The use of cannabinoids has a history spanning thousands of years, and their pharmacological and toxicological properties, particularly those of THC and CBD, are well-documented. However, their potential to induce drug-drug interactions remains underexplored. This review aims to provide a comprehensive perspective by contextualizing the historical and pharmacological significance of cannabinoids while focusing on their capacity to modulate the metabolic activity of cytochrome P450 isoforms relevant to drug metabolism. Additionally, we look at the impact of cannabinoids in neuronal circuits impacting the hypothalamic-pituitary hormonal axis, such as the locus coeruleus and raphe nuclei and their possible consequences on the cytochrome P450 system. Recognising potential interactions between cannabinoids and other drugs could enhance understanding of their pharmacological effects, improve the efficacy and safety profiles of cannabinoid-based therapies, and encourage further exploration into this under-researched area of psychopharmacology, with implications for both preclinical research and clinical practice.

• Publication type
• Journal Article MeSH
• Review MeSH

Alterations in the excitability of dorsal root ganglion (DRG) neurons are critical in the pathogenesis of acute and chronic pain. Neurotransmitter release from the terminals of DRG neurons is regulated by cannabinoid receptor 1 (CB1) and transient receptor potential vanilloid 1 (TRPV1), both activated by anandamide (AEA). In our experiments, the AEA precursor N-arachidonoylphosphatidylethanolamine (20:4-NAPE) was used to study the modulation of nociceptive DRG neurons excitability using K+-evoked Ca2+ transients. Intrathecal administration was used to evaluate in vivo effects. Application of 20:4-NAPE at lower concentrations (10 nM - 1 μM) decreased the excitability of DRG neurons, whereas the higher (10 μM) increased it. Both effects of 20:4-NAPE were blocked by the N-acylphosphatidylethanolamine phospholipase D (NAPE-PLD) inhibitor LEI-401. Similarly, lower concentrations of externally applied AEA (1 nM - 10 nM) inhibited DRG neurons, whereas higher concentration (100 nM) did not change it. High AEA concentration (10 μM) evoked Ca2+ transients dependent on TRPV1 activation in separate experiments. Inhibition of the CB1 receptor by PF514273 (400 nM) prevented the 20:4-NAPE- and AEA-induced inhibition, whereas TRPV1 inhibition by SB366791 (1 μM) prevented the increased DRG neuron excitability. In behavioral tests, lower 20:4-NAPE concentration caused hyposensitivity, while higher evoked mechanical allodynia. Intrathecal LEI-401 prevented both in vivo effects of 20:4-NAPE. These results highlight anti- and pro-nociceptive effects of 20:4-NAPE mediated by CB1 and TRPV1 in concentration-dependent manner. Our study underscores the complexity of endocannabinoid signaling in pain transmission modulation and highlights 20:4-NAPE as a potential therapeutic target, offering new insights for developing analgesic strategies.

• MeSH
• Endocannabinoids pharmacology   metabolism   MeSH
• Phosphatidylethanolamines * pharmacology   MeSH
• Phospholipase D * metabolism   antagonists & inhibitors   MeSH
• TRPV Cation Channels metabolism   MeSH
• Rats MeSH
• Arachidonic Acids * pharmacology   MeSH
• Neurons * drug effects   metabolism   MeSH
• Polyunsaturated Alkamides pharmacology   MeSH
• Rats, Sprague-Dawley MeSH
• Receptor, Cannabinoid, CB1 metabolism   MeSH
• Ganglia, Spinal * drug effects   metabolism   cytology   MeSH
• Calcium metabolism   MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Male MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH

Konopí seté (Cannabis sativa) je rostlina, která byla do 19. století v Čechách i na Moravě zdrojem suroviny pro výrobu textilního materiálu kanafasu. S rozvojem výzkumu endokanabinoidního systému se tato rostlina dostává opět do popředí zájmu. Endokanabinoidní systém ovlivňuje homeostázu celého organismu na bázi modulace aktivity jiných neurotransmiterů, např. nocicepci, kognici, spasticitu, spánek aj. Kanabinoidní receptory se nachází v periferním (CB2) i centrálním nervovém systému (CB1), ale i v pojivových tkáních a imunitním systému. Nejznámějšími účinnými molekulami je delta-9-tetrahydrokanabinol (THC) a kanabidiol (CBD). Prezentuji kazuistiku pacienta s chronickými vertebrogenními obtížemi a polyneuropatií dolních končetin doprovázenou neuropatickou bolestí. Léčebné konopí v monoterapii nebo kombinované terapii může být dobrou volbou pro pacienty při léčbě neuropatické bolesti v individualizované léčbě.

