Yes I know all of that in great detail(I study drugs and pharmacology in my free time), I was just wondering what your proposed purpose for it was and you explained it great for others who may not know about all of those things and now that I know your reasoning I can partially agree. It is just very hard to know what this thread is about when there wasn't as far as I read a real in depth description of what effects, at what time scale, we are even trying to reverse.... my point was that if one quits smoking weed and then months later(for some reason, I wouldn't know get why) wants to "reset" their receptors with an inverse agonist or antagonist, while I know it works sometimes to stop protracted benzodiazepine withdrawal using flumazenil that is a whole different ball game(and like I said it isn't always effective and sometimes detrimental. also I don't believe it is even known if the mechanism of it's success is "resetting" the receptors, which is a vague term which I don't quite understand). Yes you can upregulate receptors and downregulate them, but what does the term "resetting" them mean? Sorry, I suppose I was too vague before.
Also, fun fact: not all antagonists will cause upregulation, in fact some cause downregulation the same as agonists. I believe an example of this is the 5ht2a/c receptors, but my memory is hazy.
No not all antagonists do cause upregulation but the focus of my discussion was aimed the one's I've used and the ones research supports. No need to extrapolate.
Resetting means returning them to a state prior to agonist induced down-regulation or closer to it.
By all means don't take my subjective experiences and the available research alone. This is my experience and that of many others but it may not work for everyone and/or not everyone responses to every drug. I suggest you research it and try it yourself if it suits you.
The main focus of this thread is undoing the negative effects that cannabis can have on some users on memory with a supplement. I believe this can be possible but hard to directly effect the cause without some degree of cannabinoid receptor antagonist which is proven to enhance memory via it's reverse effects on the cb receptor.
Behav Pharmacol. 2007 Sep;18(5-6):571-80.
Short-term memory is modulated by the spontaneous release of endocannabinoids: evidence from hippocampal population codes.
Deadwyler SA, Goonawardena AV, Hampson RE.
Source
Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Winston-Salem, North Carolina 27157-1083, USA. sdeadwy@wfubmc.edu
Abstract
Population codes derived from ensembles of hippocampal neurons were assessed to determine whether endocannabinoids were active when rats performed a delayed-nonmatch-to-sample (DNMS) short-term memory task. Multivariate discriminant analyses of the firing patterns of ensembles of CA1 and CA3 hippocampal neurons extracted representations of information encoded at the time of the sample response (SmR codes) during individual DNMS trials. The 'strength' or distinctiveness of trial-specific SmR codes in normal sessions was compared with sessions in which either rimonabant, the well-characterized cannabinoid CB1 receptor antagonist, or WIN 55212-2 (WIN-2), a cannabinoid CB1 receptor agonist, were administered. Results show that performance on trials with delay intervals longer than 10 s was facilitated by rimonabant (2.0 mg/kg) owing to a significantly increased frequency of trials with stronger SmR codes. In contrast, WIN-2 (0.35 mg/kg) suppressed the strength of SmR codes necessary to perform trials with delays greater than 10 s. The positive influence of rimonabant on performance indicated that the action of endocannabinoids was to reduce SmR code strength, resulting in trials that were at risk for errors if the delay exceeded 10 s. Thus endocannabinoids, like exogenously administered cannabinoids, reduced hippocampal encoding necessary to perform long-delay trials. The findings therefore indicate a direct relationship between the actions of endocannabinoids on hippocampal processes and the ability to encode information into short-term memory. PMID: 17762525
Edited by neuropill, 14 October 2012 - 05:50 AM.