Author Topic: what is everyone's thoughts on NMDA antagonists?  (Read 888 times)

[Buddie]

Re: what is everyone's thoughts on NMDA antagonists?
« Reply #10 on: January 11, 2021, 08:35:59 am »
But regarding riluzole, are there reports about wd or issues on long term use? I read an post on IOCD that it is studied as a new drug for OCD. If this helps, I will be happy to take it instead of SSRIs.
Riluzole requires special dietary regimen. Troriluzole is a riluzole pro-drug that doesn't require any special consideration.
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[Buddie]

Re: what is everyone's thoughts on NMDA antagonists?
« Reply #11 on: May 12, 2022, 08:10:37 pm »
Anything on Agmatine?  I only see 2 posts on it

https://examine.com/supplements/agmatine/

Any news on this? I am considering it.
Suggestions, opinions and/or advice provided by the author of this post should not be regarded as medical advice; nor should it substitute for professional medical care. Consult your doctor before making any changes to your medication. Please read our Community Policy Documents board for further information.

[Buddie]

Re: what is everyone's thoughts on NMDA antagonists?
« Reply #12 on: May 18, 2022, 04:35:32 am »
From what I've read into and I accept that it may not be entirely accurate. The down-regulation of the A1 location sites on the GABAa receptors due to the agonist effect benzodiazepines exert on this location may lead to the up-regulation of certain location sites on the NMDA and AMPA receptors located in the Glutamatergic neurons. I have no information on which particular sites may be effected on these receptors.

However, it is possible that the degree of benzodiazepine withdrawal symptom severity has more to do with the up-regulation of these receptor sites than it does the down-regulation of the A1 sites on the GABAa receptors in the GABAergic neurons.

The up-regulation of the NMDA and AMPA receptor sites gives Glutamate (the brains primary excitatory neurotransmitter) more sites to bind to. This would result in an increase in cell membrane depolarization, resulting in the Voltage-gated calcium (Ca2+) channels to remain open for extended periods of time. Flooding the Axon Terminals of neurons with positively charged Calcium Ions. When too many Calcium Ions flood into the neurons, it leads to 'excitotoxicity' - https://en.wikipedia.org/wiki/Excitotoxicity

Excitotoxicity can lead to chronic over stimulation. Particularly the over stimulation of the adrenergic receptors, leading to symptoms of Anxiety, Panic Attacks and Insomnia.

In more severe cases of Excitotoxicity, the structural integrity of the neurons can become damaged or even lead to the death of the neuron cell itself. This can trigger more severe symptoms such as hallucinations, psychosis and Grand Mal Seizures.

The use of NMDA and AMPA receptor antagonists/blockers could prove to be highly beneficial in controlling benzodiazepine withdrawal symptoms, by reducing/blocking Glutamate's activation effects on these receptors, preventing excess Calcium Ion Influx into the neurons.

There is an interesting study here, where a 27 year old male suffering from severe benzodiazepine withdrawal along with Opioid poly drug use was admitted to a medical facility where a combination of benzodiazepine's were administered, but failed to get the symptoms under control. - https://www.cureus.com/articles/27151-ketamine-a-potential-adjunct-for-severe-benzodiazepine-withdrawal

The patient was then placed on a Ketamine infusion of 0.5mg/kg given over a 30-minute interval and the withdrawal symptoms were subsequently reduced dramatically.

The reason this study is so relevant is because Ketamine is a highly potent NMDA receptor antagonist and greatly inhibits Glutamate's activation on these receptors.

Supplemental sources of NMDA and AMPA receptor antagonists include Magnesium Glycinate and L-Theanine. Magnesium has an antagonistic effect on NMDA receptors as well as acting as a partial blocker of the Calcium Channels. L-Theanine has antagonistic effects on the AMPA receptors and also partially blocks the transportation of Glutamate into the Glutamatergic neurons from the Astrocyte. This is important, because any Glutamate that can't make it's way into the Glutamatergic neuron, is subsequently sent to the GABAergic neuron instead. The Glutamate is then converted into GABA through the Glutamic Acid Decarboxylase (GAD) process. Reducing Glutamate in the Glutamatergic neuron, while boosting GABA levels in the GABAergic neuron.
Suggestions, opinions and/or advice provided by the author of this post should not be regarded as medical advice; nor should it substitute for professional medical care. Consult your doctor before making any changes to your medication. Please read our Community Policy Documents board for further information.