Tag Archives: cannabidiol

Cannabidiol inhibitory effect on marble-burying behaviour: involvement of CB1 receptors.

Posted on by
Reply

“Cannabidiol (CBD) is a major non-psychotomimetic component of Cannabis sativa that has been shown to have an anxiolytic effect in human and animal models.

Earlier studies suggest that these effects involve facilitation of serotonin, a neurotransmitter that has also been related to obsessive-compulsive disorder.

On the basis of this evidence, this study investigated the effects of CBD in C57BL/6J mice submitted to the marble-burying test (MBT), an animal model proposed to reflect compulsive behaviour.

CBD induced a significant decrease in the number of buried marbles compared with controls.

These results indicated that CBD and paroxetine decrease the number of buried marbles in the MBT through distinct pharmacological mechanisms.

They also suggest a potential role of drugs acting on the cannabinoid system in modulating compulsive behaviour.”

http://www.ncbi.nlm.nih.gov/pubmed/20695034

Study: Non-Psychoactive Cannabis Could Treat OCD

Posted on by
Reply

Leaf Science

“A non-psychoactive chemical in marijuana may be able to control symptoms of obsessive-compulsive disorder, according to new research out of Brazil.

Cannabidiol (CBD) is one of the major compounds found in marijuana, but lacks the high caused by THC.

Previous studies suggest that it can be used to combat anxiety and other obsessive-compulsive behaviors.

While research has mostly involved simple animal models, a team led by Dr. Francisco Guimarães of the University of Sao Paulo’s School of Medicine decided to test cannabidiol in rats that were given mCPP – a drug that blocks the effects of traditional OCD treatments.

Interestingly, even at low doses, CBD was able to reverse the obsessive-compulsive behavior caused by mCPP. Published in the journal Fundamental & Clinical Pharmacology, the authors conclude that the study adds support to “a possible anti-compulsive effect of CBD.””

http://www.leafscience.com/2013/10/22/study-non-psychoactive-cannabis-treat-ocd/

“Cannabidiol reverses the mCPP-induced increase in marble-burying behavior.”  http://www.ncbi.nlm.nih.gov/pubmed/24118015

Cannabidiol reverses the mCPP-induced increase in marble-burying behavior

Posted on by
Reply

Fundamental & Clinical Pharmacology

“Cannabidiol (CBD), one of the main components of Cannabis sp., presents clinical and preclinical anxiolytic properties.

Recent results using the marble-burying test (MBT) suggest that CBD can also induce anticompulsive-like effects.

The results, in addition to reinforcing a possible anticompulsive effect of CBD, also suggest that mCPP-induced repetitive burying could be a useful test for the screening of compounds with presumed anticompulsive properties.”

http://onlinelibrary.wiley.com/doi/10.1111/fcp.12051/abstract

Refractory trigeminal neuralgia responsive to nabiximols in a patient with multiple sclerosis.

Posted on by
Reply

“Nabiximols is a cannabinoid compound approved for the treatment of multiple sclerosis (MS)-related spasticity.

However, additional symptoms, such as pain, urinary urgency and sleep disturbance, may benefit from treatment.

CASE REPORT:

The present report describes a patient with secondary progressive MS and severe lower limbs spasticity who was started on treatment with nabiximols. The patient also suffered from trigeminal neuralgia, which he was not treating due to inefficacy or side effects of all previously tried medications. After nabiximols initiation the patient experienced a marked benefit on trigeminal neuralgia, which completely resolved, while spasticity responded only partially to treatment.

CONCLUSION:

Nabiximols mechanism of action is based on the interaction with CB1 and CB2 receptors, which are expressed by central nervous system neurons and are known to modulate pain among other effects. The present case indicates that nabiximols and other cannabinoids need to be further tested for the treatment of trigeminal neuralgia.”

http://www.ncbi.nlm.nih.gov/pubmed/27456876

“Therapeutic potential of cannabinoids in trigeminal neuralgia. Considering the pronounced antinociceptive effects produced by cannabinoids, they may be a promising therapeutic approach for the clinical management of trigeminal neuralgia.”  http://www.ncbi.nlm.nih.gov/pubmed/15578967

Should we care about sativex-induced neurobehavioral effects? A 6-month follow-up study.

Posted on by
Reply

“Sativex® is an exclusive cannabinoid-based drug approved for the treatment of spasticity due to Multiple Sclerosis (MS).

The most common side effects include dizziness, nausea, and somnolence. However, it is still under debate whether the drug could cause negative cognitive effects.

The aim of our study was to investigate the effect of Sativex® on functional and psychological status in cannabis-naïve MS patients.

After the treatment, we did not observe any significant neurobehavioral impairment in all the patients, but one.

Our findings suggest that Sativex® treatment does not significantly affect the cognitive and neurobehavioral functions.”

http://www.ncbi.nlm.nih.gov/pubmed/27460745

Effects of Cannabidiol and Hypothermia on Short-Term Brain Damage in New-Born Piglets after Acute Hypoxia-Ischemia.

