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marijuana and acetylcholine

asecin

asecin

Bluelighter
Joined
Apr 13, 2005
Messages
1,725
i tried to search for info but too much out there and most of it its not well explained.
can someone explain or, refer me to a reliable source with good info on how marijuana effects acetylcholine ?
i wonder if its either for better or worse the way it affects it tho so i might enjoy hearing from experience, or from professional opinion
 
Also it itches a lot each time i smoke. Why am i itchy all over the body ? What is it that affects histamine ?
 
Itch?

Here's some [potentially] conflicting literature for you to ponder:

Eur J Pharmacol. 2006 Aug 7;542(1-3):179-83. Epub 2006 Jun 2.
The cannabinoid CB2 receptor inverse agonist JTE-907 suppresses spontaneous itch-associated responses of NC mice, a model of atopic dermatitis.

Maekawa T, Nojima H, Kuraishi Y, Aisaka K.

Department of Applied Pharmacology, Faculty of Pharmaceutical Sciences, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.
Abstract

JTE-907, N-(benzo[1,3]dioxol-5-ylmethyl)-7-methoxy-2-oxo-8-pentyloxy-1,2-dihydroquinoline-3-carboxamide, is a selective cannabinoid CB2 receptor antagonist/inverse agonist. The anti-pruritic activity of JTE-907 was studied in NC mice with chronic dermatitis, a model of atopic dermatitis. The oral dose of JTE-907 (1 and 10 mg/kg/day), an immunosuppressant agent tacrolimus (1 mg/kg/day) and a glucocorticoid betamethasone 17-valerate (1 mg/kg/day) for 20 days suppressed the spontaneous scratching and cutaneous nerve activity of NC mice. JTE-907 (10, but not 1, mg/kg) and tacrolimus, but not betamethasone, tended to alleviate the dermatitis. Betamethasone inhibited the body weight gain. These results suggest that JTE-907 suppresses spontaneous itch-associated responses of NC mice without adverse effects such as weight loss.
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Histamine induced responses are attenuated by a cannabinoid receptor agonist in human skin.

Dvorak M, Watkinson A, McGlone F, Rukwied R.

Unilever Research & Development Port Sunlight, Wirral, UK.
Abstract

OBJECTIVE AND DESIGN: In the present study we examined the effects of the cannabinoid receptor agonist HU210 on histamine-evoked somatosensory and vascular responses in humans. SUBJECTS: Two sets of experiments were performed, in which twelve (Study 1, iontophoresis) and six participants (Study 2, microdialysis) were recruited. TREATMENT: HU210 was administered peripherally by skin patch (50 mM) or dermal microdialysis (5 mM), whereas histamine was applied by iontophoresis (50 microAmps) or dermal microdialysis (5 microM). METHODS: Skin blood flow was monitored by laser Doppler, widespread flare reaction was evaluated planimetrically, extravasation of plasma proteins was measured in the dialysate and perceived itch was recorded using a visual analogue scale. Data were evaluated by analysis of variance. RESULTS: Experimentally induced itch was significantly reduced by peripheral administration of HU210 (p < 0.05). Additionally, skin blood flow and neurogenic mediated flare responses were attenuated (p < 0.003 and p < 0.03, respectively), whereas protein extravasation due to histamine was enhanced by co-administration of HU210, as investigated by dermal microdialysis. CONCLUSIONS: In humans peripheral administration of a cannabinoid receptor agonist attenuates histamine-induced itch. The observation that protein extravasation was not decreased demonstrates that the alleviation of itch is not due to an anti-histaminergic property of HU210. The reduced neurogenic flare reaction indicates an attenuated antidromic nerve fibre activation and neuropeptide release.
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[Topical cannabinoid agonists. An effective new possibility for treating chronic pruritus]

[Article in German]

Ständer S, Reinhardt HW, Luger TA.

Abteilung für Klinische Neurodermatologie, Klinik und Poliklinik für Hautkrankheiten, Universitätsklinikum Münster, Von-Esmarchstrasse 58, 48149 Münster. [email protected]
Abstract

BACKGROUND: Chronic, therapy-resistant pruritus often fails to respond to standard measures so new therapeutic approaches are needed. Recently, the expression of cannabinoid receptors on cutaneous sensory nerve fibers was described, so cannabinoid agonists seem a rational therapeutic option for pruritus. PATIENTS: In an open application observation 22 patients with prurigo, lichen simplex and pruritus applied an emollient cream containing N-palmitoyl ethanolamine (PEA). RESULTS: In 14/22 patients a good antipruritic effect could be documented. The average reduction in itch was 86.4%. The therapy was well-tolerated by all patients; neither burning burn nor contact dermatitis was observed. CONCLUSIONS: Topical cannabinoid agonists represent an new effective and well-tolerated therapy for refractory itching of various origins. Creams with a higher concentration may be even more effective with broader indications.
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If anything though, I'd relegate your pruritic dermal fuckup to warped neurochemistry, some dormant skin condition, or the nightmare of the placebo effect.

