Due to their similar chemical structure, CBDa and CBD have similar therapeutic effects, but there are some differences between the two. There is a growing trend of CBD being compared with CBDA, so we take a look at the two, and see how they really match up. Product 1 - 20 Cannabidiolic acid, abbreviated CBDA, is the acid form of cannabidiol, abbreviated CBD and is naturally found in cannabis plants. Structurally.
CBDa CBD and
Chemists and engineers conducting research and development in this field have been hard at work creating concoctions that consistently push the boundaries of what can be done with cannabis extractions and isolations. One question more curious extract consumers ask is this: Can pure cannabinoids be isolated and packaged for consumption? Tetrahydrocannabinolic acid THCA and cannabidiolic acid CBDA are the two most prominent cannabinoids found within the trichomes of living cannabis plants.
As a living cannabis plant cycles through the final stages of senescence, these unstable cannabinoid precursors slowly decarboxylate and become active. Once a plant is harvested and dried, various forms of heat application can also decarboxylate cannabinoids into their active compounds. Cannabis contains hundreds of active and inactive compounds that take on many shapes and structures on a microscopic level.
THCA and CBD are both similar in that their molecular composition resembles a crystalline formation with rigid and latticed structures. When completely isolated and in visible quantities, these compounds look a lot like snowflakes or crushed rock salt. This means that there are no traces or terpenes, flavonoids, fats, lipids, or anything else from the raw plant. For this reason, isolates contain little to no flavor, color, or aroma.
The specific process of creating crystalline is a well-guarded proprietary secret, but processors have divulged enough information to give us a general idea of how this complicated preparation is conducted. The process of isolating and collecting cannabinoids begins with an extract. Aside from primary cannabinoids, these extracts contain a number of other components that range from terpenes and flavonoids to fats, lipids, and a host of other particulates.
In order to remove these compounds and isolate the cannabinoids, a series of washes and separations must occur. The first wash is typically done with the popular extracting hydrocarbon hexane as well as acetic acid think super-concentrated vinegar.
Once mixed, these chemical solvents help to strip away plant particulates and impurities. To isolate cannabinoids with this method, more chemicals are introduced which must be filtered out through yet another round of rotary evaporation.
Crystalline THCA is considered inactive insofar as it does not have the same psychotropic properties as THC if ingested in its current state. The final stage in cannabinoid isolation is to prepare the product for human consumption.
The neuroprotective effects of Delta 9 -tetrahydrocannabinol but not cannabidiol were inhibited by SR, a cannabinoid CB1 receptor antagonist, and were abolished by warming of the animals to the levels observed in the controls.
Delta 9 -Tetrahydrocannabinol significantly decreased the rectal temperature, and the hypothermic effect was inhibited by SR These results surely show that the neuroprotective effect of Delta 9 -tetrahydrocannabinol are via a CB1 receptor and temperature-dependent mechanisms whereas the neuroprotective effects of cannabidiol are independent of CB1 blockade and of hypothermia.
The Dravet syndrome is a complex childhood epilepsy disorder that is associated with drug-resistant seizures and a high mortality rate. We studied cannabidiol for the treatment of drug-resistant seizures in the Dravet syndrome. In this double-blind, placebo-controlled trial, we randomly assigned children and young adults with the Dravet syndrome and drug-resistant seizures to receive either cannabidiol oral solution at a dose of 20 mg per kilogram of body weight per day or placebo, in addition to standard antiepileptic treatment.
The primary end point was the change in convulsive-seizure frequency over a week treatment period, as compared with a 4-week baseline period. The median frequency of convulsive seizures per month decreased from Adverse events that occurred more frequently in the cannabidiol group than in the placebo group included diarrhea, vomiting, fatigue, pyrexia, somnolence, and abnormal results on liver-function tests. There were more withdrawals from the trial in the cannabidiol group.