Hemp (Cannabis sativa) is a herb which was used for the production of canvas until the 19th century in Bohemia and Moravia. The progress in research focused on endocanabinoid system brings this herb into the focus again. Endocanabinoid system influences homeostasis of the whole organism due to modulation of neurotransmiter activity and subsequently the nociception, cognition, spasticity, sleep etc. Cannabinoid receptors are situated in the peripheral (CB2) and central nervous system (CB1), as well as in the connective tissue and immune system. The best-known effective molecules are delta-9-tetrahydrocanabinol (THC) and cannabidiol (CBD). I present a case report of a patient with chronic vertebrogenic problems and polyneuropathy of the lower extremities accompanied by neuropathic pain. Medical cannabis in monotherapy or in combination therapy can be a good choice for patients with neuropathic pain in individualized treatment.

• MeSH
• Cannabis * MeSH
• Endocannabinoids pharmacology   therapeutic use   MeSH
• Cannabidiol metabolism   therapeutic use   MeSH
• Case Reports as Topic MeSH
• Humans MeSH
• Medical Marijuana * pharmacology   therapeutic use   MeSH
• Neuralgia diagnosis   drug therapy   MeSH
• Receptors, Cannabinoid MeSH
• Dronabinol metabolism   therapeutic use   MeSH
• Check Tag
• Humans MeSH
• Male MeSH
• Publication type
• Review MeSH

Introduction: Rheumatoid arthritis (RA) is a chronic autoimmune disease with unknown cause. It mainly affects joints and, without proper treatment, negatively impacts their movement, causes painful deformities, and reduces the patients' quality of life. Current treatment options consist of various types of disease-modifying antirheumatic drugs (DMARDs), however 20-30% of patients are partially resistant to them. Therefore, development of new drugs is necessary. Possible option are compounds exhibiting their action via endocannabinoid system, which plays an important role in pain and inflammation modulation. One such compound - cannabidiol (CBD) has already been shown to attenuate synovitis in animal model of RA in in vivo studies. However, it has low bioavailability due to its low water solubility and lipophilicity. This issue can be addressed by preparation of a lipid containing formulation targeting lymphatic system, another route of absorption in the body. Materials and Methods: CBD-containing emulsion was prepared by high-shear homogenization and its droplet size distribution was analysed by optical microscopy. The relative oral bioavailability compared to oil solution as well as total availability of CBD were assessed in a cross-over study in rats and absorption of CBD via lymphatic system was observed. The effect of CBD on the animal model of RA was determined. Results: Compared to oil solution, the emulsion exhibited higher absolute oral bioavailability. Significant lymphatic transport of CBD was observed in all formulations and the concentrations in lymph were calculated. The therapeutic effect of CBD on RA was confirmed as an improvement in clinical symptoms as well as morphological signs of disease activity were observed during the study. Conclusion: In this work, we prepared a simple stable emulsion formulation, determined the pharmacokinetic parameters of CBD and calculated its absolute bioavailability in rats. Moreover, we successfully tested the pharmaceutical application of such a formulation and demonstrated the positive effect of CBD in an animal model of RA.

• MeSH
• Administration, Oral MeSH
• Pain drug therapy   MeSH
• Emulsions MeSH
• Cannabidiol * pharmacology   chemistry   MeSH
• Cross-Over Studies MeSH
• Rats MeSH
• Quality of Life MeSH
• Arthritis, Rheumatoid * drug therapy   MeSH
• Water MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH

