7 replies to this topic

[CIMN]

Does anyone know of any way to upregulate choline receptors??

I think i remember hearing memantine upregulates/increases nicotinic acetycholine receptors, wanted also ask what does anyone think of tobacco extract as a nootropic?

Edited by CIMN, 31 July 2012 - 05:11 AM.

[kevinseven11]

Nicotine is bad for the health but theres a metabolite of nicotine called cotinine that is used as a nootropic and isn't quite as bad. Im interested in trying.

[CIMN]

edit- double post

Edited by CIMN, 31 July 2012 - 04:43 PM.

[CIMN]

Nicotine is bad for the health but theres a metabolite of nicotine called cotinine that is used as a nootropic and isn't quite as bad. Im interested in trying.

Cotinine is interesting. i heard of it as well, i was thinking perhaps if someone were skilled enought they could get some nicotine and convert it into cotinine with a couple chemicals,
there are a couple other nicotine partial agonist that are being studied as well,

i was thinking tobbaco could be a source for some partial agonist, if a person could extract the wanted alkaloids and leave out the unwanted stuff.

[noopeptisgood]

BDNF stimulation will upregulate acetylcholine receptors. http://www.ncbi.nlm....pubmed/17029981

So you may want to look into noopept or Lion's Mane. Stimulanting BDNF will cause downregulation of TrkA and TrkB receptors, so I think only taking one of the supplements would be the smarter choice. The supplement should be cycled, too.

Edited by noopeptisgood, 01 August 2012 - 06:54 AM.

[CIMN]

BDNF stimulation will upregulate acetylcholine receptors. http://www.ncbi.nlm....pubmed/17029981

So you may want to look into noopept or Lion's Mane. Stimulanting BDNF will cause downregulation of TrkA and TrkB receptors, so I think only taking one of the supplements would be the smarter choice. The supplement should be cycled, too.

hmm very cool didnt know that bdnf increased nicotinic receptors, makes me wonder if there is some way to prevent downregulation of TrkA TrkB receptors,

found this on bdnf;

Overexpression of pitx3 upregulates expression of BDNF and GDNF in SH-SY5Y cells and primary ventral mesencephalic cultures.

The transcription factor Pitx3 plays an important role in the development of midbrain to promote the growth and differentiation of dopamine neurons. The present study has demonstrated that overexpression of Pitx3 in SH-SY5Y cells and primary ventral mesencephalic (VM) cultures significantly increased the mRNA levels of brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF), and remarkably elevated the protein levels of these two neurotrophic factors. Our data provide the first evidence that pitx3-expressing cells are able to upregulate the expression of BDNF and GDNF. Therefore, Pitx3 might be a good target for the treatment of Parkinson's disease.

Edited by CIMN, 01 August 2012 - 05:01 PM.

[CIMN]

been thinking if cycling between a antagonist and a partial agonist of muscarinic acetylcholine receptors would work as a way to upregulate them.

been thinking if cycling between a antagonist and a partial agonist of muscarinic acetylcholine receptors would work as a way to upregulate them. Whether it would be a long lasting effect is another question, perhaps some 3rd variable such as a neurotrophin or something else is needed in conjunction.

according to mr happy this is what he says about preventing homeostasis on bdnf ,
There appears to be a way to stop homeostatis for these factors, involving upregulating TrkA, TrkB, TrkC while increasing the growth factors. This hasn't been throughly explored, yet.

Piracetam unfortunately decreases nicotinic acetycholine receptors but memantine and Bupropion might partially reverse this.

[Effects of piracetam and meclofenoxate on the brain NMDA and nicotinic receptors in mice with different exploratory efficacy in the cross maze test].

A population of outbred mice of the ICR strain was divided into two subpopulations according to their high (EH mice) or low (EL mice) exploratory efficacy in the closed cross maze test. In addition, the EH and EL mice differed in the number of binding sites of (i) [G-3H]-MK-801 with NMDA receptors from hippocampus and (ii) [G-3H]-nicotine with nicotine cholinoreceptors (nACh) from neocortex. A subchronic administration of the cognition enhancer piracetam (200 mg/kg, once per day for 5 days) increased by 70% the number of binding sites of NMDA receptors in the EL mice. At the same time, this treatment decreased the density of neocortical nACh receptors in both EL and EH mice (by 55% and 40%, respectively). A subchronic administration of the cognition enhancer and anti-oxidant meclofenoxate (100 mg/kg, once per day for 5 days) also decreased the density of neocortical nACh receptors in both EL and EH mice (by 48% and 20%, respectively). However, meclofenoxate also increased by 41% the number of binding sites of NMDA receptors in the EH mice.

perhaps increasing the choline receptor mrna or gene expression might be another method.

Edited by CIMN, 01 August 2012 - 06:31 PM.

[CIMN]

another idea might be to use partial agonist with very low affinity on the agonist affinity spectrum with some acetylcholinesterase inducers such as forskolin and ecydesterone,

some pertaining links to tolerance,upregulation.

http://www.longecity...ce/page__st__60
http://www.longecity...downregulation/
http://www.longecity...ine-expierence/
http://www.longecity...st/page__st__30
http://www.longecity...on-be-an-issue/
http://www.longecity...55-cdp-choline/
http://www.longecity...20-pozanicline/

Edited by CIMN, 01 August 2012 - 07:46 PM.