal levels of glutamate can overactivate the glutamate receptors on the nerve cells. When these receptors (also known as NMDA receptors) are activated, calcium ions enter the nerve cells. Excessive activation causes a buildup of these calcium ions, which then leads to the death of the nerve cell....

 

"HD researchers believe that memantine may have strong potential to slow the progression of HD by decreasing the NMDA receptor´s sensitivity to glutamate. Memantine is an NMDA antagonist. As an antagonist, memantine prevents the excessive binding of glutamate to NMDA receptors, inhibiting the pathway to excessive NMDA activation and nerve cell death. Memantine is also a non-competitive antagonist. "Non-competitive" means that memantine binds to a site on the NMDA receptor that is different from glutatmate´s binding site. By binding to one portion of the NMDA receptor, memantine changes the overall shape of the receptor, making it more difficult for glutamate to bind to the other portion of the receptor."

 

-- (HOPES: Huntington's Outreach Project for Education, at Stanford,  5/3/2005: http://www.stanford.edu/group/hopes/treatmts/antiglut/l5.html)

 

Riluzole: An anti-glutamate drug and energy buffer.

 

"Riluzole has been shown to have energy-buffering and anti-glutamate properties. It has been associated with increased energy metabolism efficiency and inhibition of glutamate activity, and is currently used as a treatment for Amyotrophic Lateral Sclerosis (ALS) .... as well as Huntington’s disease...."

 

Riluzole is used to deal with the problem of aerobic inefficiency. "Energy metabolism is the process by which cells produce energy. Normally, cells prefer a form  energy metabolism called aerobic respiration due to its efficiency and high-energy yield. The altered huntingtin protein in people with HD is believed to interfere with aerobic respiration, resulting in the inability of HD cells to perform aerobic respiration efficiently. Instead, HD cells must resort to anaerobic respiration, another form of energy metabolism that is less efficient. This impairment in energy metabolism results in various negative effects that eventually lead to cell death.

 

"Studies have reported that riluzole treatment improves motor abnormalities associated with administration of a toxin that blocks energy metabolism. The improvements indicate that riluzole may have positive effects on cells with defective metabolism. However, the mechanism by which riluzole improves energy metabolism is still unknown....

 

Riluzole is also used to deal with the problem of glutamate sensitivity. "One of the effects of the impairment in energy metabolism in HD cells is an increased sensitivity to glutamate. Glutamate is one of the major neurotransmitters in the nervous system, used to transmit messages from nerve cell to another. Increased activation of receptors that receive glutamate has been observed in people with HD. Increased glutamate activity, in turn, has been associated with nerve cell death.

 

"Studies have demonstrated that riluzole may act as an anti-glutamate drug in two ways: 1) by inhibiting the release of glutamate and 2) by interfering with the effects of glutamate on nerve cells.

 

"It is thought that riluzole inhibits the release of glutamate by interfering with sodium (Na+) channels that are required for normal glutamate release."

 

-- (HOPES: Huntington's Outreach Project for Education, at Stanford, 12/3/2004: http://www.stanford.edu/group/hopes/treatmts/antiglut/l3.html)

 

Lamotrigine - An anti-glutamate and anticonvulsant drug

 

"Lamotrigine belongs to a group of medications called anticonvulsants, which are used to control seizure disorders. Lamotrigine acts on the central nervous system to control the number and severity of seizures. It is thought to suppress the activity of certain parts of the brain and the abnormal firing of nerve cells that cause seizures. In psychiatry, lamotrigine may be used as a mood stabilizer. In the laboratory, researchers have found that lamotrigine also inhibits release of the neurotransmitter glutamate. This is important because glutamate may play a role in nerve cell degeneration in the brains of people with HD, so reducing the amount of glutamate released makes lamotrigine a potential treatment for HD."

