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From MMJ to Special K

Brain & Ketamine

Every five months Irvin Rosenfeld has gets a FedEx shipment, courtesy of the federal government, containing six metal canisters, each with 300 perfectly rolled joints of what today would be considered rather mediocre weed. But the quality of the government-issue reefer matters less than the fact that Uncle Sam has been supplying him with it regularly since 1982, when Rosenfeld won the right to smoke cannabis for reasons of medical necessity under the auspices of the federal government’s Compassionate Investigational New Drug (IND) program. Rosenfeld smokes cannabis every day to treat a rare and excruciatingly painful bone disease called multiple congenital cartilaginous exotosis.

Medicine in a Can

A total of 15 patients with different incurable ailments would enroll in the Compassionate IND Program to study cannabis before it was officially shut down in 1992. As one of the last living IND participants, Rosenfeld remains a forthright and energetic medical cannabis advocate, a role he takes very seriously. His personal story is compelling. He has suffered with extreme pain for most of his life. At age 10, x-rays revealed more than 200 tumors sprouting from bones in his arms and legs. He would undergo a dozen surgeries and consume a steady diet of prescription narcotics and other pharmaceuticals.

When he first smoked marijuana as a teenager at a social gathering, it was a revelation. Before long he realized that if he smoked cannabis every couple of hours, his pain eased and he didn’t have to rely as much on doctor-prescribed muscle relaxants, opiates, and benzos to get by. Although he felt no euphoric effects from cannabis, the herb somehow kept his disease in check, inhibiting tumor growth and helping him live a decent life. A walking, talking refutation of the lazy stoner myth, he went to college, played sports, married his childhood sweetheart Debbie, and became a successful stockbroker.

There’s no doubt that cannabis helps Rosenfeld’s condition, but it’s not a cure. Though he has learned to live with his pain, at times its relentlessness makes him feel depressed, trapped in a lonely prison from which there’s no escape. At least that’s how it felt until one day in 2020, when Rosenfeld’s pain management specialist, Dr. Michele Weiner, mentioned a potential jailbreak: ketamine.

Dissociation Nation

Ketamine, an FDA-approved “dissociative anesthetic,” has been around since 1962 when it was first synthesized by chemist Calvin Stevens. Employed initially as a tranquilizer in veterinary medicine, the drug was widely utilized during the Vietnam War for treating wounded troops. Ketamine kept injured soldiers conscious but cognitively disconnected from their pain, all while maintaining their vital functions.

Ketamine’s efficacy against pain is attributed to the drug’s ability to induce a dissociative state. At high doses ketamine produces anesthesia; at lower doses, it relieves pain and causes hallucinations. “Special K” acquired a reputation as a party drug in the 1970s due to its psychedelic and mood-altering effects. Favored by fashionistas and Silicon Valley bros, it’s still part of the recreational drug scene.

At high doses ketamine produces anesthesia; at lower doses, it relieves pain and causes hallucinations.

Some have attributed Elon Musk’s erratic behavior of late to ketamine benders at parties. (He says he uses it to relieve depression — proof that money can’t buy everything.) Although ketamine is potentially addictive and excessive use can cause liver damage, renal failure, and psychotic episodes, it’s classified as a Schedule III controlled substance (along with anabolic steroids and some acetaminophen-codeine combinations), indicating a relatively low risk for abuse.

Unlike LSD and psilocybin, ketamine has no natural source. Lysergic acid is present in ergot (rye fungus), psilocybin is a magic mushroom compound, mescaline comes from the peyote cactus, and for MDMA (“ecstasy”) there’s sassafras. But there’s no natural correlate for synthetic ketamine, which works through different molecular pathways than the classic, naturally sourced psychedelics. Acid and ‘shrooms deliver a full-blown psychedelic experience by binding to the 5-HT2A serotonin receptor, whereas ketamine confers its powerful dissociative and psychedelic effects by blocking the N-methyl-d-aspartate (NMDA) receptor, a glutamate ion channel that manages the ebb and flow of calcium inside the cell.

Fertilizer for the Brain

By inhibiting the NMDA receptor, ketamine triggers the production of a chemical known as brain-derived neurotrophic factor (BDNF), which has been likened to “fertilizer of the brain.” The role of BDNF in adult neurogenesis (the creation of new brain cells) and neuroplasticity (the ability to reorganize neural networks and synaptic connections in response to injury and lived experience) is the subject of many scientific papers.