Cíl: Při vývoji nových anxiolytik je slibným terapeutickým cílem endokanabinoidní systém (ECS) především díky své schopnosti modulace synaptické plasticity a schopnosti retrográdně regulovat ostatní neurotransmiterové systémy. Farmakologicky lze cílit agonisticky a antagonisticky na receptory CB1 a CB2, případně inhibičně na enzymy FAAH a MAGL, které se podílejí na degradaci endokanabinoidů. Cílem tohoto sdělení je podat ucelený systematický přehled o klinickém využití endokanabinoid-ního systému jako farmakoterapeutického cíle u poruch úzkostného spektra (posttraumatická stresová porucha, generalizovaná úzkostná porucha, sociální fobie a panická porucha). Metoda: V květnu 2023 bylo provedeno systematické vyhledávání v databázích Medline (PubMed) a Web of Science (WOS). Byla použita klíčová slova "(cannabinoid* OR endocannabinoid* OR cannabidiol* OR tetrahydrocannabinol*) AND ((PTSD OR posttraumatic stress disorder) OR (GAD OR generalized anxiety disorder) OR (PA OR panic attack) OR (SAD OR social anxiety disorder))" v polích "Title OR Abstract". Mezi vylučovací kritéria patřily publikace psané v jiném jazyce než v anglickém, publikace jednotlivých kazuistik, konferenční abstrakta a preklinické studie. Do přehledového článku tak byly zařazeny prospektivní, retrospektivní, randomizované kontrolované studie, v nichž byly použity stanovené dávky kanabinoidů nebo kombinace ligandů kanabinoidních receptorů. Výsledky: Pomocí databází Medline a Web of Science bylo vyhledáno 420 a 458 publikací, z nichž bylo po přezkoumání vyřazeno 410 a 454 publikací pro nesplnění selekčních kritérií. Do přehledu bylo zařazeno 10 publikací, které se týkaly daného tématu. Bylo publikováno 6 studií, které sledovaly účinnost kanabinoidů v terapii PTSD, další 4 studie se zabývaly využitím kanabinoidů v terapii SAD a GAD. Klinické studie v terapii panické poruchy nebyly dosud provedeny. Závěr: Na základě výsledků dosud publikovaných klinických studií se ukazuje, že endokanabinoidy jsou v posledních letech testovány v klinických studiích jako alternativní nebo komplementární terapie v indikaci poruch úzkostného spektra, konkrétně PTSD, GAD a SAD. Byly provedeny čtyři randomizované klinické studie, které sledovaly efekt kanabinoidů v terapii SAD, ve kterých se prokázala účinnost kanabidiolu. Ze šesti otevřených nebo retrospektivních studií sledujících účinek kanabinoidů v terapii PTSD prokázal ve třech studiích účinnost nabilon (tetrahydrokanabinol). V dalších třech studiích se účinek prokázal, avšak nebyl statisticky hodnocen/hodnotitelný. Příznivé výsledky studií mohou být ovlivněny nízkým počtem subjektů a u některých studií také absencí kontrolní skupiny. Dále některé studie učinily závěry na základě závislosti efektu na dávce kanabinoidů s využitím neurozobrazovacích metod a subjektivního skóru při hodnocení úzkosti, aniž by byly hodnoceny plazmatické hladiny podávaných kanabinoidů. Přestože tedy dostupná data ukazují na slibný potenciál kanabinoidů v terapii úzkostných poruch, měli bychom z výše uvedených důvodů výsledky interpretovat s opatrností a pro definitivní potvrzení nálezů bude nutné vyčkat na závěry dobře designovaných prospektivních, randomizovaných a kontrolovaných studií.

