“A large body of evidence suggests that the cannabinoid CB1 receptor plays a key role in the regulation of emotional behaviors. The present study was designed to evaluate the effects of CB1 agonist and antagonist on anxiety-like behaviors in the lateral septum (LS) region of the rat brain using elevated plus maze test…
The results suggest that the cannabinoid system of the lateral septum modulates anxiety-like behavior through CB1 receptor.”
“We reported previously that both a cannabinoid receptor 2 (CB2R) agonist and a cannabinoid receptor 1 (CB1R) antagonist were protective in the treatment of transient middle cerebral artery occlusion/reperfusion injury (MCAO/R) and that they acted in a synergistic manner when administered in combination. The goal of the current study was to determine which of the potential cannabinoid receptors participate in the protective effects of this drug combination in a mouse model of MCAO/R.
The effects of administration of the CB2R agonist/CB1R antagonist combination on infarct size and cerebral blood flow during a 1-h occlusion were tested…
In conclusion, administration of the CB2R agonist/CB1R antagonist combination causes a significant reduction in infarct size in the MCAO/R model. The protective effect involves both the CB2R and the 5-HT1A receptor. Neither the CB1R nor the TRPV1 receptors appear to participate in this response.”
“The prelimbic medial prefrontal cortex (PL) is an important encephalic structure involved in the expression of emotional states. In a previous study, intra-PL injection of cannabidiol (CBD), a major non-psychotomimetic cannabinoid present in the Cannabis sativa plant, reduced the expression of fear conditioning response…
CBD caused an anxiolytic, rather than anxiogenic, effect…
Taken together, these results suggest that CBD modulation of anxiety in the PL depend on 5HT1A-mediated neurotransmission and previous stressful experience.”
“Good news for people who’ve worried that smoking too much marijuana (cannabis) — especially as a teenager — might lead to some dramatic problems in the future, even schizophrenia.
New research from Harvard Medical School, in a comparison between families with a history of schizophrenia and those without, finds little support for marijuana use as a cause of schizophrenia.
“The results of the current study suggest that having an increased familial morbid risk for schizophrenia may be the underlying basis for schizophrenia in cannabis users and not cannabis use by itself,” note the researchers.”
More: http://psychcentral.com/news/2013/12/10/harvard-marijuana-doesnt-cause-schizophrenia/63148.html
“Cannabidiol (CBD) is a non-psychoactive plant cannabinoid that inhibits cell proliferation and induces cell death of cancer cells and activated immune cells. It is not an agonist of the classical CB1/CB2 cannabinoid receptors and the mechanism by which it functions is unknown.
…using microscale thermophoresis, we showed a direct interaction between purified fluorescently labeled VDAC1 and CBD.
Thus, VDAC1 seems to serve as a novel mitochondrial target for CBD.
The inhibition of VDAC1 by CBD may be responsible for the immunosuppressive and anticancer effects of CBD.”
“To date, anticonvulsant effects of the plant cannabinoid, cannabidivarin (CBDV), have been reported in several animal models of seizure. However, these behaviourally observed anticonvulsant effects have not been confirmed at the molecular level…
These results provide the first molecular confirmation of behaviourally observed effects of the non-psychoactive, anticonvulsant cannabinoid, CBDV, upon chemically-induced seizures and serve to underscore its suitability for clinical development.”
http://www.ncbi.nlm.nih.gov/pubmed/24282673
Full-text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3840466/
“GW Pharmaceuticals plc (Nasdaq: GWPH, AIM: GWP, “GW”) announced today it has commenced a Phase 1 clinical trial of product candidate GWP42006 for the treatment of epilepsy.
Over the last five years, GW has conducted an extensive pre-clinical cannabinoid research program in the field of epilepsy in collaboration with the University of Reading in the United Kingdom. This research has led to the emergence of a number of promising cannabinoid therapeutic candidates showing anti-epileptic effects.
GWP42006, one of the most promising of those candidates, is a non-psychoactive cannabinoid extracted from specific chemotypes of the cannabis plant which has shown the ability to treat seizures in pre-clinical models of epilepsy with significantly fewer side effects than currently approved anti-epileptic drugs1.
