The cannabinoid TRPA1 agonist cannabichromene inhibits nitric oxide production in macrophages and ameliorates murine colitis.

“The non-psychotropic cannabinoid cannabichromene is known to activate the transient receptor potential ankyrin-type1 (TRPA1) and to inhibit endocannabinoid inactivation, both of which are involved in inflammatory processes. We examined here the effects of this phytocannabinoid on peritoneal macrophages and its efficacy in an experimental model of colitis…

CONCLUSION AND IMPLICATIONS:

Cannabichromene exerts anti-inflammatory actions in activated macrophages – with tonic CB1 cannabinoid signalling being negatively coupled to this effect – and ameliorates experimental murine colitis.”

http://www.ncbi.nlm.nih.gov/pubmed/23373571

Cannabinoid receptor 2 is increased in acutely and chronically inflamed bladder of rats.

“Cannabinoid receptors are expressed in the urinary bladder and may affect bladder function… CB2 receptors may be a viable target for pharmacological treatment of bladder inflammation and associated pain…

In this study, we have shown that CB1 and CB2 are present in the bladder and its innervation, and that expression of CB2 is increased in the bladders of rats with acute and chronic cystitis. Bladder inflammation and pain is the summation of a number of biological events, including participation of the endocannabinoid system.

The endocannabinoid system could play an important role in modulation of severity of bladder inflammation and pain, and it may be possible to take advantage of the cannabinoid system in the bladder to decrease inflammation and resultant pain.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2592089/

Increased cannabinoid receptor 1-immunoreactive nerve fibers in overactive and painful bladder disorders and their correlation with symptoms.

“To study the expression of cannabinoid receptor 1 (CB1) in human urinary bladder hypersensitivity and overactivity disorders, and correlate changes with symptoms. Cannabinoid receptor agonists have been shown to modulate urinary bladder contractility and reduce pain after bladder inflammation; their clinical efficacy on lower urinary tract symptoms was demonstrated in the Cannabinoids in Multiple Sclerosis study…

CONCLUSIONS:

The results of this study suggest that increased nerve fibers, which express CB1, may be related to bladder pain in PBS (painful bladder syndrome) and urgency in IDO (idiopathic detrusor overactivity).

Our findings support clinical trials of CB1 agonists in bladder disorders.”

http://www.ncbi.nlm.nih.gov/pubmed/20346490

Changes in Cerebral CB1 Receptor Availability after Acute and Chronic Alcohol Abuse and Monitored Abstinence.

“Involvement of the type 1 cannabinoid receptor (CB1R) in the effects of alcohol on the brain is supported by animal experiments…

In conclusion, whereas the acute alcohol effect is an increase in CB1R availability, chronic heavy drinking leads to reduced CB1R availability that is not reversible after 1 month of abstinence. Longer follow-up is required to differentiate whether this is a compensatory effect of repeated endocannabinoid overstimulation or an enduring trait-like feature.

An enhanced CB1R signaling may offer a new therapeutic direction for treatment of the negative affective state produced by alcohol withdrawal and abstinence, which is critical for the maintenance of alcohol addiction.”

http://www.ncbi.nlm.nih.gov/pubmed/24553924

Human orexin/hypocretin receptors form constitutive homo- and heteromeric complexes with each other and with human CB1 cannabinoid receptors.

“Human OX1 orexin receptors have been shown to homodimerize and they have also been suggested to heterodimerize with CB1 cannabinoid receptors. The latter has been suggested to be important for orexin receptor responses and trafficking. In this study, we wanted to assess the ability of the other combinations of receptors to also form similar complexes…

In conclusion, orexin receptors have a significant propensity to make homo- and heterodi-/oligomeric complexes. However, it is unclear whether this affects their signaling. As orexin receptors efficiently signal via endocannabinoid production to CB1 receptors, dimerization could be an effective way of forming signal complexes with optimal cannabinoid concentrations available for cannabinoid receptors.”

http://www.ncbi.nlm.nih.gov/pubmed/24530395

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

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

Effect of cannabinoid receptor activation on spreading depression.

“Cannabis has been used for centuries for both symptomatic and prophylactic treatment of different types of headaches including migraine…

Suppression of CSD (cortical spreading depression) by activation of CB1 receptors suggests the potential therapeutic effects of cannabinoids in migraine with aura as well as other CSD-related disorders.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3586901/