In the development of novel anxiolytics, the endocannabinoid system (ECS) is a promising therapeutic target primarily due to its ability to modulate synaptic plasticity and to act as a retrograde regulator of several neurotransmitter systems. Pharmacologically, it can target at CB1 and CB2 receptors (agonistitic or antagonistic activity) or by inhibiting FAAH and MAGL enzymes, which are involved in endocannabinoid degradation. The aim of this article is to provide a comprehensive systematic review of the clinical use of the endocannabinoid system as a pharmacotherapeutic target in anxiety spectrum disorders (posttraumatic stress disorder, generalized anxiety disorder, social phobia, and panic disorder). Method: In May 2023, a systematic search through the Medline (PubMed) and Web of Science (WOS) databases was performed. The keywords used were "(cannabinoid* OR endocannabinoid* OR cannabidiol* OR tetrahydrocannabinol*) AND ((PTSD OR posttraumatic stress disorder) OR (GAD OR generalized anxiety disorder) OR (PA OR panic attack) OR (SAD OR social anxiety disorder))" in the "Title OR Abstract" fields. Exclusion criteria included non-English language records, case reports, conference abstracts, and preclinical studies. Thus, only prospective, retrospective, randomized controlled trials using fixed doses of cannabinoids or combinations of cannabinoid receptor ligands compared with placebo were included in the review article. Results: Using the Medline and Web of Science databases, 420 and 458 publications respectively were retrieved, of which 410 and 454 were excluded from the review for not meeting the inclusion criteria. Thus, ten publications that were relevant to the topic were included in the review. There were six studies dealing with cannabinoids in the treatment of PTSD and further four studies referring to the use of cannabinoids in the treatment of SAD and GAD. Clinical trials in the treatment of panic disorder have not yet been conducted. Conclusion: Based on the results of clinical trials published to date, it appears that endocannabinoids have been tested in recent years as an alternative or complementary therapy in the indications of anxiety disorders, particularly PTSD, GAD and SAD. Four randomised clinical trials, which investigated the effect of cannabinoids in the treatment of SAD, found cannabidiol to be effective. Out of the six open-label or retrospective studies evaluating the effect of cannabinoids in the treatment of PTSD, nabilone or tetrahydrocannabinol have demonstrated efficacy in three studies. The remaining three studies showed clinical effect however not statistically significant or assessable. The favourable results of the studies may be affected by the low number of subjects and, in some studies, the absence of a control group. In addition, some studies have drawn conclusions based on the dose-response relationship with the use of measures such as neuroimaging and subjective scores on anxiety assessments, without assessing plasma levels of administered cannabinoids. Thus, although the available data suggest a promising potential for cannabinoids in the treatment of anxiety disorders, we should interpret the results with caution for the reasons mentioned above. Thus to draw evidence-based conclusions for clinical practice, it will be necessary to wait for the results of well-designed prospective, randomized, controlled trials to confirm the findings definitively.

Generalizovaná úzkostná porucha (GAD) je častá psychiatrická porucha, charakterizovaná přítomností obecných a nadměrných obav. Současná léčba se skládá z řady farmakologických a psychologických léčebných postupů. Mnoho pacientů však nereaguje na farmakologickou léčbu první linie a vyvíjejí se nová anxiolytická léčiva. V tomto přehledovém článku se autoři nejprve zabývají diagnostickými kritérii a epidemiologií GAD. Pozornost je věnována účinné farmakologické léčbě GAD a její snášenlivosti. K dispozici je řada účinných způsobů léčby GAD, zejména duloxetin, escitalopram, pregabalin, quetiapin a venlafaxin. Existuje omezená důkazní základna, která by podporovala další farmakologickou léčbu pacientů s GAD, kteří nereagovali na počáteční léčbu. Ačkoli mnoho nových anxiolytik postoupilo do klinických studií, překlad ze zvířecích modelů byl většinou neúspěšný. Potenciál má několik sloučenin včetně některých psychedelik, ketaminu, oxytocinu a látek modulujících orexin, endokanabinoidní a imunitní systém si však zaslouží další studium. Těmto látkám bude věnován příští článek.

Generalized anxiety disorder (GAD) is a frequent psychiatric condition characterized by the presence of generalized anxiety and excessive worry. Current treatment consists of a range of pharmacological and psychological treatments. However, many patients do not respond to first-line pharmacological treatment and new anxiolytic drugs are being developed. In this review article, the authors first address the diagnostic criteria and epidemiology of GAD. Attention is paid to the effective pharmacological treatment of GAD and its tolerability. A number of effective treatments for GAD are available, notably duloxetine, escitalopram, pregabalin, quetiapine and venlafaxine. There is a limited evidence base to support further pharmacological treatment of patients with GAD who have not responded to initial treatment. Although many new anxiolytics have advanced to clinical trials, translation from animal models has mostly been unsuccessful. However, the potential of several compounds including some psychedelics, ketamine, oxytocin, and orexin, endocannabinoid, and immune system modulators deserves further study. The next article will be devoted to these substances.