As for the choline, weed tends to depress acetylcholine firing where it's important, or at the very lest relevant to what I think you're wondering - cortex, hippocampus, and elsewhere if I remember right. Endogenous cannabinoid agonists also tend to noncompetitively antagonize nicotinic receptor currents, so I think you're looking at a functionally global downturn here.
 
ah ok i see. maybe you are right about warped neurochemistry.
also i dont get what "functionally global downturn here" means. care to explain a bit further ? :/
 
also i dont get what "functionally global downturn here" means. care to explain a bit further ?
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Sure. Sorry, that's some ambiguous wording for anyone who doesn't spend inordinate amounts of time poring over pharmacologic data on the internets. Having assumed that you were wondering about THC's effects on acetylcholine as a neural correlate of reduced cognitive function, I referenced its regional effects on cholinergic transmission in brain regions relevant to learning, memory, etc. By what I know, and what I tried to scrape together from Google Scholar, weed has a way of dampening choline all over the place, resulting (at least partly) in the cognitive impairment following acute and chronic use. Or is that not what you were interested in?
 
yeh i have been smoking a lot and i know from past experience it affects my memory and learning.
anyway lately i have been smoking a lot regularly together with alcohol always (if alcohol causes any extra distress on acetylcholine?) and i have been really tired but i dont feel that bad.
im wondering can a supplement of some type help me sustain adequate levels of choline and still be able to smoke and drink for a while at least or im surely crashing slowly ??
 
im wondering can a supplement of some type help me sustain adequate levels of choline and still be able to smoke and drink for a while at least
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Unfortunately, there's quite a bit more going on here than lowered levels of one particular paracrine chemical messenger. The human brain is one of the (likely the) most complex biological organs, and its respective field of study is extensive. But over one hundred years of modern research on the part of thousands of dedicated, brilliant scientists has seemingly done only slightly more than scratch the surface, at least as it pertains to the electrochemical intricacies that make such mind-boggling phenomena as consciousness and higher-order reasoning possible. Your feelings of fogginess and fatigue, while distressing and uncomfortable to you, cannot and will not be solved through reductionistic attempts to pass them off as mere neural 'deficiencies' or 'imbalances' and subsequently self-medicating them as such. Not that you asked, but here's what I think you could/should do:

1. Cut back, or eliminate one drug [or both] altogether, at least when it comes to egregious/regular use. Are you an alcoholic? Weed "addict"? If so, fuck it. You'll be tired no matter what you do, short of dumping methamphetamine into your morning coffee.
2. Go see a doctor and get a script for modafinil, a virtually side-effect free stimulant. If that doesn't pan out, or if you're not rich [shit's expensive], pick up a caffeine habit. It's good for you.
3. Exercise regularly.
4. Eat a high-nutrient diet and/or take a multivitamin, preferably one high in B-vitamins, some of which grain ethanol invariably depletes after long-term use. But again, I'm a bit confused. I interpret "crashing slowly" to mean that you're using these drugs daily and suffering the predictable consequences. If that's not what's going on, then I'm an idiot and you can forget everything you just read.

As for cholinergic drugs/supplements (99% of which I'm 100% positive will NOT help you) you're looking at a wide range of molecules. Just to list a few: huperzine, arecoline, nicotine, acetylcarnitine, donepezil, tacrine, centrophenoxine, citicoline, dimethylaminoethanol, and the racetams. Type any of those into Pubmed or Medline, read the literature, and find out which one most appeals to you - my guess would be none, unless you're interested in expensive, long-term nootropic use, something which would do little to offset sedative-induced fatigue.
 
P A said:
By what I know, and what I tried to scrape together from Google Scholar, weed has a way of dampening choline all over the place, resulting (at least partly) in the cognitive impairment following acute and chronic use. Or is that not what you were interested in?
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^-------LOL......And see...choline is what......and you get it from where and what happens in your brain........o ya right now you see my point.........
 
I always wonder how weed damages memory and the brain.
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Cannabis sativa does not cause brain damage in 99% of those who use it regularly. Its varied effects on cognition and memory are typically short-lived following withdrawal and prolonged abstinence after regular use.
 
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