According to a 2012 study by University of Bonn scientist Andras Bilkei-Gorzo: “On the cellular level, the cannabinoid system regulates the expression of brain-derived neurotrophic factor and neurogenesis.” Subsequent reports by Brazilian investigators established that ketamine’s central and peripheral painkilling effects are mediated by the endocannabinoid system. When scientists blocked the CB1 cannabinoid receptor, ketamine did not prevent pain. The same group of researchers also found that ketamine caused anandamide (one of two major endocannabinoids) to be released in certain brain areas. And when anandamide levels increased, so did ketamine’s analgesic effect.

“CBD significantly augmented the activating effects of ketamine.”

Plant cannabinoids have also been shown to potentiate ketamine’s painkilling properties. A 2011 report on “The interplay of cannabinoid and NMDA glutamate receptor systems” examined “the interactive effects of cannabidiol and ketamine in healthy human subjects.” The report concluded that “CBD significantly augmented the activating effects of ketamine.” Other studies have noted that CBD boosts endocannabinoid levels and CB1 receptor signaling by delaying the metabolic breakdown and reuptake of anandamide.

CBD and ketamine are both neurogenic compounds, and this may factor into how they confer antidepressant effects. Impaired neurogenesis has been linked to clinical depression, substance abuse, and other mental health conditions. Ketamine’s rapid antidepressant effects involve enhanced BDNF-induced (and cannabinoid-regulated) neurogenesis and neuroplasticity. The drug is currently being administered off-label for refractory depression at numerous ketamine clinics around the country.

Common Biological Mechanisms

“Pain and depression share common biological mechanisms,” explains Dr. Michelle Weiner, a double board-certified physician who specializes in interventional pain medicine, physical medicine, and rehabilitation. In addition to her clinical practice at five locations in southern Florida, Dr. Weiner is an Assistant Professor at Nova Southeastern University College of Osteopathic Medicine.

Take a spin on her website and you’ll find a group photo picturing Dr. Weiner and her team of practitioners, a bevy of Florida beauties who look as though they could’ve been cast as the Real Housewives of Miami. There’s a lot going on behind the glamor. When interviewed by Project CBD, Dr. Weiner’s enthusiasm for her calling is obvious, her expertise backed by years of on-the-ground research and a vast knowledge rooted in pain studies and cutting-edge neuroscience.

While building her practice, Dr. Weiner grew increasingly frustrated with the limited tools available beyond conventional pain pills and injections. When medical cannabis was legalized in Florida in 2016, she became one of the first licensed physicians to include it in her treatment plans. She found that cannabis was an effective therapeutic option for helping chronic pain patients, especially seniors, decrease their dependence on opioids.

“It really changed my practice,” says Weiner, who is a member of Florida’s Medical Cannabis Advisory Committee. Weiner’s experience as a cannabis clinician encouraged her to explore other mind-body healing modalities, including psychedelic drugs. Today she is vice president of Mr. Psychedelic Law, a not-for-profit that advocates for responsible legal reform of psilocybin prohibition in the Sunshine State.

Teaching Resilience

Dr. Weiner’s interest in ketamine began during a residency and training fellowship at the University of Miami. “Back then we used ketamine differently than we do now,” she says. “We’d give patients a benzodiazepine sedative beforehand to tone down the hallucinatory experiences common with ketamine.” But after learning of ketamine’s potential as treatment for anxiety, depression, and PTSD, she changed her approach to encompass a dual-pronged focus on pain and mental health.

“Eighty-five percent of chronic pain patients also suffer from depression,” says Dr. Weiner. “You can’t successfully treat pain without concurrently treating mental health.” From her perspective, it’s all interconnected: chronic pain adversely impacts how the brain functions, causing maladaptive changes in the central nervous system and weakening synaptic circuitry between brain regions — and these changes often lead to depression, according to a 2017 study published in the journal Neural Plasticity. Not only does it offer rapid relief from both depression and pain, ketamine also appears to refresh and reset neural circuitry.

But the benefits of a single ketamine treatment are often short-lived (seven days on average for depression), and the drug may be contraindicated for certain conditions. Some people can’t tolerate ketamine’s intense hallucinogenic effects. Another major drawback: MediCare and health insurance companies don’t cover ketamine treatments, so patients must pay out of pocket. For those who can’t afford it, there are DIY at-home ketamine kits with medicine procured from less-than-reliable online sources, which is problematic.

“When used mindfully, ketamine, through its dissociative effects, allows patients a time-out from their pain.”

