Peripheral interactions between cannabinoid and opioid systems contribute to the antinociceptive effect of crotalphine.

“Crotalphine is an antinociceptive peptide… we evaluated the involvement of the peripheral cannabinoid system in the crotalphine effect and its interaction with the opioid system…

Crotalphine-induced antinociception involves peripheral CB2 cannabinoid receptors and local release of dynorphin A, which is dependent on CB2 receptor activation.

These results enhance our understanding of the mechanisms involved in the peripheral effect of crotalphine, as well as the interaction between the opioid and cannabinoid systems.”

http://www.ncbi.nlm.nih.gov/pubmed/24460677

Selective inhibition of FAAH produces antidiarrheal and antinociceptive effect mediated by endocannabinoids and cannabinoid-like fatty acid amides.

“The endogenous cannabinoid system (ECS) plays a crucial role in multiple physiological processes in the central nervous system and in the periphery. The discovery that selective cannabinoid (CB) receptor agonists exert a potent inhibitory action on gastrointestinal (GI) motility and pain has placed the ECS in the center of attention as a possible target for the treatment of functional GI diseases…

These data expand our understanding of the ECS function and provide a novel framework for the development of future potential treatments of functional GI disorders.”

http://www.ncbi.nlm.nih.gov/pubmed/24460851

Cannabinoid system and neuroinflammation: implications for multiple sclerosis.

“There is a growing amount of evidence suggesting that cannabinoids may be neuroprotective in central nervous system inflammatory conditions.

Advances in the understanding of the physiology and pharmacology of the cannabinoid system have potentiated the interest in cannabinoids as potential therapeutic targets.

…The effects of cannabinoids on cytokine brain work and on the regulation of neuroinflammatory processes may affect chronic inflammatory demyelinating diseases such as multiple sclerosis.”

http://www.ncbi.nlm.nih.gov/pubmed/18073512

5-Lipoxygenase and anandamide hydrolase (FAAH) mediate the antitumor activity of cannabidiol, a non-psychoactive cannabinoid.

“It has been recently reported that cannabidiol (CBD), a non-psychoactive cannabinoid, is able to kill glioma cells, both in vivo and in vitro, independently of cannabinoid receptor stimulation.

…the present investigation indicates that CBD exerts its antitumoral effects through modulation of the LOX pathway and of the endocannabinoid system…”

http://www.ncbi.nlm.nih.gov/pubmed/18028339

Cannabinoids induce glioma stem-like cell differentiation and inhibit gliomagenesis.

“Glioma stem-like cells constitute one of the potential origins of gliomas, and therefore, their elimination is an essential factor for the development of efficient therapeutic strategies.

Cannabinoids are known to exert an antitumoral action on gliomas that relies on at least two mechanisms: induction of apoptosis of transformed cells and inhibition of tumor angiogenesis…

The discovery of an endogenous cannabinoid system, together with the great improvement in our understanding of the signaling mechanisms responsible for cannabinoid actions, has fostered the interest in the potential therapeutic applications of cannabinoids.

Several studies have demonstrated a significant antitumoral action of cannabinoid ligands in animal models. Thus, cannabinoid administration to nude mice curbs the growth of different tumors, including gliomas…

Cannabinoids are known to exert an antitumoral action against gliomas…

Overall, our results demonstrate that cannabinoids target glioma stem-like cells, promote their differentiation, and inhibit gliomagenesis, thus giving further support to their potential use in the management of malignant gliomas.

In conclusion, our results demonstrate the action of cannabinoids on glioma stem-like cells and thus may open new avenues for cannabinoid-based antitumoral strategies.”

http://www.jbc.org/content/282/9/6854.long

Medical marijuana as protection against the H1N1 swine flu virus?

“When the immune system attacks a flu virus, it causes widespread inflammation throughout the body. This inflammation presents itself in runny noses, soar throats, and body aches that accompany influenza. Runaway inflammation can cause the immune system to destroy the body it was meant to protect and lead to death.

 “When inflammation goes off the handle, the body releases endocannabinoids, which are natural chemicals that suppress the immune system, taking down the inflammation before it does more harm than good. This endocannabinoid system, as it’s called, is one of the many systems responsible for maintaining balance and health in the body,” ABC News reported.

If the endocannabinoid system cannot keep up – which often happens in very severe influenza infections – organ failure, particularly lung failure, may result.

 “They die not from the virus itself but from their own immune response,” Melamede told ABC News.
Cannabis Science intends to solve this threat. Marijuana contains natural, plant-based cannabinoids, called phytocannabinoids. A medical marijuana lozenge provides the body with a boost of endocannabinoids and helps to relieve the dangerous inflammation.
While viruses like the H1N1 swine flu bug are clever in their ability to mutate and outsmart even the latest vaccines, the human body’s response – with regard to inflammation management – does not change. Cannabis Science may be on to something here.”

http://digitaljournal.com/article/276928

Cannabinoid type-1 receptor ligands, alone or in combination with cocaine, affect vigilance-related behaviors of marmoset monkeys.

“Endocannabinoids (eCB) have been functionally linked to cocaine’s rewarding effects.

…changes in CB1r function – alone and in combination with cocaine – affected stereotyped vigilance-related behaviors… further implicating the eCB system in the neurobiological mechanisms of cocaine addiction.”

http://www.ncbi.nlm.nih.gov/pubmed/24445195

Beyond radio-displacement techniques for Identification of CB1 Ligands: The First Application of a Fluorescence-quenching Assay.

“Cannabinoid type 1 Receptor (CB1) belongs to the GPCR family and it has been targeted, so far, for the discovery of drugs aimed at the treatment of neuropathic pain, nausea, vomit, and food intake disorders. Here, we present the development of the first fluorescent assay enabling the measurement of kinetic binding constants for CB1orthosteric ligands…

…a sustainable valid alternative to the expensive and environmental impacting radiodisplacement techniques and paves the way for an easy, fast and cheap high-throughput drug screening toward CB1 for identification of new orthosteric and allosteric modulators.”

http://www.ncbi.nlm.nih.gov/pubmed/24441508

Expression of cannabinoid receptor 2 and its inhibitory effects on synovial fibroblasts in rheumatoid arthritis.

“Recent studies have suggested immunomodulatory and anti-inflammatory effects of cannabinoid receptor 2 (CB2R) activation, which shows no psychoactivity…

These data suggest that CB2R may be a potential therapeutic target of RA.”

http://www.ncbi.nlm.nih.gov/pubmed/24440992

Cannabinoid modulation of predator fear: involvement of the dorsolateral periaqueductal gray.

“The present study investigated the effects of systemic or intra-dorsolateral periaqueductal gray (dlPAG) administration of CB1 agonists on behavioural changes induced in rats by predator (a live cat) exposure, a model of panic responses…

These results suggest that modulation of the cannabinoid system could be a target in the treatment of panic disorders…”

http://www.ncbi.nlm.nih.gov/pubmed/24438603