Cannabidiol as a Potential New Type of an Antipsychotic. A Critical Review of the Evidence. There is urgent need for the development of mechanistically different and less side-effect prone antipsychotic compounds. The endocannabinoid system has been suggested to represent a potential new target in this indication.
Although, results from animal studies are inconsistent to a certain extent and seem to depend on behavioral paradigms, treatment duration and experimental conditions applied, cannabidiol has shown antipsychotic properties in both rodents and rhesus monkeys.
After some individual treatment attempts, the first randomized, double-blind controlled clinical trial demonstrated that in acute schizophrenia cannabidiol exerts antipsychotic properties comparable to the antipsychotic drug amisulpride while being accompanied by a superior, placebo-like side effect profile.
As the clinical improvement by cannabidiol was significantly associated with elevated anandamide levels, it appears likely that its antipsychotic action is based on mechanisms associated with increased anandamide concentrations. Although, a plethora of mechanisms of action has been suggested, their potential relevance for the antipsychotic effects of cannabidiol still needs to be investigated. The clarification of these mechanisms as well as the establishment of cannabidiol 's antipsychotic efficacy and its hopefully benign side-effect profile remains the subject of a number of previously started clinical trials.
Cannabidiol as potential treatment in refractory pediatric epilepsy. In recent years there has been great scientific and public interest focused on the therapeutic potential of compounds derived from cannabis for the treatment of refractory epilepsy in children.
From in vitro and in vivo studies on animal models, cannabidiol CBD appears to be a promising anticonvulsant drug with a favorable side-effect profile. In humans, CBD efficacy and safety is not supported by well-designed trials and its use has been described by anecdotal reports. It will be necessary to investigate CBD safety, pharmacokinetics and interaction with other anti-epileptic drugs AEDs alongside performing double-blinded placebo-controlled trials in order to obtain conclusive data on its efficacy and safety in children.
Does cannabidiol have a role in the treatment of schizophrenia? Schizophrenia is a debilitating psychiatric disorder which places a significant emotional and economic strain on the individual and society-at-large. Unfortunately, currently available therapeutic strategies do not provide adequate relief and some patients are treatment-resistant. In this regard, cannabidiol CBD , a non-psychoactive constituent of Cannabis sativa, has shown significant promise as a potential antipsychotic for the treatment of schizophrenia.
However, there is still considerable uncertainty about the mechanism of action of CBD as well as the brain regions which are thought to mediate its putative antipsychotic effects. We argue that further research on CBD is required to fast-track its progress to the clinic and in doing so, we may generate novel insights into the neurobiology of schizophrenia. Cannabidiol in humans-the quest for therapeutic targets.
Cannabidiol CBD , a major phytocannabinoid constituent of cannabis, is attracting growing attention in medicine for its anxiolytic, antipsychotic, antiemetic and anti-inflammatory properties. However, up to this point, a comprehensive literature review of the effects of CBD in humans is lacking.
The aim of the present systematic review is to examine the randomized and crossover studies that administered CBD to healthy controls and to clinical patients. Both monotherapy and combination studies e. A total of 34 studies were identified: Potential pharmacokinetic and pharmacodynamic explanations for these results are discussed.
Abstract Cannabidiol CBD , a major cannabinoid of hemp, does not bind to CB1 receptors and is therefore devoid of psychotomimetic properties.
It has been argued that this may occur also after oral administration in humans. However, the experimental conversion of CBD to THC and delta8-THC in simulated gastric fluid SGF is a highly artificial approach that deviates significantly from physiological conditions in the stomach; therefore, SGF does not allow an extrapolation to in vivo conditions. In addition, the typical spectrum of side effects of THC, or of the very similar synthetic cannabinoid nabilone, as listed in the official Summary of Product Characteristics e.
Cannabidiol CBD , a major cannabinoid of hemp, does not bind to CB1 receptors and is therefore devoid of psychotomimetic properties. Potential protective effects of cannabidiol on neuroanatomical alterations in cannabis users and psychosis: Cannabis use and the development of schizophrenic psychoses share a variety of similarities. Both start during late adolescence; go along with neuropsychological deficits, reduced activity, motivation deficits, and hallucinations suggesting impairment of similar brain structures.