Ketamine treatment needs to be monitored by an experienced practitioner, says Dr. Weiner. Most of her patients come into the clinic once or twice a week for at least a month to receive ketamine by intramuscular or intravenous infusion, along with therapy sessions and lifestyle counseling for a better long-term outcome. Treatment is tapered off over time, and the benefits are maintained with occasional ketamine “boosters,” an approach backed by research. The goal is to relieve pain while helping patients learn new strategies for how to live with it.

“When used mindfully,” says Dr. Weiner, “ketamine, through its dissociative effects, allows patients a time-out from their pain. Yes, it’s temporary, but being able to take a break from intense pain also gives them a chance to see it from a different perspective. It’s not who they are. It’s not their identity. Ketamine disrupts the static and unproductive patterns with which patients deal with their pain and encourages the development of better life strategies. What we’re really doing is teaching them resilience.”

A Remarkable Drug

Unlike Dr. Weiner’s other patients, Irv Rosenfeld has her blessing to treat himself orally with ketamine at his own home. The fact that she makes an exception in Irv’s case is a testament to her admiration and respect for Rosenfeld, who has been under Dr. Weiner’s pain management care for many years.

Every five days or so, when the pain in his bones gets really bad, Irv texts his wife Debbie before he drives home from work: I’m doing ketamine tonight. Debbie knows to stay close by yet out of his way. In order to “do ketamine,” Rosenfeld needs complete isolation and quiet. Once at his house in Fort Lauderdale, he will put on some classical music. Then he’ll place one-and-a-half sublingual tablets containing a total of 300 milligrams of ketamine between his cheek and gum, sit down in a comfortable armchair, and wait for the portal to open. His flight from pain is about to take off.

About an hour passes before Rosenfeld notices any effects. When they arrive, the feelings are both physical and emotional. He can see “the pain flow out and float far away,” he tells Project CBD. Under the influence of “forgetamine,” existential agony and exhaustion are replaced by euphoric hallucinations lasting several hours with his eyes closed.

Rosenfeld accepts that the relief he gets from ketamine won’t last beyond his solitary, three-to-four-hour sit-down sessions. But the knowledge that he can occasionally be whisked away from the Land of Pain is in and of itself transformative, nourishing his innate resilience and helping him tackle life’s daily challenges.

“It’s a remarkable drug,” he says with an obvious tone of gratitude. Just as pain has influenced the course of Rosenfeld’s life, so has his outspoken activism, his efforts to get the word out about the therapeutic benefits of cannabis before most people knew much about it. And now he’s also singing the praises of ketamine. Listening to him talk is uplifting, like getting a dose of medicine you really need.

Melinda Misuraca is a Project CBD contributing writer with a past life as an old-school cannabis farmer specializing in CBD-rich cultivars. Martin A. Lee is the director of Project CBD. He’s authored and edited several books, including Smoke Signals, Acid Dreams, and The Essential Guide to CBD. © Copyright, Project CBD. May not be reprinted without permission.


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Cannabinoids for Tinnitus?

Recently my wife returned from a night out with a ringing in one ear and significantly diminished hearing. It was a sure sign of injury caused by standing too close to a speaker. She was upset with herself for being so careless and concerned that the condition would persist. For the next couple days, she got extra sleep to aid recovery, and for good measure took an extra dose or two of CBD.

For many other people of all ages, tinnitus is indeed a chronic condition that has nothing to do with loud ‘80s cover bands in small clubs. Risk factors span a wide range of physical and psychological conditions including concussion, smoking, certain medications, ear infection, high blood pressure, anxiety, depression, and, most commonly, age-related hearing loss.

And it’s not just ringing. Technically, tinnitus (pronounced tih-NITE-us or TIN-ih-tus) is the perception of sound originating from within the nervous system that’s unrelated to external stimulation. Tinnitus can also be experienced as buzzing, whirring, humming, whooshing, clicking, and hissing. Whatever the precise nature of the phantom sound, it often comes with a constellation of symptoms related to the disruption such a condition can bring: sleep problems, difficulty concentrating, low mood, etc. Estimates vary, but tens of millions of people in the United States alone likely suffer from chronic tinnitus.

My wife’s ringing tinnitus did fade, and her hearing gradually improved over the course of a few days. The CBD she took may or may not have helped, but according to a recent survey of tinnitus patients, she wasn’t alone in trying — or at least in being interested in cannabis as a potential remedy.