“We are pleased to have advanced GWP42006 to first dose in man, a significant milestone in the development of this novel product candidate. The decision to progress into Phase 1 follows several years of highly promising pre-clinical research,” stated Dr. Stephen Wright, Director of Research and Development at GW. “We believe that GWP42006 has the potential to become an important advance in the treatment of epilepsy, a condition for which there remains a substantial unmet medical need.””
More: http://www.gwpharm.com/Phase1Epilepsy.aspx
“Driving directions to GW Pharma Limited and product information about EPIDIOLEX is provided. EPIDIOLEX is a product created by GW Pharma Limited in Porton Down Science Park , Salisbury, , SP4OJR. The EPIDIOLEX is a product related to Pharmaceutical and veterinary preparations and substances for the treatment of epilepsy, convulsions, seizures, Dravet syndrome, Lennox-Gastaut syndrome, intractable childhood epilepsy with generalized tonic-clonic seizures, generalized epilepsy with febrile seizures plus, Doose syndrome and chromosome disorders; pharmaceutical preparations and substances for the treatment of pediatric epilepsy; herbs for medicinal purposes; medicinal herbs; medicinal oils; medicinal infusions for the treatment of epilepsy; pure extracts of medicinal plants and herbs used for the treatment of epilepsy, convulsions and seizures; herb teas for medicinal purposes. The EPIDIOLEX product is now being marketed in the United States for sale. The EPIDIOLEX is in the category of Pharmaceutical Products..
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“Malignant gliomas are the most common primary brain tumors… Recently, we have shown that the non-psychoactive cannabinoid compound cannabidiol (CBD) induced apoptosis of human glioma cells in vitro and tumor regression in vivo…the present study was to investigate the anti-migratory action of CBD…
In conclusion, the present investigation adds further insights into the antitumoral action of the non-psychoactive CBD, showing multiple mechanisms through which the cannabinoid inhibits glioma cell growth and motility.
As CBD is a natural compound without psychotropic and side effects, these data lead us to consider CBD as a new potential anticancer drug useful in the management of gliomas.”
“The active ingredient in marijuana appears to reduce tumor growth…
The researchers showed giving THC to mice with cancer decreased tumor growth and killed cells off in a process called autophagy.
“Our findings support that safe, therapeutically efficacious doses of THC may be reached in cancer patients,” Guillermo Velasco of Complutense University in Madrid and colleagues reported in the Journal of Clinical Investigation…
Other research has shown benefits, such as staving off Alzheimer’s, and many doctors view THC as a valuable way to treat weight loss associated with AIDS, and nausea and vomiting associated with chemotherapy in cancer patients.
Velasco and his team’s study included an analysis of two tumors from two people with a highly aggressive brain cancer which showed signs of autophagy after receiving THC.
The researchers said the findings could pave the way for cannabinoid-based drugs to treat cancer…”
“Multiple sclerosis (MS) is a neurodegenerative disease that is characterised by repeated inflammatory/demyelinating events within the central nervous system (CNS). In addition to relapsing-remitting neurological insults, leading to loss of function, patients are often left with residual, troublesome symptoms such as spasticity and pain. These greatly diminish “quality of life” and have prompted some patients to self-medicate with and perceive benefit from cannabis.
Recent advances in cannabinoid biology are beginning to support these anecdotal observations, notably the demonstration that spasticity is tonically regulated by the endogenous cannabinoid system.
Recent clinical trials may indeed suggest that cannabis has some potential to relieve, pain, spasms and spasticity in MS. However, because the CB(1) cannabinoid receptor mediates both the positive and adverse effects of cannabis, therapy will invariably be associated with some unwanted, psychoactive effects.
In an experimental model of MS, and in MS tissue, there are local perturbations of the endocannabinoid system in lesional areas. Stimulation of endocannabinoid activity in these areas either through increase of synthesis or inhibition of endocannabinoid degradation offers the positive therapeutic potential of the cannabinoid system whilst limiting adverse events by locally targeting the lesion.
In addition, CB(1) and CB(2) cannabinoid receptor stimulation may also have anti-inflammatory and neuroprotective potential as the endocannabinoid system controls the level of neurodegeneration that occurs as a result of the inflammatory insults.
Therefore cannabinoids may not only offer symptom control but may also slow the neurodegenerative disease progression that ultimately leads to the accumulation of disability.”