“Positron emission tomography (PET) can visualize and quantify receptors and other targets in the living human brain, and recent progress in radioligand development has enabled measurement of cannabinoid CB1 receptors. Cannabinoid CB1 receptors have been implicated in multiple human diseases, such as obesity, mood disorders, and addiction. First in vivo human studies have shown distinctive spatial and temporal alterations in cannabinoid CB1 receptor binding in addictive disorders.”
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Spinal neuronal cannabinoid receptors mediate urodynamic effects of systemic fatty acid amide hydrolase (FAAH) inhibition in rats.
“To test if urodynamic effects from systemic Fatty Acid Amide Hydrolase (FAAH) inhibition involve sacral spinal cannabinoid type 1 (CB1) or type 2 (CB2) receptors…
Urodynamic effects of systemic FAAH inhibition involve activities at spinal neuronal CB1 and CB2 receptors in normal and obstructed rats.
Endogenous spinal CB receptor ligands seem to regulate normal micturition and bladder overactivity (BO). Altered spinal CB receptor functions may be involved in the pathogenesis of obstruction-induced BO.”
Assessing the public health impacts of legalising recreational cannabis use in the USA.
“Some US states have created de facto legal supply of cannabis for medical use. So far this policy does not appear to have increased cannabis use or cannabis-related harm.”
http://www.ncbi.nlm.nih.gov/pubmed/25777798
Synthetic cannabis: a comparison of patterns of use and effect profile with natural cannabis in a large global sample.
“Natural cannabis was preferred to synthetic cannabis by 93% of users, with natural cannabis rated as having greater pleasurable effects when high and being more able to function after use. Synthetic cannabis was associated with more negative effects, hangover effects, and greater paranoia…
Users report a strong preference for natural over synthetic cannabis…”
Risk of emergency medical treatment following consumption of cannabis or synthetic cannabinoids in a large global sample.
“Synthetic cannabinoids (SCs) have become increasingly popular in recent years. Often marketed to reflect their similar effects to cannabis, their use has been associated with a range of negative health effects. We sought to determine the relative risk of seeking emergency medical treatment (EMT) following use of SCs and natural cannabis.
The relative risk associated with the use of SCs was 30 (95% CI 17.5-51.2) times higher than that associated with cannabis. Significantly more symptoms (p=0.03) were reported by respondents seeking treatment for SCs than for cannabis.
CONCLUSIONS:
Whilst these findings must be treated with caution, SCs potentially pose a greater risk to users’ health than natural forms of cannabis. Regulation is unlikely to remove SCs from the market, so well-informed user-focused health promotion messages need to be crafted to discourage their use.”
The cannabinoid receptor 2 is involved in acute rejection of cardiac allografts.
“Acute rejection of cardiac allografts is a major risk factor limiting survival of heart transplant recipients. Rejection is triggered by dendritic cell (DC) mediated activation of host T cells, amongst others CD4+ T helper (TH)1- and TH17 cells.
The cannabinoid receptor 2 (CB2) is an important modulator of cellular immune responses…
These results demonstrate that CB2 modulates in vitro cytokine responses via DCs and directly via its influence on TH1/TH17 differentiation.
These findings and the fact that allograft rejection is enhanced in Cnr2-/- mice suggest that CB2 may be a promising therapeutic target in organ transplantation.”
Protective effects of Delta(9)-tetrahydrocannabinol against N-methyl-d-aspartate-induced AF5 cell death.
“One of the most promising potential medical applications of cannabinoids involves their ability to protect cells from a variety of toxic events.
Cannabinoids have been reported to protect neurons from death…
Cannabinoids, such as the pharmacologically active component of marijuana (-)Δ9-tetrahydrocannabinol (THC)…
The neuroprotective effects of Δ9-tetrahydrocannabinol (THC) were examined…
Protective effects of Delta(9)-tetrahydrocannabinol… THC may function as an antioxidant to increase cell survival…
THC can produce receptor-independent neuroprotective or cellular protective effects at micromolar concentrations as a result of its antioxidant properties…
In conclusion, THC produces a potent neuroprotective effect…”
Delta9-tetrahydrocannabinol protects hippocampal neurons from excitotoxicity.
“Excitotoxic neuronal death underlies many neurodegenerative disorders…
Delta9-tetrahydrocannabinol protects hippocampal neurons from excitotoxicity…
…desensitization of CB(1) receptors diminishes the neuroprotective effects of cannabinoids.
This study demonstrates the importance of agonist efficacy and the duration of treatment on the neuroprotective effects of cannabinoids.
It will be important to consider these effects on neuronal survival when evaluating pharmacologic treatments that modulate the endocannabinoid system.”
http://www.ncbi.nlm.nih.gov/pubmed/17140550
“Molecular Mechanisms of Cannabinoid Protection from Neuronal Excitotoxicity” http://molpharm.aspetjournals.org/content/69/3/691.long
Molecular Mechanisms of Cannabinoid Protection from Neuronal Excitotoxicity
“Cannabinoids protect neurons from excitotoxic injury…
Endogenous or exogenous cannabinoids have shown neuroprotective effects…
The main finding reported here is that cannabinoids protect neurons from excitotoxic injury by a mechanism that involves the activation of CB1R and inhibition of NOS and PKA….
Cannabinoid receptor agonist drugs protect neurons…
By identifying the signaling pathways responsible for cannabinoid effects in animal models of disease and their human counterparts, it may be possible to design more specific and therefore more efficacious cannabinoid-based therapies.”
http://molpharm.aspetjournals.org/content/69/3/691.long
“Delta9-tetrahydrocannabinol protects hippocampal neurons from excitotoxicity.” http://www.ncbi.nlm.nih.gov/pubmed/17140550
Hypothalamic POMC neurons promote cannabinoid-induced feeding.
“Hypothalamic pro-opiomelanocortin (POMC) neurons promote satiety. Cannabinoid receptor 1 (CB1R) is critical for the central regulation of food intake.
Here we test whether CB1R-controlled feeding in sated mice is paralleled by decreased activity of POMC neurons.
We show that chemical promotion of CB1R activity increases feeding, and notably, CB1R activation also promotes neuronal activity of POMC cells…
Together, these results uncover a previously unsuspected role of POMC neurons in the promotion of feeding by cannabinoids.”
http://www.ncbi.nlm.nih.gov/pubmed/25707796