Auditory & Other Symptoms

The survey, whose findings were published in February 2023 in the Journal of Otolaryngology – Head & Neck Surgery1evaluated cannabis perceptions and consumption among 45 adult tinnitus patients randomly selected and recruited from an outpatient ear, nose, and throat clinic in Ontario, Canada.

Among the 45 respondents, median age 55, only 10 said they were current cannabis users (19 had never used, and 16 had used in the past). But of the 10 current users, eight reported that cannabis did help with some of their tinnitus-related symptoms — if not necessarily the sound itself. Seven of the eight found it helpful for sleep disturbances, seven for pain, six for emotional complaints, four for functional difficulties, and three for dizziness symptoms. Only three of the ten found cannabis helpful for the actual auditory symptoms characterizing tinnitus.

But many more patients were willing to try, perhaps as an indication of the intractability of chronic tinnitus. All but two of the 45 respondents said they’d consider cannabis as a treatment, with 29 seeking help for sleep disturbances, 27 for emotional complaints, 25 for functional disturbances, and nine for pain. Of note, however, 41 of the 45 said they’d turn to cannabis for auditory symptoms — the primary concern for most tinnitus patients yet the least improved by cannabis according to the survey’s 10 current users.

Interestingly, and perhaps unfortunately for patients, previous reviews in 2020 and 20192 also concluded there was insufficient evidence that cannabis can diminish chronic tinnitus.

Mixed Findings

A December 2020 review in the journal Laryngoscope Investigative Otolaryngology3 by researchers at Yale University and nearby University of Connecticut tackles the question head-on. Its title: “Does cannabis alleviate tinnitus? A review of the current literature.”

And its conclusion? “While animal studies have revealed that cannabinoid receptors likely have a role in modulating auditory signaling, there is no compelling data either from animal or human studies for the use of cannabinoids to alleviate tinnitus.”

There could be a role for cannabinoids in the management of tinnitus through their anticonvulsant effects.

In fact, there’s some evidence from animal research that cannabinoid administration may actually induce or exacerbate tinnitus. That’s what appeared to happen in rats injected with the synthetic CB1 agonists WIN55,212‐2 and CP55,940 in a 2010 study4 and THC and CBD in a 1:1 ratio in a 2011 follow-up study.5

As far as human studies, the review authors also summarize two previous surveys in 2010 and 2019, a 1975 clinical trial and a 2006 case study — whose cumulative findings are, at best, entirely unclear.

Despite all this, there is a potential biological rationale for the treatment of tinnitus with cannabinoids, the authors explain. Other animal studies have suggested that cannabinoid receptor expression in the cochlear nucleus may vary with tinnitus symptomatology. And since the most widely accepted hypothesis for the pathophysiology of tinnitus relates to something called “neuronal hyperexcitability” — a mechanism that has also been observed in epilepsy, they note — “there is a potential role of cannabinoids in the management of tinnitus through its anticonvulsant effects.”

Cannabinoid Receptors Influence Hearing

Finally, a November 2020 review in Frontiers in Neurology6 adds more complexity and subtlety to the issue. The article wisely notes that animal studies showing cannabinoids to potentially worsen tinnitus have focused on CB1 agonists. This excludes compounds that target, among others:

  • CB2 receptors, which influence immune function and are “increasingly recognized as essential in understanding nervous system pathological responses”
  • and “non-classical” cannabinoid targets like TRP (“trip”) channels, which mediate processes including vision, taste, olfaction, touch and hearing.

While the collective evidence to date is mixed and inconclusive, it’s also incomplete. The potential is huge for new animal studies using cannabinoids other than CB1 agonists, and for more robust human studies (indeed any clinical trial at all) to contribute fresh insights to this burning, buzzing question.

Nate Seltenrich, an independent science journalist based in the San Francisco Bay Area, covers a wide range of subjects including environmental health, neuroscience, and pharmacology. Copyright, Project CBD. May not be reprinted without permission.