Posted on by
Reply

“Hypothermia is a standard treatment for neonatal encephalopathy, but nearly 50% of treated infants have adverse outcomes.

Pharmacological therapies can act through complementary mechanisms with hypothermia improving neuroprotection.

Cannabidiol could be a good candidate.

Our aim was to test whether immediate treatment with cannabidiol and hypothermia act through complementary brain pathways in hypoxic-ischemic newborn piglets.

Individually, the hypothermia and the cannabidiol treatments reduced the glutamate/Nacetyl-aspartate ratio, as well as TNFα and oxidized protein levels in newborn piglets subjected to hypoxic-ischemic insult. Also, both therapies reduced the number of necrotic neurons and prevented an increase in lactate/N-acetyl-aspartate ratio.

The combined effect of hypothermia and cannabidiol on excitotoxicity, inflammation and oxidative stress, and on cell damage, was greater than either hypothermia or cannabidiol alone.

The present study demonstrated that cannabidiol and hypothermia act complementarily and show additive effects on the main factors leading to hypoxic-ischemic brain damage if applied shortly after the insult.”

http://www.ncbi.nlm.nih.gov/pubmed/27462203

Cannabidiol is an allosteric modulator at mu- and delta-opioid receptors.

Posted on by
Reply

“The mechanism of action of cannabidiol, one of the major constituents of cannabis, is not well understood but a noncompetitive interaction with mu opioid receptors has been suggested on the basis of saturation binding experiments.

The aim of the present study was to examine whether cannabidiol is an allosteric modulator at this receptor, using kinetic binding studies, which are particularly sensitive for the measurement of allosteric interactions at G protein-coupled receptors.

In addition, we studied whether such a mechanism also extends to the delta opioid receptor. For comparison, (-)-Delta9-tetrahydrocannabinol (THC; another major constituent of cannabis) and rimonabant (a cannabinoid CB1 receptor antagonist) were studied.

The present study shows that cannabidiol is an allosteric modulator at mu and delta opioid receptors. This property is shared by THC but not by rimonabant.”

http://www.ncbi.nlm.nih.gov/pubmed/16489449

Arachidonylcyclopropylamide increases microglial cell migration through cannabinoid CB2 and abnormal-cannabidiol-sensitive receptors.

Posted on by
Reply

“Microglial cells, the macrophages of the brain, express low, yet detectable levels of cannabinoid CB(1) receptors, which are known to modulate cell migration.

To determine if cannabinoid CB(1) receptors expressed by microglial cells modulate their migration, we assessed whether arachidonylcyclopropylamide (ACPA, an agonist shown to selectively activate CB(1) receptors) affects the migration of BV-2 cells, a mouse microglial cell line.

Our results suggest that cannabinoid CB(2) receptors and abn-CBD receptors, rather than cannabinoid CB(1) receptors, regulate microglial cell migration, and that ACPA is a broad cannabinoid receptor agonist.”

http://www.ncbi.nlm.nih.gov/pubmed/12921861

Complex pharmacology of natural cannabinoids: evidence for partial agonist activity of delta9-tetrahydrocannabinol and antagonist activity of cannabidiol on rat brain cannabinoid receptors.

Posted on by
Reply

“Delta9-tetrahydrocannabinol (delta9-THC), cannabinol and cannabidiol are three important natural cannabinoids from the Marijuana plant (Cannabis sativa).

Using [35S]GTP-gamma-S binding on rat cerebellar homogenate as an index of cannabinoid receptor activation we show that: delta9-THC does not induce the maximal effect obtained by classical cannabinoid receptor agonists such as CP55940.

Moreover at high concentration delta9-THC exhibits antagonist properties.

Cannabinol is a weak agonist on rat cerebellar cannabinoid receptors and cannabidiol behaves as an antagonist acting in the micromolar range.”

http://www.ncbi.nlm.nih.gov/pubmed/9667767

Nonpsychotropic cannabinoids, abnormal cannabidiol and canabigerol-dimethyl heptyl, act at novel cannabinoid receptors to reduce intraocular pressure.

Posted on by
Reply

 

“The objective of our study was to examine the pharmacology of the intraocular pressure (IOP)-lowering actions of the behaviorally inactive cannabinoids, abnormal cannabidiol (abn-CBD), and a cannabigerol analog, cannabigerol-dimethyl heptyl (CBG-DMH), in comparison to that of the nonselective cannabinoid 1 receptor (CB(1)R) and CB(2)R agonist, WIN55,212-2, in Brown Norway rats.

These results indicate that both CBG-DMH and abn-CBD have the potential for further investigation as novel ocular hypotensive cannabinoids devoid of CB(1)R-mediated side-effects.”

http://www.ncbi.nlm.nih.gov/pubmed/21770780