In cannabis heavy users diminished regional gray and white matter volume was reported. Similar alterations were observed in the large literature addressing structural abnormalities in schizophrenia. Furthermore, in cannabis using schizophrenic patients, these brain alterations were especially pronounced.
Close relatives of schizophrenic patients showed greater cannabis-associated brain tissue loss than non-relatives indicating a genetically mediated particular sensitivity to brain tissue loss. Possible mechanisms for the induction of structural brain alterations are here discussed including impairments of neurogenesis, disturbance of endocannabinoids and diminished neuroplasticity. Especially direct THC effects or via endocannabinoids may mediate diminished glutamatergic neurotransmission usually driving neuroplasticity.
Correspondingly, alterations of the kynurenic acid blocking NMDA receptors may contribute to brain structure alterations. However, different cannabis compounds may exert opposite effects on the neuroanatomical changes underlying psychosis. This finding is further supported by several animal experiments supporting neuroprotective properties of CBD mainly via anti-oxidative effects, CB2 receptors or adenosine receptors.
We will discuss here the mechanisms by which CBD may reduce brain volume loss, including antagonism of THC, interactions with endocannabinoids, and mechanisms that specifically underlie antipsychotic properties of CBD. Anti-inflammatory effects of the cannabidiol derivative dimethylheptyl- cannabidiol - studies in BV-2 microglia and encephalitogenic T cells.
The expression levels of selected genes involved in stress regulation and inflammation were determined by quantitative real-time PCR. DMH-CBD downregulates the expression of inflammatory cytokines and protects the microglial cells by inducing an adaptive cellular response against inflammatory stimuli and oxidative injury. Memory-rescuing effects of cannabidiol in an animal model of cognitive impairment relevant to neurodegenerative disorders.
Cannabidiol , the main nonpsychotropic constituent of Cannabis sativa, possesses a large number of pharmacological effects including anticonvulsive, sedative, hypnotic, anxiolytic, antipsychotic, anti-inflammatory, and neuroprotective, as demonstrated in clinical and preclinical studies. Many neurodegenerative disorders involve cognitive deficits, and this has led to interest in whether cannabidiol could be useful in the treatment of memory impairment associated to these diseases.
We used an animal model of cognitive impairment induced by iron overload in order to test the effects of cannabidiol in memory-impaired rats. Rats received vehicle or iron at postnatal days At the age of 2 months, they received an acute intraperitoneal injection of vehicle or cannabidiol 5.
In order to investigate the effects of chronic cannabidiol , iron-treated rats received daily intraperitoneal injections of cannabidiol for 14 days.
Twenty-four hours after the last injection, they were submitted to object recognition training. Retention tests were performed 24 h after training.
A single acute injection of cannabidiol at the highest dose was able to recover memory in iron-treated rats. Chronic cannabidiol improved recognition memory in iron-treated rats. Acute or chronic cannabidiol does not affect memory in control rats.
The present findings provide evidence suggesting the potential use of cannabidiol for the treatment of cognitive decline associated with neurodegenerative disorders. Further studies, including clinical trials, are warranted to determine the usefulness of cannabidiol in humans suffering from neurodegenerative disorders.
Cannabidiol protects liver from binge alcohol-induced steatosis by mechanisms including inhibition of oxidative stress and increase in autophagy. Acute alcohol drinking induces steatosis, and effective prevention of steatosis can protect liver from progressive damage caused by alcohol. Increased oxidative stress has been reported as one mechanism underlying alcohol-induced steatosis.
We evaluated whether cannabidiol , which has been reported to function as an antioxidant, can protect the liver from alcohol-generated oxidative stress-induced steatosis. Cannabidiol can prevent acute alcohol-induced liver steatosis in mice, possibly by preventing the increase in oxidative stress and the activation of the JNK MAPK pathway.