-- (HOPES: Huntington's Outreach Project for Education, at Stanford, 6/24/05: http://www.stanford.edu/group/hopes/treatmts/antiglut/l4.html)

 

Budipine

 

Budipine and Other Glutamate Blockers. A number of experimental drugs are being investigated for Parkinsons disease because they block the actions of glutamate, an amino acid that is a particularly potent nerve cell killer. Some of these drugs block a receptor group to glutamate called N-methyl-D-aspartate (NMDA). Investigative NMDA antagonists include remacemide, memantine, riluzole, and budipine. Budipine is of particular interest. It not only blocks NMDA, but it increases levels of two enzymes involved in the production of dopamine. Studies suggest that it reduces tremor in PD and it proving to be beneficial in combination with levodopa.

 

-- (About.com, 3/12/06): http://adam.about.com/reports/000051_7.htm)

 

Gabapentin

 

"Gabapentin - [brand Name: Neurotin] is a FDA approved medication for the treatment of seizures (epilepsy). Gabapentin is thought to decrease the production of glutamate. Glutamate is an excitatory amino acid in the brain. It acts as the major excitory neurotransmitter in the central nervous system. Glutamate, in excessive amounts, is toxic to motor neurons. Studies have shown that ALS patients have high levels of glutamate in their brain as well as a defect in the glutamate transport mechanism. Gabapentin is hoped to slow the rate of motor neuron death. A small number of patients on gabapentin report decreased muscle spasms and/or decreased muscle fasciculations and improved sleep."

 

--(The University of Miami ALS Clinical and Research Center: http://www.miami-als.org/drugs.htm)

..I'll pass on any other drugs..

how about cream of tartar?

Iggy

Sorry but nobody is going to be taking harmful drugs to block glutamate and increase our neurological damage, we are looking for natural ways to do it.

Sorry but nobody is going to be taking harmful drugs to block glutamate and increase our neurological damage, we are looking for natural ways to do it.

 

Scooby, your use of the word "nobody" is highly judgmental and just plain wrong. A close friend of mine died of Amyotrophic Lateral Sclerosis (ALS). It is a terrible way to die. https://en.wikipedia.org/wiki/Amyotrophic_lateral_sclerosis

 

He was an educator and a musician. He tried nearly every imaginable treatment (natural and pharmacological). Before his death while taking a pharmacological medication to prolong his painful existence and with the use of computer assisted technology to transcribe and publish most of his songs, he found some solace and also brought enjoyment to many of his friends who had not heard his previously unpublished music.

 

imo, people should be free to experiment and treat their symptoms of distress as they see fit so long as they do no harm to others.

best wishes

 

Edit: Another case in point; Jason Becker who can no longer perform due to ALS but, he is still composing music:

 

 

People should be informed of the consequences of pharmaceutical drugs to treat glutamate overload especially those in benzodiazepine withdrawal. The drugs used for glutamate blocking cause severe side effects and withdrawal symptoms like benzodiazepines, this is not something others with damaged nervous systems want.

 

 

 

 

People should be informed of the consequences of pharmaceutical drugs to treat glutamate overload especially those in benzodiazepine withdrawal. The drugs used for glutamate blocking cause severe side effects and withdrawal symptoms like benzodiazepines, this is not something others with damaged nervous systems want.

 

How is it that you speak for anyone besides yourself?

 

 

People should be informed of the consequences of pharmaceutical drugs to treat glutamate overload especially those in benzodiazepine withdrawal. The drugs used for glutamate blocking cause severe side effects and withdrawal symptoms like benzodiazepines, this is not something others with damaged nervous systems want.

 

How is it that you speak for anyone besides yourself?

 

I agree with Nathan Arizona, your writing style could use an upgrade to conform with forum policy.

 

Although our focus is indeed support, members are bound to have questions, will wish to discuss practical issues and problems, and share information. There is no limit upon reasonable discussion, but you should consider how your writing style might affect those reading your words. Since individuals are highly variable in how they react to benzodiazepine use and withdrawal, and some people taking benzodiazepines are more suggestible than they might be under different circumstances, you should avoid making blanket statements.

 

 

On the surface since glutamate does the opposite of GABA, it seems like blocking glutamate would be a good thing for anxiety and panic sufferers.

 

OTOH, When you start fooling around with these neurotransmitters in the brain with Rx drugs, you are probably asking for trouble. LOL

 

Look at what benzos do to GABA after the brain adapts and you become tolerant to the drug's effect. Might the same thing happen using a glutamate blocker? You initially get some relief. Then, the brain adapts to the drug and slowly stops working due to tolerance. Does glutamate then go into overdrive? Yikes--

 

Interesting thread!