• Keywords
• generalizovaná úzkostná porucha,
• MeSH
• Anti-Anxiety Agents * pharmacology   classification   adverse effects   therapeutic use   MeSH
• Clinical Studies as Topic MeSH
• Humans MeSH
• Drug Tolerance MeSH
• Anxiety Disorders * diagnosis   epidemiology   drug therapy   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Review MeSH

Three decades ago, the first endocannabinoid, anandamide (AEA), was identified, and its analgesic effect was recognized in humans and preclinical models. However, clinical trial failures pointed out the complexity of the AEA-induced analgesia. The first synapses in the superficial laminae of the spinal cord dorsal horn represent an important modulatory site in nociceptive transmission and subsequent pain perception. The glutamatergic synaptic transmission at these synapses is strongly modulated by two primary AEA-activated receptors, cannabinoid receptor 1 (CB1) and transient receptor potential vanilloid 1 (TRPV1), both highly expressed on the presynaptic side formed by the endings of primary nociceptive neurons. Activation of these receptors can have predominantly inhibitory (CB1) and excitatory (TRPV1) effects that are further modulated under pathological conditions. In addition, dual AEA-mediated signaling and action may occur in primary sensory neurons and dorsal horn synapses. AEA application causes balanced inhibition and excitation of primary afferent synaptic input on superficial dorsal horn neurons in normal conditions, whereas peripheral inflammation promotes AEA-mediated inhibition. This review focuses mainly on the modulation of synaptic transmission at the spinal cord level and signaling in primary nociceptive neurons by AEA via CB1 and TRPV1 receptors. Furthermore, the spinal analgesic effect in preclinical studies and clinical aspects of AEA-mediated analgesia are considered.

• MeSH
• Endocannabinoids * metabolism   MeSH
• TRPV Cation Channels metabolism   MeSH
• Arachidonic Acids * metabolism   pharmacology   MeSH
• Humans MeSH
• Spinal Cord * metabolism   drug effects   MeSH
• Synaptic Transmission * physiology   drug effects   MeSH
• Nociception physiology   drug effects   MeSH
• Nociceptors metabolism   drug effects   physiology   MeSH
• Polyunsaturated Alkamides * metabolism   MeSH
• Receptor, Cannabinoid, CB1 metabolism   MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Review MeSH

Hypofunctioning of NMDA receptors, and the resulting shift in the balance between excitation and inhibition, is considered a key process in the pathophysiology of schizophrenia. One important manifestation of this phenomenon is changes in neural oscillations, those above 30 Hz (i.e., gamma-band oscillations), in particular. Although both preclinical and clinical studies observed increased gamma activity following acute administration of NMDA receptor antagonists, the relevance of this phenomenon has been recently questioned given the reduced gamma oscillations typically observed during sensory and cognitive tasks in schizophrenia. However, there is emerging, yet contradictory, evidence for increased spontaneous gamma-band activity (i.e., at rest or under baseline conditions). Here, we use the sub-chronic phencyclidine (PCP) rat model for schizophrenia, which has been argued to model the pathophysiology of schizophrenia more closely than acute NMDA antagonism, to investigate gamma oscillations (30-100 Hz) in the medial prefrontal cortex of anesthetized animals. While baseline gamma oscillations were not affected, oscillations induced by train stimulation of the posterior dorsal CA1 (pdCA1) field of the hippocampus were enhanced in PCP-treated animals (5 mg/kg, twice daily for 7 days, followed by a 7-day washout period). This effect was reversed by pharmacological enhancement of endocannabinoid levels via systemic administration of URB597 (0.3 mg/kg), an inhibitor of the catabolic enzyme of the endocannabinoid anandamide. Intriguingly, the pharmacological blockade of CB1 receptors by AM251 unmasked a reduced gamma oscillatory activity in PCP-treated animals. The findings are consistent with the observed effects of URB597 and AM251 on behavioral deficits reminiscent of the symptoms of schizophrenia and further validate the potential for cannabinoid-based drugs as a treatment for schizophrenia.