Importantly, cannabidiol can prevent the decrease in autophagy induced by alcohol. In conclusion, these results show that cannabidiol protects mouse liver from acute alcohol-induced steatosis through multiple mechanisms including attenuation of alcohol-mediated oxidative stress, prevention of JNK MAPK activation, and increasing autophagy.
We have previously reported that cannabidiol CBD lowers the incidence of diabetes in young non-obese diabetes-prone NOD female mice. In the present study we show that administration of CBD to 11—14 week old female NOD mice, which are either in a latent diabetes stage or with initial symptoms of diabetes, ameliorates the manifestations of the disease.
In addition, the level of the proinflammatory cytokine IL produced by splenocytes was significantly reduced, whereas the level of the anti-inflammatory IL was significantly elevated following CBD-treatment. Histological examination of the pancreata of CBD-treated mice revealed more intact islets than in the controls.
Our data strengthen our previous assumption that CBD, known to be safe in man, can possibly be used as a therapeutic agent for treatment of type 1 diabetes. Accumulating evidence suggests that cannabidiol CBD may be an effective and safe anxiolytic agent and potentially also an antidepressant.
The objective of this study was to further examine these properties of CBD using the 'depressive-like' Wistar-Kyoto WKY rat, focusing on the drug's effect on anhedonia-like behaviors. These findings extend the limited knowledge on the antidepressant effect of CBD, now shown for the first time in a genetic animal model of depression.
These results suggest that CBD may be beneficial for the treatment of clinical depression and other states with prominent anhedonia.
The astrocytes have gained in recent decades an enormous interest as a potential target for neurotherapies, due to their essential and pleiotropic roles in brain physiology and pathology. The cannabinoid system and its ligands have been shown to interact and affect activities of astrocytes. Cannabidiol CBD is the main non-psychotomimetic cannabinoid derived from Cannabis.
Here, we attempt to sum up the current findings on the effects of CBD on astrocyte activity, and in this way on central nervous system CNS functions, across various tested models and neuropathologies. The collected data shows that increased astrocyte activity is suppressed in the presence of CBD in models of ischemia, Alzheimer-like and Multiple-Sclerosis-like neurodegenerations, sciatic nerve injury, epilepsy, and schizophrenia.
Moreover, CBD has been shown to decrease proinflammatory functions and signaling in astrocytes. Cannabis, cannabidiol , and epilepsy--from receptors to clinical response. Recreational cannabis use in adults with epilepsy is widespread. The use of cannabis for medicinal purposes is also becoming more prevalent. For this purpose, various preparations of cannabis of varying strengths and content are being used.
The recent changes in the legal environment have improved the availability of products with high cannabidiol CBD and low tetrahydrocannabinol THC concentrations. There is some anecdotal evidence of their potential efficacy, but the mechanisms of such action are not entirely clear.
The mechanism of action of CBD is less clear but is likely polypharmacological. The scientific data support the role of the endocannabinoid system in seizure generation, maintenance, and control in animal models of epilepsy. There are clear data for the negative effects of cannabis on the developing and mature brain though these effects appear to be relatively mild in most cases. In the past five years, an increasing number of publications have focused on the discovery of the anti-inflammatory, anti-oxidant, and neuroprotective effects of CBD.
In particular, CBD exerts positive pharmacological effects in ischemic stroke and other chronic diseases, including Parkinson's disease, Alzheimer's disease, and rheumatoid arthritis.
Importantly, CBD use does not lead to tolerance. In this review, we will discuss the therapeutic possibility of CBD as a cerebroprotective agent, highlighting recent pharmacological advances, novel mechanisms, and therapeutic time window of CBD in ischemic stroke. Controlled clinical trial of cannabidiol in Huntington's disease. Based on encouraging preliminary findings, cannabidiol CBD , a major nonpsychotropic constituent of Cannabis, was evaluated for symptomatic efficacy and safety in 15 neuroleptic-free patients with Huntington's Disease HD.