  1. Mavedatnia, Dorsa et al. “Cannabis use amongst tinnitus patients: consumption patterns and attitudes.” Journal of otolaryngology – head & neck surgery vol. 52,1 19. 24 Feb. 2023, doi:10.1186/s40463-022-00603-8
  2. Zheng, Yiwen, and Paul F Smith. “Cannabinoid drugs: will they relieve or exacerbate tinnitus?.” Current opinion in neurology vol. 32,1 (2019): 131-136. doi:10.1097/WCO.0000000000000631
  3. Narwani, Vishal et al. “Does cannabis alleviate tinnitus? A review of the current literature.” Laryngoscope investigative otolaryngology vol. 5,6 1147-1155. 30 Oct. 2020, doi:10.1002/lio2.479
  4. Zheng, Yiwen et al. “The effects of the synthetic cannabinoid receptor agonists, WIN55,212-2 and CP55,940, on salicylate-induced tinnitus in rats.” Hearing research vol. 268,1-2 (2010): 145-50. doi:10.1016/j.heares.2010.05.015
  5. Zheng, Y et al. “Acoustic trauma that can cause tinnitus impairs impulsive control but not performance accuracy in the 5-choice serial reaction time task in rats.” Neuroscience vol. 180 (2011): 75-84. doi:10.1016/j.neuroscience.2011.02.040
  6. Perin, Paola et al. “Cannabinoids, Inner Ear, Hearing, and Tinnitus: A Neuroimmunological Perspective.” Frontiers in neurology vol. 11 505995. 23 Nov. 2020, doi:10.3389/fneur.2020.505995

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Mental Health & the CB2 Receptor

In the first part of this series, we reviewed recent research into the role of the CB2 cannabinoid receptor in cancer proliferation. This week we turn our attention to another fascinating aspect of CB2 function: its impact on psychiatric and mood disorders despite not being concentrated in the central nervous system (CNS).

After all, the CNS is the domain of its sibling, the CB1 cannabinoid receptor — the primary target of THC and the mediator of cannabis’ intoxicating effects. CB2, by contrast, is more prominently expressed in the peripheral nervous system, where it regulates inflammation, pain, and neuroprotection. CB2 is found to a much lesser extent in the brain, where it modulates dopamine signaling, neuroinflammation, and neurogenesis.

The CB2 receptor was of particular interest to visionary cannabinoid scientist Raphael Mechoulam. In the year prior to his recent passing at age 92, Mechoulam was still actively involved in research investigating CB2 in a variety of disease models. Here we look at a couple of his final papers on CB2 and mental health, as well as two related reviews published in the same timeframe.

CB2 & Schizophrenia

First comes a paper on CB2’s role in schizophrenia, a condition related to psychosis whose symptoms include hallucinations, delusions, disorganized thinking, social withdrawal, decreased emotional expression, and apathy. Coauthored by Brazilian scientists affiliated with the University of São Paulo, it appeared in the journal Progress in Neuro-Psychopharmacology & Biological Psychiatry1 in July 2022.

“The CB2 receptor modulates dopaminergic neurotransmission, which is abnormally enhanced in schizophrenia patients,” the authors explain. That much is clear. Given this, they wanted to know, how might “HU-910,” a synthetic research compound that selectively activates the CB2 receptor, affect behavior in a rodent model of the disease?

Through a series of tests, they found that HU-910 administration did indeed produce an anti-psychotic-like effect through the CB2 receptor. The authors suggest that these results “support further research on the potential therapeutic properties of this compound to treat schizophrenia.”

But their conclusion that HU-910 could serve as a drug warrants some caution. Cannabinoid receptors don’t function simply as on/off switches. As Project CBD has addressed in the past relative to proposed therapies for bone disease, Alzheimer’s Disease, and autoimmune dysfunction, selective CB2 agonists thus far have been disappointing in the clinical context due to unintended consequences and other unwelcome outcomes resulting from the receptor’s wide reach in the body.

CB2 & Depression

The very last paper bearing Mechoulam’s name before his death — among a body of work encompassing 379 total articles listed at Pubmed — concerns the role of the CB2 receptor in mediating the antidepressive effect of cannabidiolic acid-methyl ester (CBDA-ME). Titled “Cannabinoid Receptor 2 Blockade Prevents Anti-Depressive-like Effect of Cannabidiol Acid Methyl Ester in Female WKY Rats,” it appeared in the February 2023 special issue of the International Journal of Molecular Sciences,2 which explored the biological mechanisms of cannabinoids in mental health.

CBDA-ME is a stable synthetic analogue of cannabidiolic acid (CBDA), the raw, unheated version of CBD present in cannabis flower. (The fact that CBDA becomes CBD in the presence of sunlight or heat makes it difficult to study, hence the need for a more stable CBDA-related compound.) First described in 19693 by Mechoulam and a coauthor, CBDA-ME has in recent years been shown to exert anxiolytic,4 anti-hyperalgesic,5 and anti-depressive6 effects in male rodents at low doses.