 

 

On the surface since glutamate does the opposite of GABA, it seems like blocking glutamate would be a good thing for anxiety and panic sufferers.

 

OTOH, When you start fooling around with these neurotransmitters in the brain with Rx drugs, you are probably asking for trouble. LOL

 

Look at what benzos do to GABA after the brain adapts and you become tolerant to the drug's effect. Might the same thing happen using a glutamate blocker? You initially get some relief. Then, the brain adapts to the drug and slowly stops working due to tolerance. Does glutamate then go into overdrive? Yikes--

 

Interesting thread!

 

Exactly.

On 22/01/2022 at 06:53, [[A...] said:

On the surface since glutamate does the opposite of GABA, it seems like blocking glutamate would be a good thing for anxiety and panic sufferers.

OTOH, When you start fooling around with these neurotransmitters in the brain with Rx drugs, you are probably asking for trouble. LOL

Look at what benzos do to GABA after the brain adapts and you become tolerant to the drug's effect. Might the same thing happen using a glutamate blocker? You initially get some relief. Then, the brain adapts to the drug and slowly stops working due to tolerance. Does glutamate then go into overdrive? Yikes--

Interesting thread!

It depends on wether the drug up or down regulates glutamate receptors, in case of benzos gaba receptors are downregulated and glutamate receptors are upregulated so if a drug would do the opposite, there is a chance that it wouldn't be so bad.

The real problem is in the fact that the brain isn't so simple and adaptations go well beyond these 2 receptor sites, even if You could reverse adaptations there, there are probably hundreds of other downstream adaptations that happened and could generate negative symptoms due to this new abnormal state.

It is true that most people recover from withdrawal naturally but there always be a group that won't no matter how long they wait, because brains aren't perfect and if every brain had a way to correct every maladaptation back to baseline we wouldn't have degenerative brain disorders for example. How do we know it's true that not everyone can heal naturally? For example from studies on natural course of depression like this one:

https://www.cambridge.org/core/journals/the-british-journal-of-psychiatry/article/duration-of-major-depressive-episodes-in-the-general-population-results-from-the-netherlands-mental-health-survey-and-incidence-study-nemesis/406A1D35C7346CB742DFF42A90DE2462

20% of people doesn't recover after 24 months. While it is true that probably some of them will recover yet it is certain that it won't be all of them, so for this group it makes sense to try to find a drug that will modify the incorrect homeostasis that their brain created.

I don't really get why so many people got on the bandwagon of "low serotonin theory of depression is wrong" as it somehow discredits the notion that there is some kind of a problem with neurotransmitters in the brain of a depressed person, of course it is wrong, it doesn't matter what is the level of serotonin or any other neurotransmitter in someone's brain in relation to general population, what matters is the level of neurotransmitters and number and function of their respective receptors and how it all works together in this particular person. Really simplistic example:

We have a person A with 1000 serotonin and 1000 receptors, person A is fine and we have a person B with 1000 serotonin and 2000 receptors and person B while having the same level of serotonin is depressed.

I personally really hate psychiatry and we can see why looking at the study I've linked - if 80% of people recover naturally over 2 years then giving antidepressants as a first line treatment is wrong on so many levels. Don't get me wrong I get that depression is awful but I would trade feeling as I've felt when I had it to the rest of my life over how I am feeling now, back then I at least had some days of feeling better, could exercise without invoking hellish symptoms, could eat what I wanted. There is no other branch of medicine that has such a track of harmful treatments like psychiatry. I said earlier that for those that don't recover from depression (and I would add withdrawal here also as I think they are not so unlike in principle, but withdrawal is worse in symptoms and duration) trying a drug to at least alleviate the suffering isn't necessarily bad, but I would much rather live in a world where it isn't an option, ergo there are no psychotropic drugs of any kind legal or not and I am sure it would have been a net positive and it wouldn't even be close.

This turned out to be a little tangent so I will end it here.

V.

Edited March 23 by [Va...]
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