A comparison of the effects of CBD and placebo on chorea severity and other therapeutic outcome variables, and on a Cannabis side effect inventory, clinical lab tests and other safety outcome variables, indicated no significant p greater than 0. Cannabis contains the psychoactive component delta9-tetrahydrocannabinol delta9-THC , and the non-psychoactive components cannabidiol CBD , cannabinol, and cannabigerol.
It is well-known that delta9-THC and other cannabinoid CB1 receptor agonists are neuroprotective during global and focal ischemic injury. Additionally, delta9-THC also mediates psychological effects through the activation of the CB1 receptor in the central nervous system.
In addition to the CB1 receptor agonists, cannabis also contains therapeutically active components which are CB1 receptor independent. The cerebroprotective action of CBD is CB1 receptor-independent, long-lasting, and has potent anti-oxidant activity.
Cannabidiol promotes browning in 3T3-L1 adipocytes. Recruitment of the brown-like phenotype in white adipocytes browning and activation of existing brown adipocytes are currently being investigated as a means to combat obesity. Thus, a wide variety of dietary agents that contribute to browning of white adipocytes have been identified.
The present study was designed to investigate the effects of cannabidiol CBD , a major nonpsychotropic phytocannabinoid of Cannabis sativa, on induction of browning in 3T3-L1 adipocytes. These data suggest possible roles for CBD in browning of white adipocytes, augmentation of lipolysis, thermogenesis, and reduction of lipogenesis.
In conclusion, the current data suggest that CBD plays dual modulatory roles in the form of inducing the brown-like phenotype as well as promoting lipid metabolism. Thus, CBD may be explored as a potentially promising therapeutic agent for the prevention of obesity. Is there a role for cannabidiol in psychiatry? Understanding whether cannabidiol CBD is useful and safe for the treatment of psychiatric disorders is essential to empower psychiatrists and patients to take good clinical decisions.
Our aim was to conduct a systematic review regarding the benefits and adverse events AEs of CBD in the treatment of schizophrenia, psychotic disorders, anxiety disorders, depression, bipolar disorder and substance-use disorders. We conducted a literature search in PubMed, Scielo, and Clinicaltrials. Bibliographic research yielded records. After analysis, we included six case reports and seven trials, comprising subjects. Most the studies published presented several drawbacks and did not reach statistical significance.
We have not found evidence regarding major depressive and bipolar disorders. The level of evidence for cannabis withdrawal is B; cannabis addiction is C2; treatment of positive symptoms in schizophrenia and anxiety in social anxiety disorder is C1. Discrete or no AEs were reported. The most frequently reported AEs are sedation and dizziness. The evidence regarding efficacy and safety of CBD in psychiatry is still scarce. Further larger well-designed randomised controlled trials are required to assess the effects of CBD in psychiatric disorders.
Could cannabidiol be used as an alternative to antipsychotics? Individuals with this disorder often present signs such as hallucination, anxiety, reduced attention, and social withdrawal. Although antipsychotic drugs remain the cornerstone of schizophrenia treatment, they are associated with severe side effects. Recently, the endocannabinoid system ECS has emerged as a potential therapeutic target for pharmacotherapy that is involved in a wide range of disorders, including schizophrenia.
Since its discovery, a lot of effort has been devoted to the study of compounds that can modulate its activity for therapeutic purposes. Among them, cannabidiol CBD , a non-psychoactive component of cannabis, shows great promise for the treatment of psychosis, and is associated with fewer extrapyramidal side effects than conventional antipsychotic drugs.
The overarching goal of this review is to provide current available knowledge on the role of the dopamine system and the ECS in schizophrenia, and to discuss key findings from animal studies and clinical trials investigating the antipsychotic potential of CBD. Cannabidiol , a Cannabis sativa constituent, as an antipsychotic drug. A high dose of delta9-tetrahydrocannabinol, the main Cannabis sativa cannabis component, induces anxiety and psychotic-like symptoms in healthy volunteers.
