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upregulate muscarinic acetylcholine

acetylcholine

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#1 metabrain

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Posted 23 November 2018 - 12:18 PM


Is it possible to upregulate muscarinic acetylcholine on a permanent basis i.e. the receptors will be denser or more activated even after the substance upregulating them is removed?



#2 MankindRising

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Posted 23 November 2018 - 04:24 PM

Some of the well known herbal supps/noots do this:

 

* piracetam (study didnt say which subtypes get upregulated)

* ginkgo (m1 muscarainic)

* alpha lipoic acid (m1 and m2)

* probably lots more but those 3 are the ones that came to mind.


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#3 CWF1986

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Posted 26 November 2018 - 11:45 PM

Do keep in mind that upregulating Machr is not beneficial for everyone.  For some it does everything that the noot sites tell you like increased energy, focus, and concentration.  For me, anything with the exception of racetams that's M-cholinergic is extreme anxiety, IBS type symptoms, and despair in a pill/powder.  

 

There's a few threads/posters that suggest that there might be a sort of spectrum ranging from low dopamine, high ach to high dopamine, low ach.  They work in sort of a seesaw pattern.  In fact, old school parkinson's meds were very powerful anti-cholinergics as a way of increasing dopamine and this would reduce the shaking.  There's even a theory that depression can be caused by an cholinergic/adrenergic imbalance.  

 

I'm not saying it's a bad idea, but I would find out how I respond to the regular more vanilla cholinergics before looking into more permanent ways of doing this.  This is a process that I can't imagine taking less than months.

 

Regardless of your choice, I hope it works out well for you.  



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#4 Pereise1

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Posted 30 November 2018 - 05:17 PM

From examine.com, Magnolia Bark Extract upregulates muscarinic receptors:

 

The neolignans (magnolol and honokiol) appear to increase the affinity of muscarine to its receptor (the muscarinic acetylcholine receptors) due to allosterically modifying low affinity receptors to a higher binding capacity, thus causing a greater amount of overall binding.[25] Honokiol and magnolol were both effective, and increased binding 3.2-fold and 2.8-fold (respectively) in rat forebrains and 71% and 64% (respectively) in the cerebellum.[25]

 

 

Curcumin activates M1 receptors, not too sure if it upregulates it at all (https://www.ncbi.nlm...pubmed/19765405)

 

Berberine activates M2 receptors (https://www.ncbi.nlm...pubmed/21168503)

 

Some antipsychotics upregulates muscarinic receptors:

 

 
Effects of antipsychotic medication on muscarinic M1 receptor mRNA expression in the rat brain.
Abstract

Alterations in muscarinic M1 receptor protein and mRNA expression have been revealed in post-mortem brains of schizophrenia patients. Most patients had been treated with antipsychotics, so medication effects cannot be excluded as a possible explanation for these results. With in situ hybridization, this study investigated M1 receptor mRNA expression in rats treated with the typical antipsychotic haloperidol (0.3 mg/kg/day) and the atypical antipsychotics olanzapine (1.5 mg/kg/day) and aripiprazole (2.25 mg/kg/day) for 1 or 12 weeks. Compared with the control group, haloperidol significantly increased (approximately 13-21%, P < 0.05) M1 mRNA expression in the CA1, CA2, and CA3 regions of the hippocampus after both 1 and 12 weeks of treatment, and it also increased (approximately 17%, P < 0.01) M1 mRNA expression in the substantia nigra compacta after 1 week of treatment. Olanzapine significantly increased (14-22%, P < 0.05) M1 mRNA expression in the hippocampus (CA1, CA2, and CA3) and substantia nigra compacta after 12 weeks of treatment, but not after 1 week. Aripiprazole significantly increased (17%, P < 0.01) M1 mRNA expression in the hippocampus (CA1) after both 1 and 12 week treatments and increased (12%, P < 0.05) M1 mRNA expression in the nucleus accumbens after 1 week of treatment. Despite their different affinities for muscarinic M1 receptors, all three antipsychotic medications induced a similar trend of change in M1 mRNA expression in selected brain regions. These data suggest that the decreased M1 receptor protein and mRNA expression observed in schizophrenia patients is unlikely to be a consequence of drug treatments and implicates muscarinic M1 receptors in the pharmacotherapy of the disease.

 







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