Research has also shown that past claims of brain damage from cannabis use fail to hold up to the scientific method.[35] Instead, recent studies with synthetic cannabinoids show that activation of CB1 receptors can facilitate neurogenesis,[36] as well as neuroprotection[37], and can even help prevent natural neural degradation from neurodegenerative diseases such as MS, Parkinson's, and Alzheimer's. This, along with research into the CB2 receptor (throughout the immune system), has given the case for medical marijuana more support.[38][39] THC is both a CB1 and CB2 agonist.[40]

http://en.wikipedia.org/wiki/Tetrahydrocannabinol

http://www.webmd.com/mental-health/news/20030701/heavy-marijuana-use-doesnt-damage-brain

Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects
Wen Jiang,1,2 Yun Zhang,1 Lan Xiao,1 Jamie Van Cleemput,1 Shao-Ping Ji,1 Guang Bai,3 and Xia Zhang1
J Clin Invest. 2005 November 1; 115(11): 3104–3116.
Published online 2005 October 13. doi: 10.1172/JCI25509
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1253627/

Cannabinoids: Between Neuroprotection and Neurotoxicity

Abstract:
Cannabinoids, such as the ?9- tetrahydrocannabinol (THC), present in the cannabis plant, as well as anandamide and 2-arachidonoyl glycerol, produced by the mammalian body, have been shown to protect the brain from various insults and to improve several neurodegenerative diseases. The current review summarizes the evidence for cannabinoid neuroprotection in vivo, and refers to recent in vitro studies, which help elucidate possible molecular mechanisms underlying this protective effect. Some of these mechanisms involve the activation of CB1 and CB2 cannabinoid receptors, while others are not dependent on them. In some cases, protection is due to a direct effect of the cannabinoids on neuronal cells, while in others, it results from their effects on non-neuronal elements within the brain. In many experimental set-ups, cannabinoid neurotoxicity, particularly by THC, resides side by side with neuroprotection. The current review attempts to shed light on this dual activity, and to dissociate between the two contradictory effects.

http://www.ingentaconnect.com/content/ben/cdtcnsnd/2005/00000004/00000006/art00008

Cannabinoid CB2 receptor: a new target for controlling neural cell survival?

Two types of cannabinoid receptor have been cloned and characterized. Whereas CB1 receptors are ubiquitously expressed in neurons of the CNS, CB2 receptors have been thought to be absent from the CNS. Recent data now question this notion and support the expression of CB2 receptors in microglial cells, astrocytes and even some neuron subpopulations. This discrete distribution makes CB2 receptors interesting targets for treating neurological disorders because CB2-selective agonists lack psychoactivity. Here, we review evidence supporting the idea that CB2 receptors are implicated in the control of fundamental neural cell processes, such as proliferation and survival, and that their pharmacological manipulation might be useful for both delaying the progression of neurodegenerative disorders and inhibiting the growth of glial tumors.
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T1K-4MG6NYP-1&_user=10&_coverDate=01/31/2007&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=73429df3237e83252ba7bceaf8ebf372


I have found many more alot of them involving the neuroprotective qualities of HU-210, it is an exciting time regarding this research. As finally there is some unbiased medical research going into cannabinoids and the synthesis of the synthetic cannabinoids allowed proper testing and dispelling of many old propaganda myths! As they had been medically testing morphinans ect why not marijuana? But that has apparently changed within the last couple of years.

It's just that many of the articles pertain to "cannabanoids" in general or marijuana as a whole. Since these chemicals are not cannabanoids but rather just act upon those receptors can you still infer the same benefits?

We do have members with MS, chronic pain, Crohns and such and I would like to be able to put this in terms the majority would understand. Thanks for the links. I will look at them and dig deeper. I guess it would have been batter stated as Pharmacodynamics because it is the physiological effects my med patients are interested in.

Then we go to the next paper,
Cannabinoids: Between Neuroprotection and Neurotoxicity

Cannabinoids, such as the ?9- tetrahydrocannabinol (THC), present in the cannabis plant, as well as anandamide and 2-arachidonoyl glycerol, produced by the mammalian body, have been shown to protect the brain from various insults and to improve several neurodegenerative diseases. The current review summarizes the evidence for cannabinoid neuroprotection in vivo, and refers to recent in vitro studies, which help elucidate possible molecular mechanisms underlying this protective effect. Some of these mechanisms involve the activation of CB1 and CB2 cannabinoid receptors, while others are not dependent on them. In some cases, protection is due to a direct effect of the cannabinoids on neuronal cells, while in others, it results from their effects on non-neuronal elements within the brain. In many experimental set-ups, cannabinoid neurotoxicity, particularly by THC, resides side by side with neuroprotection. The current review attempts to shed light on this dual activity, and to dissociate between the two contradictory effects.

delta-9-THC was specifically tested, and it is clearly stated "have been shown to protect the brain from various insults and to improve several neurodegenerative diseases" so that part is not up for debate the mechanism of its action is! If the mechanism of their action in this case was through activation of CB1 and CB2, then the synthetic cannabinoids discussed prior would also be attractive here!(but I only have that abstract, not the paper).

The third paper is trying to take advantage of the already known benefits of CB1 agonists and trying to use that to create CB2 agonists with the same benefits. Because CB2 agonists lack psycoactivity the boring bastards think that is more attractive for a medicament (and also found that CB2 recptors are involved in the control of fundamental neural cell processes) but still no need to spoil the party!

Cant we have our cake and eat it too?
Cant we have our agonists CB1 and 2?

A very good document on CB receptors,

http://www.tocris.com/pdfs/cannabinoid_receptor_review/page_001.html

I don't have all the technical details at hand right now, but I did a lot of research into the HPA axis and stress responses.  I kept running into the endocannabinoids as potential cures of stress related problems. 

When you experience threat or trauma, there is a kind of programming that gets done in the amydalga (sp).  The programming happens when you experience/interpret an event as life threatening and thereby activate your flight or fight response.  Your primative brain records potentially trivial sensory information and associates it with threat.  If you experience enough trauma in this way your HPA wires your body to be on a hair trigger - an evolutional response to a dangerous environment.   You wind up sleeping less soundly, eating less etc and can get a variety of physiological symptoms from the wiring.  You can also begin over responding to trivial triggers in your environment.

That is why I believe some people may respond to an endocannabinoid with anxiety.  If you are one of those individuals with the hyperalert HPA it would percieve the relaxing of your defenses through the use of an endocannabinoid (which typically disarm the HPA responses) as a threat and therefore you would be anxious at the perceived vulnerability.

Got the documentation somewhere to back some of this up, but there was just too much of it - would have to write a paper (may do that some day).

Salat