These effects of delta9-tetrahydrocannabinol are significantly reduced by cannabidiol CBD , a cannabis constituent which is devoid of the typical effects of the plant. Studies in animal models and in healthy volunteers clearly suggest an anxiolytic-like effect of CBD. The antipsychotic-like properties of CBD have been investigated in animal models using behavioral and neurochemical techniques which suggested that CBD has a pharmacological profile similar to that of atypical antipsychotic drugs.
The results of two studies on healthy volunteers using perception of binocular depth inversion and ketamine-induced psychotic symptoms supported the proposal of the antipsychotic-like properties of CBD. In addition, open case reports of schizophrenic patients treated with CBD and a preliminary report of a controlled clinical trial comparing CBD with an atypical antipsychotic drug have confirmed that this cannabinoid can be a safe and well-tolerated alternative treatment for schizophrenia.
Future studies of CBD in other psychotic conditions such as bipolar disorder and comparative studies of its antipsychotic effects with those produced by clozapine in schizophrenic patients are clearly indicated. Gene duplication and divergence affecting drug content in Cannabis sativa. Marijuana and hemp were crossed to evaluate competing models of cannabinoid inheritance and to explain the predominance of tetrahydrocannabinolic acid THCA in marijuana compared with cannabidiolic acid CBDA in hemp.
Individuals in the resulting F2 population were assessed for differential expression of cannabinoid synthase genes and were used in linkage mapping. Genetic markers associated with divergent cannabinoid phenotypes were identified.
Phylogenetic analysis further suggests a history of duplication and divergence affecting drug content. Marijuana is distinguished from hemp by a nonfunctional CBDA synthase that appears to have been positively selected to enhance psychoactivity. An unlinked QTL for cannabinoid quantity may also have played a role in the recent escalation of drug potency. Performance of schizophrenic patients in the Stroop Color Word Test and electrodermal responsiveness after acute administration of cannabidiol CBD.
The last decade has seen increasing evidence of dysfunctions in the endogenous cannabinoid system in schizophrenia and of its relationship with the typical cognitive impairment of the disorder. Studies in animal models, healthy volunteers, and psychotic patients clearly suggest an antipsychotic-like effect of cannabidiol.
This study investigated the effects of cannabidiol on selective attention in 28 schizophrenic patients using the Stroop Color Word Test and on these patients' electrodermal responsiveness to auditive stimuli. The subjects attended two experimental sessions, the first one without the administration of drugs. In the second session the subjects were divided into three groups that received either a single dose of cannabidiol mg or cannabidiol mg or placebo.
The three groups did not differ significantly with respect to electrodermal measures in the two experimental sessions. When the first and second sessions were compared improved performance was found in all three groups, with patients who received placebo and cannabidiol mg performing better than those who received cannabidiol mg.
The single, acute administration of cannabidiol seems to have no beneficial effects on the performance of schizophrenic patients in the Stroop Color Word Test, although the hypothesis that chronic administration may lead to improvement cannot be disregarded.
Neuroprotection and reduction of glial reaction by cannabidiol treatment after sciatic nerve transection in neonatal rats. In neonatal rats, the transection of a peripheral nerve leads to an intense retrograde degeneration of both motor and sensory neurons. Most of the axotomy-induced neuronal loss is a result of apoptotic processes. The clinical use of neurotrophic factors is difficult due to side effects and elevated costs, but other molecules might be effective and more easily obtained.
Among them, some are derived from Cannabis sativa. Cannabidiol CBD is the major non-psychotropic component found on the surface of such plant leaves. The present study aimed to investigate the neuroprotective potential of CBD. Thus, 2-day-old Wistar rats were divided into the following experimental groups: In line with such results, the terminal deoxynucleotidyl transferase dUTP nick end labeling reaction revealed a reduction of apoptotic cells, mostly located in the spinal cord intermediate zone, where interneurons promote sensory-motor integration.