The Israel-based authors assessed the antidepressant effect of CBDA-ME in mice through a common laboratory model known as the “forced swim test.” Among the authors’ findings, one stands out (and makes its way into the paper’s title): a synthetic CB2 antagonist called “AM-630” blocked CBDA-ME’s anti-depressive effect in female rats, but not in males, indicating that the CB2 receptor is involved in mediating the compound’s effect.

Does this suggest that CB2 activation — perhaps indirectly triggered by CBD or CBDA as well as CBDA-ME — could help fight depression, at least in women? Possibly, the authors conclude, but “the cumulative data indicate that these pathways are still ambiguous and require future research in order to fully understand the mechanisms of action of acute CBDA-ME in relieving the symptoms of depression.”

Targeting CB2 in CNS Disorders

Two other reviews from 2022 provide a broader perspective on CB2’s role in several emotional, cognitive, and psychiatric disorders — from addiction and anxiety to Huntington’s and Parkinson’s diseases.

A report published in the International Journal of Molecular Sciences, coauthored by Emmanuel Onaivi at William Patterson University in New Jersey and a team of Japanese scientists, concludes that CB2 receptors “are highly expressed in neuropsychiatric and neurodegenerative disorders, and that selective CB2 ligands have promising effects on the symptomatic management of these disorders.”

However, given the potential for such drugs to have significant side effects, the authors also recommend further study of cannabis-derived compounds to target CB2 in tandem with CB1, as well as less directly through the broader endocannabinoid system.

Next, an April 2022 review in Frontiers in Psychiatry7 notes that recent findings of CB2’s presence in several brain areas and different brain cell types, including neurons and glia, indicate that “CB2 may closely relate the immune system and the brain circuits regulating inflammation, mood, and cognitive functions.” This receptor is particularly implicated in neuropsychiatric diseases associated with neuroinflammation, according to the European scientists, who conclude that future research should continue to zero in on the critical link between CB2, inflammation, and psychiatric disorders.

Read part 1 of this 2-part series: Cancer & the CB2 Receptor

Nate Seltenrich, an independent science journalist based in the San Francisco Bay Area, covers a wide range of subjects including environmental health, neuroscience, and pharmacology. Copyright, Project CBD. May not be reprinted without permission.


  1. Cortez, Isadora Lopes et al. “HU-910, a CB2 receptor agonist, reverses behavioral changes in pharmacological rodent models for schizophrenia.” Progress in neuro-psychopharmacology & biological psychiatry vol. 117 (2022): 110553. doi:10.1016/j.pnpbp.2022.110553
  2. Hen-Shoval, Danielle et al. “Cannabinoid Receptor 2 Blockade Prevents Anti-Depressive-like Effect of Cannabidiol Acid Methyl Ester in Female WKY Rats.” International journal of molecular sciences vol. 24,4 3828. 14 Feb. 2023, doi:10.3390/ijms24043828
  3. Mechoulam, R et al. “Carboxylation of resorcinols with methylmagnesium carbonate. Synthesis of cannabinoid acids.” Journal of the chemical society D: chemical communications vol. 1,7 (1969): 343-344. doi:10.1039/C29690000343
  4. Pertwee, Roger G et al. “Cannabidiolic acid methyl ester, a stable synthetic analogue of cannabidiolic acid, can produce 5-HT1A receptor-mediated suppression of nausea and anxiety in rats.” British journal of pharmacology vol. 175,1 (2018): 100-112. doi:10.1111/bph.14073
  5. Zhu, Yong Fang et al. “An evaluation of the anti-hyperalgesic effects of cannabidiolic acid-methyl ester in a preclinical model of peripheral neuropathic pain.” British journal of pharmacology vol. 177,12 (2020): 2712-2725. doi:10.1111/bph.14997
  6. Hen-Shoval, D et al. “Acute oral cannabidiolic acid methyl ester reduces depression-like behavior in two genetic animal models of depression.” Behavioural brain research vol. 351 (2018): 1-3. doi:10.1016/j.bbr.2018.05.027
  7. Kibret, Berhanu Geresu et al. “New Insights and Potential Therapeutic Targeting of CB2 Cannabinoid Receptors in CNS Disorders.” International journal of molecular sciences vol. 23,2 975. 17 Jan. 2022, doi:10.3390/ijms23020975
  8. Morcuende, Alvaro et al. “Immunomodulatory Role of CB2 Receptors in Emotional and Cognitive Disorders.” Frontiers in psychiatry vol. 13 866052. 15 Apr. 2022, doi:10.3389/fpsyt.2022.866052

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