Evaluation of the Effects of Charged Amino Acids on Uncontrolled Seizures

Danny Boy

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Oct 12, 2014
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Ear infection
"Two products of arginine: glutamic acid and agmatine may be involved for anticonvulsant effects of arginine.

Administration of arginine and glutamic acid can be effective in reducing the seizure frequency of uncontrolled epilepsy patients, without triggering considerable complications."

http://www.hindawi.com/journals/nri/2015/124507/

"Agmatine was found to exert modulatory actions directly and/or indirectly at multiple key molecular targets"

  • Neurotransmitter receptors and receptor ionophores. Nicotinic, imidazoline I1 and I2, α2- adrenergic, glutamate NMDAr, and serotonin 5-HT2A and 5HT-3 receptors.
  • Ion channels. Including: ATP-sensitive K+ channels (Potassium channel)
    , voltage-gated Ca2+ channels, and acid-sensing ion channels (ASICs)."

"Glutamic Acid is converted into GABA (gamma aminobutyric acid) or glutamine both of which serve essential purposes in passing messages around the brain.

Like all amino acids, Glutamic acid is one of the numerous components of our proteins and while it is synthesised naturally inside the body, we often find ourselves with depleted levels."
 
Concerning neuroprotection, agmatine's effects are thought to involve modulation of receptors (NMDA, alpha 2, and imidazoline) and ion channels (ATP sensitive potassium channels and voltage-gated calcium channels) as well as blocking nitric oxide synthesis. Agmatine blocks nitric oxide synthesis by reducing the nitric oxide synthase -2 (NOS-2) protein in astroglial cells and macrophages. With respect to agmatine's benefit in psychiatric disorders, it is suggested that the mechanism involves neurotransmitter receptor modulation of the NMDA, alpha-2, serotonin, opioid, and imidazoline receptors. Specifically when agmatine binds to the imidazoline and alpha 2 receptors, it acts as a neurotransmitter and releases catecholamines from the adrenal gland.

As an experimental drug, agmatine is being studied for several indications such as cardioprotection, diabetes, decreased kidney function, neuroprotection (stroke, severe CNS injuries, epilepsy, glaucoma, and neuropathic pain), and psychiatric conditions (depression, anxiety, schizophrenia, and cognition). The exact mechanism of action is still being investigated for all of the potential indications of agmatine.



http://www.drugbank.ca/drugs/DB08838

Hm...So Agmatine works on the potassium channels and NDMA receptors as well as calcium channels.
 
Aren't you also on Trobalt and possibly other drugs, @Danny Boy? Doesn't that make it more or less impossible for anyone to know what is doing what effect, what interactions there might be, etc?

Sorry, but it seems like every week you have some new supplement, drug or approach which you become convinced is "helping" -- and yet you still have tinnitus, and you're still on Trobalt?
 
Aren't you also on Trobalt and possibly other drugs, @Danny Boy? Doesn't that make it more or less impossible for anyone to know what is doing what effect, what interactions there might be, etc?

Sorry, but it seems like every week you have some new supplement, drug or approach which you become convinced is "helping" -- and yet you still have tinnitus, and you're still on Trobalt?

I don't want a cure, just a reduction. Plus, I found it quite interesting.

Also, here are the biointeractions
http://www.drugbank.ca/drugs/DB08838/biointeractions
 
Where does it say that?
it says it's a potassium channel antagonist, so there's some kind of direct/secondary interaction there. It also says it's an NMDAR antagonist, which means it's got secondary/tertiary interactions with RTG's GABA activity (NMDA and GABA work in opposition).

edit; ah, it's a Kv1.1 targeter, so, possibly not much direct interaction with RTG at Kv channels... but, it's hitting a whole ton of buttons, and clearly has significant overlap at least along GABA-mediated inhibition. Until evidence to the contrary emerges, I will remain convinced that a big part of RTG's tinnitus impact relates to GABA. Kv channels have been pretty conclusively shown to be part of the problem that initially creates tinnitus, but I also remain convinced that the long-term maintenance of tinnitus hyperactivity has more to do with LTP and problems with inhibition.

Interesting stuff, anyway.
 
it says it's a potassium channel antagonist, so there's some kind of direct/secondary interaction there. It also says it's an NMDAR antagonist, which means it's got secondary/tertiary interactions with RTG's GABA activity (NMDA and GABA work in opposition).

edit; ah, it's a Kv1.1 targeter, so, possibly not much direct interaction with RTG at Kv channels... but, it's hitting a whole ton of buttons, and clearly has significant overlap at least along GABA-mediated inhibition. Until evidence to the contrary emerges, I will remain convinced that a big part of RTG's tinnitus impact relates to GABA. Kv channels have been pretty conclusively shown to be part of the problem that initially creates tinnitus, but I also remain convinced that the long-term maintenance of tinnitus hyperactivity has more to do with LTP and problems with inhibition.

Interesting stuff, anyway.

It does work on the calcium channels, so there'd be a gabapentin interaction.
 
Hey Danny Boy, good job on look for new drugs which could work for Tinnitus suffers. Continue this please I read all your post and get some hope even they are not the final cure for us.
 
Hey Danny Boy, good job on look for new drugs which could work for Tinnitus suffers. Continue this please I read all your post and get some hope even they are not the final cure for us.

Thank you for your support. I will ^_^.
 

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