The present results show that CBD possesses neuroprotective characteristics that may, in turn, be promising for future clinical use. Effects of cannabidiol plus naltrexone on motivation and ethanol consumption. The aim of this study was to explore if the administration of naltrexone NTX together with cannabidiol CBD may improve the efficacy in reducing alcohol consumption and motivation rather than any of the drugs given separately.
The effects of low doses of NTX 0. The combination of low doses of CBD plus NTX resulted more effective to reduce ethanol consumption and motivation to drink. These effects, appears to be mediated, at least in part, by 5-HT 1A receptors. This article is protected by copyright. Medical use of cannabis.
The medical properties of cannabis have been known for many centuries; its first documented use dates back to BC when it was described for its hallucinogenic and pain-relieving properties. In the first half of the twentieth century, a number of pharmaceutical companies marked cannabis for indications such as asthma and pain, but since then its use has sharply declined, mainly due to its unpredictable effects, but also for socio-political issues.
Evidence suggests an association between cannabis and schizophrenia: Additionally, the use of marijuana can trigger psychotic episodes in schizophrenic patients, and this has been ascribed to THC. Given the need to reduce the side effects of marketed antipsychotics, and their weak efficacy on some schizophrenic symptoms, cannabinoids have been suggested as a possible alternative treatment for schizophrenia. CBD, a non-psychoactive constituent of the Cannabis sativa plant, has been receiving growing attention for its anti-psychotic-like properties.
Evidence suggests that CBD can ameliorate positive and negative symptoms of schizophrenia. Behavioural and neurochemical models suggest that CBD has a pharmacological profile similar to that of atypical anti-psychotic drugs and a clinical trial reported that this cannabinoid is a well-tolerated alternative treatment for schizophrenia.
Cannabidiol effects in the prepulse inhibition disruption induced by amphetamine. The information processing appears to be deficient in schizophrenia. Prepulse inhibition PPI , which measures the inhibition of a motor response by a weak sensory event, is considered particularly useful to understand the biology of information processing in schizophrenia patients.
Drugs that facilitate dopaminergic neurotransmission such as amphetamine induce PPI disruption in human and rodents. Clinical and neurobiological findings suggest that the endocannabinoid system and cannabinoids may be implicated in the pathophysiology and treatment of schizophrenia.
Cannabidiol CBD , a non-psychotomimetic constituent of the Cannabis sativa plant, has also been reported to have potential as an antipsychotic. Since one possible mechanism of CBD action is the facilitation of endocannabinoid-mediated neurotransmission through anandamide, we tested the effects of an anandamide hydrolysis inhibitor URB in the amphetamine-induced PPI disruption.
Pretreatment with CBD attenuated the amphetamine-disruptive effects on PPI test after systemic or intra-accumbens administration. Similar effects were also found with the inhibitor of anandamide hydrolysis. These results corroborate findings indicating that CBD induces antipsychotic-like effects. In addition, they pointed to the nucleus accumbens as a possible site of these effects.
The increase of anandamide availability may be enrolled in the CBD effects. Several antiepileptic drugs AEDs , about 25, are currently clinically available for the treatment of patients with epilepsy. Despite this armamentarium and the many recently introduced AEDs, no major advances have been achieved considering the number of drug resistant patients, while many benefits have been indeed obtained for other clinical outcomes e.
Cannabinoids have long been studied for their potential therapeutical use and more recently phytocannabinoids have been considered a valuable tool for the treatment of several neurological disorders including epilepsy. Among this wide class, the most studied is cannabidiol CBD considering its lack of psychotropic effects and its anticonvulsant properties.
Analyse the currently available literature on CBD also in light of other data on phytocannabinoids, reviewing data spanning from the mechanism of action, pharmacokinetic to clinical evidences.
Several preclinical studies have tried to understand the mechanism of action of CBD, which still remains largely not understood. CBD has shown significant anticonvulsant effects mainly in acute animal models of seizures; beneficial effects were reported also in animal models of epileptogenesis and chronic models of epilepsy, although not substantial.
