Ever wanted to learn what each cannabinoid does?

Thanks a lot BIOhazard! I too have seen pre 98 bubba tested very high at multiple clubs in cali.

As time goes along, I'll keep posting very interesting research on cannabinoids and the body's natural endocannabinoid system: (that is activated whether or not you use cannabis). This article is very important.

Cannabidiol and 9-tetrahydrocannabinol are neuroprotective antioxidants (1998)
Full Article: http://www.pnas.org/content/95/14/8268.full

This abstract is a little technical, but a great resource:

Study's Abstract:

Abstract

The neuroprotective actions of cannabidiol and other cannabinoids were examined in rat cortical neuron cultures exposed to toxic levels of the excitatory neurotransmitter glutamate. Glutamate toxicity was reduced by both cannabidiol, a nonpsychoactive constituent of marijuana, and the psychotropic cannabinoid (−)Δ9-tetrahydrocannabinol (THC). Cannabinoids protected equally well against neurotoxicity mediated by N-methyl-d-aspartate receptors, 2-amino-3-(4-butyl-3-hydroxyisoxazol-5-yl)propionic acid receptors, or kainate receptors. N-methyl-d-aspartate receptor-induced toxicity has been shown to be calcium dependent; this study demonstrates that 2-amino-3-(4-butyl-3-hydroxyisoxazol-5-yl)propionic acid/kainate receptor-type neurotoxicity is also calcium-dependent, partly mediated by voltage sensitive calcium channels. The neuroprotection observed with cannabidiol and THC was unaffected by cannabinoid receptor antagonist, indicating it to be cannabinoid receptor independent. Previous studies have shown that glutamate toxicity may be prevented by antioxidants. Cannabidiol, THC and several synthetic cannabinoids all were demonstrated to be antioxidants by cyclic voltametry. Cannabidiol and THC also were shown to prevent hydroperoxide-induced oxidative damage as well as or better than other antioxidants in a chemical (Fenton reaction) system and neuronal cultures. Cannabidiol was more protective against glutamate neurotoxicity than either ascorbate or α-tocopherol, indicating it to be a potent antioxidant. These data also suggest that the naturally occurring, nonpsychotropic cannabinoid, cannabidiol, may be a potentially useful therapeutic agent for the treatment of oxidative neurological disorders such as cerebral ischemia.

Cannabinoid components of marijuana are known to exert behavioral and psychotropic effects but also to possess therapeutic properties including analgesia (1), ocular hypotension (2), and antiemesis (3). This report examines another potential therapeutic role for cannabinoids as neuroprotectants and describes their mechanism of action in rat cortical neuronal cultures.

During an ischemic episode, large quantities of the excitatory neurotransmitter glutamate are released. This event causes neuronal death by over-stimulating N-methyl-d-aspartate receptors (NMDAr) and 2-amino-3-(4-butyl-3-hydroxyisoxazol-5-yl)propionic acid (AMPA) and kainate-type receptors and results in metabolic stress and accumulation of toxic levels of intracellular calcium (4). In vitro and in vivo studies (4, 5, 6) have demonstrated that such neurotoxicity can be reduced by antioxidants or antagonists to NMDAr and AMPA/kainate receptors. Antioxidants such as α-tocopherol (5, 6) are effective neuroprotectants because of their ability to reduce the toxic reactive oxygen species (ROS) formed during ischemic metabolism. Cannabinoids like (−)Δ9-tetrahydrocannabinol (THC) and its psychoactive analogues also have been reported to be neuroprotective against glutamate toxicity in vitro (7). Cannabinoids have been suggested to prevent glutamate neurotoxicity by activating cannabinoid receptors (7, 8), which can reduce calcium influx through voltage sensitive calcium channels (8, 9). A synthetic cannabinoid (HU-211) also has been demonstrated to be neuroprotective even though it does not activate cannabinoid receptors. This compound is an atypical cannabinoid, however, in that it, unlike other cannabinoids, directly antagonizes NMDAr (10) and possesses some antioxidant properties (11). The present study examines classical cannabinoids as neuroprotectants in vitro but focuses on the nonpsychoactive cannabinoid cannabidiol. Like THC, cannabidiol is a natural component of the marijuana plant, Cannabis sativa, although unlike THC, cannabidiol does not activate cannabinoid receptors and so is devoid of psychoactive effects (12). This study reports that cannabidiol and other cannabinoids such as THC are potent antioxidants that protect neurons from glutamate-induced death without cannabinoid receptor activation.

Not many other active chemicals in the world are known for neurogenesis in adults. It is incredible that certain cannabinoids actually grow new Hippocampus neurons, which are associated with Short and long term memory. This could also be connected to how CBD helps reverse the memory issues caused by high THC to CBD ratios?

::Small Neuropsychology Primer::

This study below doesn't use direct cannabinoids but rather uses CB1 and CB2 Antagonists (Block the function of specific brain receptor sites like CB1) and Agonists (Which activate a specific brain receptor site like CB1- sometimes through out the brain, sometimes only in select areas.) The selective ones are usually refereed to as Selective Agonists or Antagonists and can be used to test certain areas of brain activation vs others. This is very useful - for instance if they want to see if a function mouses CNS or brain is related to the CB1 cannabinoid pathway: they can use CB1 antagonists and block any CB1 activity (which would shut down anything that uses CB1 to operate) to see if the function is still there or shut down showing it operates through CB1 activation =]

Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects (2005)
Full Article: http://www.jci.org/articles/view/25509

Greetings!

I am a long time lurker and now first time poster. I suffer from severe symptoms of Willis-Ekbom Disease (RLS). Currently, I am prescribed Mirapex which is a dopamine agonist. The problem with this drug I have is that it does not work effectively nor in a timely fashion upon onset of the symptoms.

I have done much reading on the topic of cannabis and it's medicinal attributes; moreso it's effects on dopamine. I also have experimented with smoking cannabis when the symptoms arise and have found that it has profound and almost immediate relief.

What I can't find is information regarding which specific cannibanoid is responsible for the increase in dopamine. Armed with this information I can better choose what strain would be most effective in treating the symptoms of my affliction.

Harley,

Here are the article I could dig up on Restless Leg Syndrome. You definitely want to get an indica dominant usually, as sativas can be speedy. Also take it at the longer end of the flowering range to get a more relaxing, non-restless state. Strains with CBD are going to help.[FONT=&quot]

Restless Leg Syndrome: Medical Marijuana Patients‘ Say it Works (news - 2007)
http://www.salem-new...tless_81807.php

Restless Leg Syndrome (news/anecdotal- 2007)
http://medicalcannab...try34.html#body
[/FONT]

Biohazard,

Thank you for your reply. The links that you have provided seem to be dead. Given the info that you have provided will send me on the path to "indicaville" to find relief from this horrendous disease.

While strain searching, I surfed to TGA Subcool's site and read that one of their strains "Jack the Ripper" has remarkable amounts of THCV and that Subcool states that this cannibanoid has been studied and found helpful in Parkinson's. Although this strain is more sativa-leaning, and since Mirapex is a Parkinson's drug, I wonder if there is any correlation between THCV acting as a dopamine agonist?

Fixed the links, I'll check into the relationship between THC-V and dopamine. =)