• MeSH
• Amidohydrolases * antagonists & inhibitors   metabolism   MeSH
• Excitatory Amino Acid Antagonists pharmacology   administration & dosage   MeSH
• Benzamides * pharmacology   MeSH
• Endocannabinoids metabolism   MeSH
• Phencyclidine * pharmacology   MeSH
• Gamma Rhythm physiology   drug effects   MeSH
• Carbamates * pharmacology   MeSH
• Rats MeSH
• Arachidonic Acids metabolism   pharmacology   MeSH
• Disease Models, Animal MeSH
• Piperidines * pharmacology   MeSH
• Polyunsaturated Alkamides metabolism   pharmacology   MeSH
• Rats, Sprague-Dawley MeSH
• Prefrontal Cortex drug effects   metabolism   physiopathology   MeSH
• Pyrazoles pharmacology   MeSH
• Schizophrenia * physiopathology   metabolism   drug therapy   MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Male MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH

Anandamide (AEA) is an important modulator of nociception in the spinal dorsal horn, acting presynaptically through Cannabinoid (CB1) and Transient receptor potential vanilloid (TRPV1) receptors. The role of AEA (1 μM, 10 μM, and 30 μM) application on the modulation of nociceptive synaptic transmission under control and inflammatory conditions was studied by recording miniature excitatory postsynaptic currents (mEPSCs) from neurons in spinal cord slices. Inhibition of the CB1 receptors by PF514273, TRPV1 by SB366791, and the fatty acid amide hydrolase (FAAH) by URB597 was used. Under naïve conditions, the AEA application did not affect the mEPSCs frequency (1.43±0.12 Hz) when all the recorded neurons were considered. The mEPSC frequency increased (180.0±39.2%) only when AEA (30 μM) was applied with PF514273 and URB597. Analysis showed that one sub-population of neurons had synaptic input inhibited (39.1% of neurons), the second excited (43.5%), whereas 8.7% showed a mixed effect and 8.7% did not respond to the AEA. With inflammation, the AEA effect was highly inhibitory (72.7%), while the excitation was negligible (9.1%), and 18.2% were not modulated. After inflammation, more neurons (45.0%) responded even to low AEA by mEPSC frequency increase with PF514273/URB597 present. AEA-induced dual (excitatory/inhibitory) effects at the 1st nociceptive synapse should be considered when developing analgesics targeting the endocannabinoid system. These findings contrast the clear inhibitory effects of the AEA precursor 20:4-NAPE application described previously and suggest that modulation of endogenous AEA production may be more favorable for analgesic treatments.

• MeSH
• Amidohydrolases MeSH
• Analgesics pharmacology   MeSH
• Benzamides * MeSH
• Endocannabinoids * pharmacology   MeSH
• Carbamates * MeSH
• Arachidonic Acids * MeSH
• Humans MeSH
• Nociception * MeSH
• Polyunsaturated Alkamides pharmacology   MeSH
• Spinal Cord Dorsal Horn MeSH
• Inflammation drug therapy   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH

Kanabinoidy, aktivní složky rostliny Cannabis, ovlivňují širokou škálu fyziologických procesů prostřednictvím endokanabinoidního systému, který zahrnuje receptory CB1 a CB2, endogenní ligandy a regulační enzymy. Tento přehledový článek shrnuje mechanismy působení fytokanabinoidů, syntetických kanabinoidů a endokanabi noidů, včetně jejich farmakologických vlastností, terapeutického potenciálu a rizik spojených s jejich použitím. Diskutována je také toxicita syntetických kanabinoidů, jejichž rekreační užívání představuje významnou hrozbu pro veřejné zdraví. Závěrem jsou uvedeny současné aplikace kanabinoidů v klinické praxi, zejména při léčbě bolesti, nevolnosti a neurologických onemocnění.

Cannabinoids, active compounds of the Cannabis plant, influence a wide range of physiological processes through the endocannabinoid system, comprising CB1 a CB2 receptors, endogenous ligands, and regulatory enzymes. This review summarizes the mechanisms of action of phytocannabinoids, synthetic cannabinoids, and endo­cannabinoids, including their pharmacological properties, therapeutic potential, and associated risks. The article also discusses the toxicity of synthetic cannabinoids, highlighting the public health threat posed by their recreational use. Finally, it explores current clinical applications of cannabinoids, particularly in the treatment of pain, nausea, and neurological disorders.

• Keywords
• syntetické kanabinoidy,
• MeSH
• Endocannabinoids pharmacology   therapeutic use   MeSH
• Cannabinoids pharmacology   therapeutic use   MeSH
• Humans MeSH
• Medical Marijuana * pharmacology   therapeutic use   MeSH
• Receptor, Cannabinoid, CB1 MeSH
• Receptor, Cannabinoid, CB2 MeSH
• Check Tag
• Humans MeSH
• Publication type
• Review MeSH