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Chemicals to upregulate receptors..

rickolasnice, I don't think there's any way besides sleep, time, good nutrition, and exercise.
 
MeDieViL said:
Tianeptine wont work as it doesnt lower serotonin.
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It does enchance serotonin reuptake, which I believe means more available serotonin to be stored in synaptic vesicles. SSRI:s do the opposite.
 
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I actually found something interesting about a study on opiate tolerace on another site, I'll throw it up here in case it interests someone. I don't think it would apply to the op, but I certainly thought it was sort of cool.

"In the study, mice were treated repeatedly with morphine until a tolerance was developed such that the mice required 3x the amount of morphine to experience the same analgesic effect

Trifluoperazine (Stelazine) is an already existing antipsychotic drug used to treat schizophrenia.
When Trifluoperazine was given to the morphine-tolerant mice 30 minutes before administration of morphine, the morphine-tolerance was completely 100% reversed. The morphine-tolerant mice taking Trifluoperazine experienced the same analgesic sensitivity and effect as an opiate-naive mice. The doses of Trifluoperazine given to the mice were similar to the (equivalent) doses used for treatment of schizophrenia.

Mice treated with trifluoperazine on a daily basis showed a great reduction or slowing in the development of the morphine tolerance in the first place

Finally, naloxone-induced withdrawal symptoms were nearly completed attenuated in morphine-tolerant mice treated with trifluoperazine."
 
preliminary research would suggest that reverse agonists could hypothetically lead to receptor upregulation. receptor antagonists wouldnt really do shit; i mean, they COULD, but probably not much. but there's basically no fucking research in this area, and the only reverse agonist i know of offhand where any research has been done is with naloxone.

as far as i know, this type of reseach isnt even to infancy yet, but i feel there's the potential for there to be many great things that could come from it.

uberpenguin - include links to articles like that when you post them please.
 
Anonyymi said:
IMHO just antagonizing (blocking) receptors is not a working way most of the time. There are some interesting substances though.

Sulpiride, amisulpride and sultopride seem to directly up-regulate GHB-receptors.

Proglumide and other cholecystokinin antagonist seem to to slow down development of opioid tolerance.

St. John's wort and tianeptine could be useful for SRA-substance related tolerance.

Atypical antipsychotics with 5HT2A affinity are not useful for reversing LSD, psilocybin, mescaline, etc. tolerance. 5HT2A downregulates upon exposure to agonist or antagonist.

I don't understand how tyramine would be able to reverse stimulant tolerance, since tyramine indeed causes spontaneous monoamine release, somewhat like amphetamines. It is not able to cross BBB either.

So far, the only guaranteed way to reverse substance tolerance is abstaining from drug use although I can see some interesting development on these substances.
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IIRC 5HT2A receptors normally come back to baseline after just a week or so of abstinence. I guess psychedelic tollerance is mostly due to receptor density rather than receptor sensitivity.
This reminds me of the first time I took LSD, I had to take twice the dose my friends took to reach a reasonable high.

Your statement about 5HT2A antagonist downregulation is kind of peculiar, got any reference? Would the same apply for inverse agonists?
 
Buspirone (Buspar) supposedly upregulates serotonergic neurons by desensitizing and down-regulating their 5-ht1a autoreceptors. For some reason, post-synaptic 5-ht1a receptors are not downregulated by its action.

I've never taken Buspirone, but from what I've heard, whatever it is doing is not much.
 
it has been shown to also slow/stop tolerance of other drugs as well - but of course this is all iffy/trial stuff so take with a grain of salt


and of course I wasn't saying "hey go eat some mk-801 with your percocets kids." It was simply food for thought
 
What's the difference between up-regulating a receptor and what benzodiazepines do (receptor modulation)? They make the GABA receptor more sensitive as we all know, which is why they combine so well with other GABA agonists. Or are benzodiazepines considered receptor up-regulators?
 
kakti said:
What's the difference between up-regulating a receptor and what benzodiazepines do (receptor modulation)? They make the GABA receptor more sensitive as we all know, which is why they combine so well with other GABA agonists.
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Almost all so-called GABA-A agonists are actually GABA-A positive allosteric modulators -- this includes benzos, barbs, nonbenzos, alkyhawl, kavalactones, etc; the only real GABA-A agonists on the market are Amanita muscaria, which produce quite different effects!

However, the difference is that upregulation is a lasting effect (usually involves increased receptor density), whereas benzodiazepines et al produce their effects only as long as they remain bound to the receptor -- when usage of benzodiazepines is abruptly halted, GABA-A receptors are downregulated, resulting in potentially lethal seizures...
 
Low doses of naltrexone are being researched for their potential to create a boost to endorphin levels.

When administered in Ultra Low Doses (15mcg), a variety of sources have been seeing an attenuation, and even reversa,l of opiate tolerance in addicted users.

Low dose Naltrexone (1-3mg taken before sleeping at night)is being used by doctors to treat AIDS, as well as certain types of cancers because of a supposed mechanism that increases endorphin levels by up to 200 percent - and the inherent boost to the immune system that this brings.

The reading i have been doing lately is pointing to naltrexone as a bit of a wonder drug.

Anyone else have knowledge of this?
 
Perhaps it was psychosomatic, but I swear that after 2 months of subtly mindfucking use of the L-Dopa containing Mucuna pruriens, which lead pretty much straight to anhedonia (I assume from receptor desensitization / downregulation), a 2nd plateau DXM trip put my head back on straight. It was truly a relief.

I can also attest that NMDA receptor antagonists slow, but by no means stop or reverse, amphetamine tolerance.
 
acetylcholine said:
Buspirone (Buspar) supposedly upregulates serotonergic neurons by desensitizing and down-regulating their 5-ht1a autoreceptors. For some reason, post-synaptic 5-ht1a receptors are not downregulated by its action.

I've never taken Buspirone, but from what I've heard, whatever it is doing is not much.
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i've heard somewhere that 5-ht1a post synaptic receptors will not downregulate, even with ssri treatment. I wonder if its true?
 
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