The cannabinoid receptors CB(1) and CB(2) are class A G-protein-coupled receptors. It is well known that cannabinoid receptor agonists produce relief of pain in a variety of animal models by interacting with cannabinoid receptors. CB(1) receptors are located centrally and peripherally, whereas CB(2) receptors are expressed primarily on immune cells and tissues. A large body of preclinical data supports the hypothesis that either CB(2)-selective agonists or CB(1) agonists acting at peripheral sites, or with limited CNS exposure, will inhibit pain and neuroinflammation without side effects within the CNS. There has been a growing interest in developing cannabinoid agonists. Many new cannabinoid ligands have been synthesized and studied covering a wide variety of novel structural scaffolds. This review focuses on the present development of cannabinoid agonists with an emphasis on selective CB(2) agonists and peripherally restricted CB(1) or CB(1)/CB(2) dual agonists for treatment of inflammatory and neuropathic pain.

Cheng Y, Hitchcock SA. Targeting cannabinoid agonists for inflammatory and neuropathic pain. Expert Opin Investig Drugs. 2007 Jul;16(7):951–65.
http://www.ncbi.nlm.nih.gov/pubmed/17594182

This bit is also interesting:

… A large body of preclinical data supports the hypothesis that either CB(2)-selective agonists or CB(1) agonists acting at peripheral sites, or with limited CNS exposure, will inhibit pain and neuroinflammation without side effects within the CNS. …

Peripherally acting CB1 agonists / CB2 agonists –> no psychoactive “side effects”.

Surely then the difference between the JWH-xxx’s is due to binding at novel cannabinoid receptors or other receptors we haven’t considered.

COMMENTS IN THIS THREAD ARE NOW CLOSED. YOU CAN CONTINUE DISCUSSING SYNTHETIC CANNABINOIDS HERE OR INDIVIDUAL SMOKING MIXTURES HERE.

The 018 hits as cerebral…but it also hits the body. I have read it described as a sativa/indica hybrid tilting more toward sativa. Whereas I have read 073 described more as indica, body-oriented, without the cerebral or manic edge of 018. But these are inadequate, rough generalizations. And you certainly can’t gauge the experiential differences by peering at a binding affinity chart. I think Synch’s point about novel receptors is timely, because there is recent evidence for such, which dramatically complexificates the whole shebang.

And now at the risk of falling back into the forced crude interpretation black hole, can it be said that CB1 is the gateway to stoningham, and CB2 is the bridge to painkillerton? And mixing complementary agonists is like having a carefully planned orgy at the commons, but without reckoning that all the homeless who live in the woods nearby would drop trow and storm the flesh pile?

k2 works but still there is something to be said about the nice red hairs and purple buds that u can never beat„ best upside is drug testing

KEEP IT REAL lol

IcYA is correct, if youve ever tried 81, youll know the difference. the 81 is a very “peppy” compound

check out this forum, it lays out all the synthetic compounds and shows their binding affinity

http://www.drugs-forum.com/forum/showthread.php?t=117873

I read that in a couple of other places, but it is also stated in Posts 55 and 95 above.

From Wiki: When smoked or orally ingested, JWH-018 produces some effects similar to those of cannabis. Its effects are by some persons considered as very similar to those of cannabis, but more of a general body high with unusually clear cerebral effects, the difference being analogous to that between cannabis that has a higher component ratio of cannabis sativa to cannabis indica.

JWH-073 is an analgesic chemical from the naphthoylindole family, which acts as a cannabinoid agonist at both the CB1 and CB2 receptors. It is somewhat selective for the CB2 subtype, with affinity at this subtype approximately 5x the affinity at CB1.[2] The abbreviation JWH stands for John W. Huffman, one of the inventors of the compound

Who is right?

Its just my opinion that any cannabinoid will not be helpful if the migraines are in fact migraines. now if they are anxiety related, absolutely some of these compounds would help!

i do have a few suggestions for you though. A friend of mine used to have terrible migraines and it turns out she was extremely magnesium deficient! any form of magnesium would do however i would suggest magnesium bicarbonate. You actually have to make that form of magnesium but its verrrrryyyy simple! here is a post about it, and do your own search on magnesium bicarbonate and ull see why i sugggest it… its great stuff!
http://www.socialanxietysupport.com/forum/f11/make-your-own-magnesium-bicarbonate-drink-tastes-sweet-46555/

hope it helps

My main issue was that saying CB1 receptors only “targeted” by one type of weed. CB1 receptors do lead to reduced GABA release, but CB1 receptors are responsible for most of the effects of Indica AND sativa strains.

I’m pretty sure that a highly selective CB2 agonist (not just selective for CB2 over CB1, but selective like salvinorin-a is for the k opioid receptor) would have negligable psychoactive effect. Like I mentioned before, other compounds could be binding to other receptors. What I forgot to mention, and perhaps probably more importantly, the different compounds could also bind to novel cannabinoid receptors not yet classified. That could be the case for JWH-018 too.

I personally do not agree with the above statement from Synchronium. Yes IcYA was incorrect about the nervous system, however saying no effects come from the CB2 activation is trying to tell everyone who has tried JWH18 that they are feeling nothing and it is all a placebo effect. I have found an excellent link from another forum showing the various binding affinities for numerous cannabinoid compounds.
http://www.drugs-forum.com/forum/showthread.php?t=117873

About the GABA. Its my opinion both of you are correct, IcYA wasnt being precise about his word choices and did not explain it correctly. However he is correct about GABA making you tired. Thus why GHB and all sleep medications work through GABA.

To all those following this blog it is my suggestion for you to do your own research through various medical publications. JWH as well as the various other cannabonoids are classified as a “research chemical.” I would suggest to all to do your own research through alternative methods as opposed to taking any individuals posting as the the definitive truth on JWH.