In contrast, data coming from some studies raise questions on the effects of other cannabinoids and above all marijuana. There is indeed sufficient supporting data for clinical development and important antiepileptic effects and the currently ongoing clinical studies will permit the real usefulness of CBD and possibly other cannabinoids. Undoubtedly, several issues also need to be addressed in the next future e. Finally, shading light on the mechanism of action and the study of other cannabinoids might represent an advantage for future developments.
Cannabidiol rather than Cannabis sativa extracts inhibit cell growth and induce apoptosis in cervical cancer cells. Cervical cancer remains a global health related issue among females of Sub-Saharan Africa, with over half a million new cases reported each year. Different therapeutic regimens have been suggested in various regions of Africa, however, over a quarter of a million women die of cervical cancer, annually.
This makes it the most lethal cancer amongst black women and calls for urgent therapeutic strategies. In this study we compare the anti-proliferative effects of crude extract of Cannabis sativa and its main compound cannabidiol on different cervical cancer cell lines. Results obtained indicate that both cannabidiol and Cannabis sativa extracts were able to halt cell proliferation in all cell lines at varying concentrations.
Apoptosis was confirmed by overexpression of p53, caspase 3 and bax. In conclusion, these data suggest that cannabidiol rather than Cannabis sativa crude extracts prevent cell growth and induce cell death in cervical cancer cell lines.
High dosage of cannabidiol CBD alleviates pentylenetetrazole-induced epilepsy in rats by exerting an anticonvulsive effect. The study was designed to investigate the effect of various concentrations of cannabidiol CBD in rats with chronic epilepsy. Behavioral measurements of convulsion following pentylenetetrazole treatment and morphological changes of the hippocampal neurons with hematoxylin and eosin staining were used to observe the epileptic behaviour.
Immunohistochemistry was used to detect the expression levels of glial fibrillary acidic protein and inducible nitric oxide synthase iNOS in the hippocampus. The neuronal loss and astrocyte hyperplasia in the hippocampal area were also decreased. Thus, CBD administration inhibited the effect of pentylenetetrazole in rats, decreased the astrocytic hyperplasia, decreased neuronal damage in the hippocampus caused by seizures and selectively reduced the expression of the NR1 subunit of NMDA.
Therefore, CBD exhibits an anticonvulsive effect in the rats with chronic epilepsy. Cannabidiol improves brain and liver function in a fulminant hepatic failure-induced model of hepatic encephalopathy in mice. We investigated the effects of cannabidiol , a non-psychoactive constituent of Cannabis sativa with anti-inflammatory properties that activates the 5-hydroxytryptamine receptor 5-HT1A, on brain and liver functions in a model of hepatic encephalopathy associated with fulminant hepatic failure induced in mice by thioacetamide.
Neurological and motor functions were evaluated 2 and 3 days, respectively, after induction of hepatic failure, after which brains and livers were removed for histopathological analysis and blood was drawn for analysis of plasma liver enzymes. In a separate group of animals, cognitive function was tested after 8 days and brain 5-HT levels were measured 12 days after induction of hepatic failure. Similarly, decreased motor activity in thioacetamide-treated mice was partially restored by cannabidiol.
Increased plasma levels of ammonia, bilirubin and liver enzymes, as well as enhanced 5-HT levels in thioacetamide-treated mice were normalized following cannabidiol administration. Likewise, astrogliosis in the brains of thioacetamide-treated mice was moderated after cannabidiol treatment. Sign-up for our free cannabis investment newsletter to discover the latest opportunities in the space.
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CBD vs. CBDA: What’s the Difference?
Cannabidiolic acid (CBDA) is a non-psychoactive cannabinoid and the acidic precursor to CBD. CBDA can be found in the live or raw form of. Do you know the difference between CBD vs CBDa. Learn more about the difference between both of these molecules. Shop Oils with CBDa. Effects of CBD and CBDA. A completely natural and vegetable substance that provides a healing effect as food supplement: discover CBD! For an even better.