LONGECITY

What would be the distinct difference between the two in correlation with depression/anhedonia symptoms and Glutamate?

 

I feel constantly spaced out and unconnected with the world, but don't ever feel lethargic. Almost too serious and hyper vigilant

Edited by Derin105, 01 March 2016 - 01:38 AM.

Well, weakly use of ketamine works for anhedonia in bipolar which under treatments dont fix but thats not something you take chronically and its effects are downstream mediated.

 

I havent read about memantine working for anhedonia but absolutely for depresion, glutamate activation can also help, its absolutely individual what would allevate your symptions, youd have to experiment thats the onyl way to figure out what works for you and indicates in a way what causes your issues.

 

Have you got any adhd symptions?

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I don't have ADHD, but it's no surprise a 20mg adderall brings back emotions and reward

Sounds like hypoactivity 

Well this was caused by marijuana is there any way to modulate or repair the NMDA system to normalize glutamate throughout the brain?

NMDA antagonists are often nAchRs antagonists, too. nAchRs have bigger impact on anhedonia and depression. 

For example instead of a mood lift or improvement of anhedonia after a hard workout, I feel even more spacey and my tinnitus gets louder. What could that indicate?

Sounds like thyroid problems to me.

My thyroid and endocrines are perfect

Tinnitus has a weird direct connection to NMDA. There were efforts to develop an antagonist (neramexane) as a treatment, unfortunately the trial failed. Strangely many, including me, get often an actual worsening of tinnitus while using an antagonist (or, to be exact, probably when passing a certain threshold. While under stress, a tiny dose of memantine would help, but any stronger antagonist makes it worse again- indicating a non-linear somewhat).

 

Somehow I think now that the NMDA system is far too complex to just speak about under- or overactivity. Probably it has more to do with balancing of receptor activity (there are even 5 or so subunits) throughout the brain, in relation to overall glutamate (you'll never have all NMDARs blocked or you'd be in anaesthesia, and antagonism leads to release of more glutamate through probably autoreceptors, which then at least causes more AMPAR activation, but maybe also a shift in the activity of the non-blocked NMDARs etc). What does this mean? I can't say.

Edited by dopamimetiq, 09 March 2016 - 12:27 PM.

I got the exact same problem, accept i don't suffer from tinnitus 

Why are you making the assumption that your symptoms stem from NMDA hyper or hypo activity in the first place? If the symptoms don't fit into either paradigm, then perhaps it's best to look elsewhere.

About hypoactivity what do you suggest?

Tinnitus has a weird direct connection to NMDA. There were efforts to develop an antagonist (neramexane) as a treatment, unfortunately the trial failed. Strangely many, including me, get often an actual worsening of tinnitus while using an antagonist (or, to be exact, probably when passing a certain threshold. While under stress, a tiny dose of memantine would help, but any stronger antagonist makes it worse again- indicating a non-linear somewhat).

 

Somehow I think now that the NMDA system is far too complex to just speak about under- or overactivity. Probably it has more to do with balancing of receptor activity (there are even 5 or so subunits) throughout the brain, in relation to overall glutamate (you'll never have all NMDARs blocked or you'd be in anaesthesia, and antagonism leads to release of more glutamate through probably autoreceptors, which then at least causes more AMPAR activation, but maybe also a shift in the activity of the non-blocked NMDARs etc). What does this mean? I can't say.

I too get tinnitus from lack of nmda activity however there is a fine balance between too much and too little and too much can also cause tinnitus.

I think it has to do with loss of brain cells with NMDA receptors. Thus we are more sensitive to antagonism. However we are genetically predisposed to exctitoxicity and thus with more NMDA activity we get even more tinnitus.

Magnesium, carnitine give me tinnitus.

 

For me there's a very sensitive balance between hyper and hypo. Hypo makes me schizo with pseudohallucinations, hyper makes me autistic with irritability, ocd and rage fits.

Anyone check their GAD1 mutations? All 5 of mine catalyzes production of GABA from Glutamate leading to increased Glutamate and low GABA.

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Anyone check their GAD1 mutations? All 5 of mine catalyzes production of GABA from Glutamate leading to increased Glutamate and low GABA.

GAD mutation leading to reduced enzymatic function is very frequent in the European population and is one out of thousands of mutations that increase our iq.