Potential protective effects of cannabidiol on neuroanatomical alterations in cannabis users and psychosis: a critical review.

“…different cannabis compounds may exert opposite effects on the neuroanatomical changes underlying psychosis. In particular, cannabidiol (CBD) was shown to prevent THC associated hippocampal volume loss… This finding is further supported by several animal experiments supporting neuroprotective properties of CBD mainly via anti-oxidative effects, CB2 receptors or adenosine receptors… mechanisms by which CBD may reduce brain volume loss, including antagonism of THC, interactions with endocannabinoids, and mechanisms that specifically underlie antipsychotic properties of CBD.”

http://www.ncbi.nlm.nih.gov/pubmed/22716143

Peripheral, but not central effects of cannabidiol derivatives: mediation by CB(1) and unidentified receptors.

“Delta-9 tetrahydrocannabinol (Delta(9)-THC) and (-)-cannabidiol ((-)-CBD) are major constituents of the Cannabis sativa plant with different pharmacological profiles…

We tested a series of (+)- and (-)-CBD derivatives for central and peripheral effects in mice…

We suggest that (+)-CBD analogues have mixed agonist/antagonist activity in the brain.

Second, (-)-CBD analogues which are devoid of cannabinoid receptor affinity but which inhibit intestinal motility, suggest the existence of a non-CB(1), non-CB(2) receptor.

Therefore, such analogues should be further developed as antidiarrheal and/or antiinflammatory drugs.

We propose to study the therapeutic potential of (-)- and (+)-CBD derivatives for complex conditions such as inflammatory bowel disease and cystic fibrosis.”

http://www.ncbi.nlm.nih.gov/pubmed/15910887

Δ9-Tetrahydrocannabinol Treatment During Human Monocyte Differentiation Reduces Macrophage Susceptibility to HIV-1 Infection

“The major psychoactive component of marijuana, Δ9-tetrahydrocannabinol (THC), also acts to suppress inflammatory responses. Receptors for THC, CB1, CB2, and GPR55, are differentially expressed on multiple cell types including monocytes and macrophages, which are important modulators of inflammation in vivo and target cells for HIV-1 infection. Use of recreational and medicinal marijuana is increasing, but the consequences of marijuana exposure on HIV-1 infection are unclear. Ex vivo studies were designed to investigate effects on HIV-1 infection in macrophages exposed to THC during or following differentiation.

THC treatment of primary human monocytes during differentiation reduced HIV-1 infection…

THC treatment of monocytes during differentiation into MDMs suppresses HIV-1 infection. 
Ultimately, the mechanism of THC suppression of HIV-1 infection was traced to a reduction in cell surface HIV receptor (CD4, CCR5 and CXCR4) expression that diminished entry efficiency.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4019698/

Nabiximols (THC/CBD Oromucosal Spray, Sativex®) in Clinical Practice – Results of a Multicenter, Non-Interventional Study (MOVE 2) in Patients with Multiple Sclerosis Spasticity.

“Nabiximols (Sativex®), a cannabinoid-based oromucosal spray, is an add-on therapy for patients with moderate to severe multiple sclerosis spasticity (MSS) resistant to other medications. The primary objective was to provide real-life observational data of clinical experience of nabiximols in contrast to formal clinical trials of effectiveness…

Conclusion: Real-life data confirm nabiximols as an effective and well-tolerated treatment option for resistant MSS in clinical practice.”

http://www.ncbi.nlm.nih.gov/pubmed/24525548

Anticoagulant effects of a Cannabis extract in an obese rat model.

“Blood coagulation studies were conducted to determine the possible anti-/prothrombotic effect of an organic cannabis extract and the three major cannabinoids, THC, CBD and CBN…

The study thus shows that Cannabis sativa and the cannabinoids, THC and CBN, display anticoagulant activity and may be useful in the treatment of diseases such as type 2 diabetes in which a hypercoagulable state exists.”

 http://www.ncbi.nlm.nih.gov/pubmed/16644197

The Neuroscience Of Munchies: Why The Scent Of A Burger Gives Us A High – npr

We Didn't Make This Up: The scientists who performed the study on how cannabis triggers the munchies through the sense of smell commissioned an artist to put this illustration together.

“From cinnamon buns in the morning to a burger after a long run, food never smells as good as when you’re superhungry.

Now scientists have uncovered a clue as to why that might be — and it lies in the munchies and marijuana.

Receptors in the brains of mice that light up when the animals are high are also activated when the critters are fasting, French scientists reported Sunday in the journal Nature Neuroscience.

In other words, skipping a meal triggered the same hunger-inducing brain receptors that marijuana does. And it works, at least in mice, by boosting the sense of smell, neuroscientist Giovanni Marsicano and his team at the Universite de Bordeaux report.

That’s because the receptors that get activated are located in the smelling center of the brain. And sense of smell is known to be a key factor driving appetite.

In case you’re wondering, the mice didn’t toke up. The researchers injected the rodents withTHC, the active ingredient in marijuana.”

http://www.npr.org/blogs/thesalt/2014/02/10/274660785/munchies-neuroscience-why-the-scent-of-a-burger-gives-us-a-high?live=1&utm_content=socialflow&utm_campaign=nprfacebook&utm_source=npr&utm_medium=facebook

“The endocannabinoid system controls food intake via olfactory processes.” http://www.ncbi.nlm.nih.gov/pubmed/24509429

Cannabinoids inhibit cholinergic contraction in human airways through prejunctional CB1 receptors

“Here, we sought to assess the effects of natural and synthetic cannabinoids on cholinergic bronchial contraction…

Delta-9-tetrahydrocannabinol, WIN55,212-2 and CP55,940 induced concentration-dependent inhibition of cholinergic contraction… 

Conclusions and implications

Activation of prejunctional CB1-receptors appears to mediate the inhibition of electrical field stimulation-evoked cholinergic contraction in human bronchus.

This feature may explain the acute bronchodilation produced by marijuana smoking.”

http://onlinelibrary.wiley.com/doi/10.1111/bph.12597/abstract

Use of Dronabinol for Cannabis Dependence: Two Case Reports and Review

“Based on recent laboratory studies, dronabinol (delta-9-tetrahydrocannabinol) has been shown to reduce cannabis withdrawal symptoms and the subjective effects of marijuana.

Given that agonist agents have been found to be effective for opiate and nicotine dependence, the clinical utility of dronabinol for cannabis dependence is a reasonable approach…

It is clear from the two cases that both patients found the induction onto dronabinol helpful.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2733248/

Dronabinol for the Treatment of Cannabis Dependence: A Randomized, Double-Blind, Placebo-Controlled Trial

“… there are no effective medications for cannabis dependence. The purpose of this study was to evaluate the safety and efficacy of dronabinol, a synthetic form of delta-9-tetrahydrocannabinol, a naturally occurring pharmacologically active component of marijuana, in treating cannabis dependence.

This is the first trial using an agonist substitution strategy for treatment of cannabis dependence. Dronabinol showed promise, it was well-tolerated, and improved treatment retention and withdrawal symptoms…

In conclusion, agonist substitution pharmacotherapy with dronabinol, a synthetic form of THC, showed promise for treatment of cannabis dependence, reducing withdrawal symptoms and improving retention in treatment…

The trial showed that among adult cannabis-dependent patients, dronabinol was well accepted, with good adherence and few adverse events.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3154755/