Detailed characterization of the endocannabinoid system in human macrophages and foam cells, and anti-inflammatory role of type-2 cannabinoid receptor.

“Here, we sought to ascertain whether different elements of the endocannabinoid system (ECS) were activated in human lipid-laden macrophages, and whether CB2R played any role in atherogenesis and inflammation of these cells…

CONCLUSIONS:

A fully active ECS is present in human macrophages and macrophage-derived foam cells. Selective activation of CB2R reduces CD36-dependent oxLDL accumulation and modulates production of inflammatory cytokines, thus representing a potential therapeutic strategy to combat atherosclerosis.”

http://www.ncbi.nlm.nih.gov/pubmed/24529123

Endocannabinoid Modulation of Cortical Up-States and NREM Sleep.

“We hypothesized that the endocannabinoid (EC) system, a neuromodulatory system intrinsic to the cortical microcircuitry, is an important regulator of up-states and sleep…

Overall, these findings demonstrate that the EC system actively regulates cortical up-states and important features of NREM sleep such as its duration and low frequency cortical oscillations.”

http://www.ncbi.nlm.nih.gov/pubmed/24520411

1,2-Dihydro-2-oxopyridine-3-carboxamides: The C-5 substituent is responsible for functionality switch at CB2 cannabinoid receptor.

“The relevance of CB2R-mediated therapeutic effects is well-known for the treatment of inflammatory and neuropathic pain and neurodegenerative disorders. In our search for new cannabinoid receptor modulators, we report the optimization of a series of 1,2-dihydro-2-oxopyridine-3-carboxamide derivatives as CB2R ligands…”

http://www.ncbi.nlm.nih.gov/pubmed/24518874

Modulation of Fear Memory by Dietary Polyunsaturated Fatty Acids via Cannabinoid Receptors.

“…several studies have suggested benefits of n-3 long-chain polyunsaturated fatty acid (PUFA) for patients with anxiety disorders.

Elevated fear is thought to contribute to the pathogenesis of particular anxiety disorders. The aim of the present study was to evaluate whether the dietary n-3 to n-6 PUFA (3/6) ratio influences fear memory…

These results suggest that the ratio of n-3 to n-6 PUFA is a factor regulating fear memory via cannabinoid CB1 receptors.”

http://www.ncbi.nlm.nih.gov/pubmed/24518289

Pro-resolution, protective and anti-nociceptive effects of a cannabis extract in the rat gastrointestinal tract.

“Cannabis is widely used for treating a number of gastrointestinal ailments…

In the present study, we tested the effects (in rats) of a simple extract of medicinal cannabis (called “MFF”) for its ability to promote resolution of colitis…

These results demonstrate that a simple extract of medicinal cannabis can significantly enhance resolution of inflammation and injury, as well as prevent injury, in the gastrointestinal tract. Interestingly, different cannabinoid receptors were involved in some of the effects. MFF may serve as the basis for a simple preparation of cannabis that would produce beneficial effects in the GI tract with reduced systemic toxicity.”

http://www.ncbi.nlm.nih.gov/pubmed/23756391

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

The endocannabinoid system controls food intake via olfactory processes.

“Hunger arouses sensory perception, eventually leading to an increase in food intake, but the underlying mechanisms remain poorly understood. We found that cannabinoid type-1 (CB1) receptors promote food intake in fasted mice by increasing odor detection.

CB1 receptors were abundantly expressed on axon terminals of centrifugal cortical glutamatergic neurons that project to inhibitory granule cells of the main olfactory bulb (MOB).

Local pharmacological and genetic manipulations revealed that endocannabinoids and exogenous cannabinoids increased odor detection and food intake in fasted mice by decreasing excitatory drive from olfactory cortex areas to the MOB.

Consistently, cannabinoid agonists dampened in vivo optogenetically stimulated excitatory transmission in the same circuit.

Our data indicate that cortical feedback projections to the MOB crucially regulate food intake via CB1 receptor signaling, linking the feeling of hunger to stronger odor processing.Thus, CB1 receptor-dependent control of cortical feedback projections in olfactory circuits couples internal states to perception and behavior.”

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

Altered Expression of the CB1 Cannabinoid Receptor in the Triple Transgenic Mouse Model of Alzheimer’s Disease.

“The endocannabinoid system has gained much attention as a new potential pharmacotherapeutic target in various neurodegenerative diseases, including Alzheimer’s disease (AD).

…The altered CB1 levels appear, rather, to be age-and/or pathology-dependent, indicating an involvement of the endocannabinoid system in AD pathology and supporting the ECS as a potential novel therapeutic target for treatment of AD.”

http://www.ncbi.nlm.nih.gov/pubmed/24496074