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Identifying the implicated neurotransmitter??

Stephen Stahl - Essential Neuropharmacology?
The Prescribers Guide.
Both available on library genesis.

It came recommended.

Saplosky?
Has he got any lectures specifically on NE receptor saturation?
 
Woodburner said:
I guess you know what caused your problems then? You do know that you don't have to be hyperactive to have it?
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Does ADHD normally result in chronic fatigue?

If I had ADHD, would I not have a postiive reaction to methylphenidate?
Which I didn't.


I've been reading a lot of material on some forms of chronic fatigue, which seems to be effectively treated with and NRI..... + L-phenylalaline (incorrect spelling).


So I tried adding L-phenylalaline - 1000mg daily, starting this morning.


Will see how that goes.


Other meds are:
45 mg remeron
70 mg lofepramine (desipramine pro-drug)
 
If we thought ADHD/ADD was simply a deficit of DA and NE then Ritalin might be expected to be a fabulous treatment for all, and improvement with Ritalin would be diagnostic, but I think ADHD/ADD is much more complicated than that - and co-morbid illnesses complicate medication responses as well.
 
Enough amphetamine leaves me zoning out listening to music of a teenage girl because anything else is too abrasive
 
johnboy2000 said:
does adhd normally result in chronic fatigue?

perhaps not officially but fatigue is top of the list of symptoms dopamine of dopamine deficiency, and adhd is very strongly linked to dopamine deficiency.
I was certainly suffering from fatigue for a very long time.

if i had adhd, would i not have a postiive reaction to methylphenidate?

not necessarily; medication is ineffective in a very large proportion of cases. It was borderline ineffective for me, and actually, seriously increasing my protein intake has been more effective!

which i didn't.


I've been reading a lot of material on some forms of chronic fatigue, which seems to be effectively treated with and nri..... + l-phenylalaline (incorrect spelling).


So i tried adding l-phenylalaline - 1000mg daily, starting this morning.

phenylalanine should help with dopamine production, but why not just eat more high protein foods?

will see how that goes.

any help?

other meds are:
45 mg remeron
70 mg lofepramine (desipramine pro-drug

looking up research on those drugs it looks like they could be helpful for adhd/low dopamine. Do they help at all? )
Click to expand...
 
Cotcha Yankinov said:
If we thought ADHD/ADD was simply a deficit of DA and NE then Ritalin might be expected to be a fabulous treatment for all, and improvement with Ritalin would be diagnostic, but I think ADHD/ADD is much more complicated than that - and co-morbid illnesses complicate medication responses as well.
Click to expand...
Agreed :)
 
Woodburner said:
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Those
drugs, lofepramine and remeron, implicate more so noradrenaline and serotonin.

bupropion - which I've previously taken to little effect, and methylphenidate - again to little effect - both implicate dopamine.

Noradrenergic action specifically incited benefit in my case.

I've replaced remeron with its older sister - Mianserin - which is going much better.

I don't know my diagnosis - I personally think it's either depression or CFS - but in any case, the only neurotransmitter to benefit me, is noradrenaline/epinephrine.

The phenylalanine experiment was not good.
Just made me more tired, exacerbated symptoms.
I cut that out.
 
I know NE works for me but - just given the primary symptoms of lethargy - would an amino acid neurotransmitter such as glutamate potentially provide any benefit?

Glutamate blocker, I believe it is but - ketamine - NMDA blocker.

I recently have met a dude that uses this recreationally.
I'm curious as to whether it would be feasible to use alongside my currents meds of desipramine and mianserin???

I assume I would also take a very small dose of it.

It doesn't have to be administered intravenously to incite a therapeutic effect, right?
 
Is the effect of NMDA blockers, basically the opposite of the activation of NE enhancers?
i.e. sedation?

That's what I seem to be getting from the wiki page on nmda blockers.

Atomoxetine - is an NE enhancer, that does have some sedation associated with it.
I wonder is that because of it's secondary property of acting as a NMDA channel blocker?
 
JohnBoy2000 said:
Is the effect of NMDA blockers, basically the opposite of the activation of NE enhancers?
i.e. sedation?

That's what I seem to be getting from the wiki page on nmda blockers.

Atomoxetine - is an NE enhancer, that does have some sedation associated with it.
I wonder is that because of it's secondary property of acting as a NMDA channel blocker?
Click to expand...
Often, sedative side effects occur because of off-target effects on histamine H1, muscarinic, or alpha2 adrenergic receptors.
 
JohnBoy2000 said:
Is the effect of NMDA blockers, basically the opposite of the activation of NE enhancers?
i.e. sedation?

That's what I seem to be getting from the wiki page on nmda blockers.

Atomoxetine - is an NE enhancer, that does have some sedation associated with it.
I wonder is that because of it's secondary property of acting as a NMDA channel blocker?
Click to expand...

NMDA antagonists can result in release of neurotransmitters (including NE) because normally NMDA receptors provide excitatory input to inhibitory neurons - so when you block NMDA receptors it can turn off inhibitory interneuorns, and hence their downstream inhibitory influence diminishes.

JohnBoy2000 said:
I know NE works for me but - just given the primary symptoms of lethargy - would an amino acid neurotransmitter such as glutamate potentially provide any benefit?

Glutamate blocker, I believe it is but - ketamine - NMDA blocker.

I recently have met a dude that uses this recreationally.
I'm curious as to whether it would be feasible to use alongside my currents meds of desipramine and mianserin???

I assume I would also take a very small dose of it.

It doesn't have to be administered intravenously to incite a therapeutic effect, right?
Click to expand...

There is probably some dose-dependent risk of seizures and/or serotonin syndrome.

Some of the anti-depressant effects of ketamine are thought to be a bit independent of NMDA antagonism (a metabolite called HNK). Depending on route of administration you may get more or less of the metabolite but my brain isn't producing much useful info on that matter right now.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4922311/
 
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