Relevant bibliographies by topics / Cannabinoid CB1 receptor

Academic literature on the topic 'Cannabinoid CB1 receptor'

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Published: 11 March 2023

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Journal articles on the topic "Cannabinoid CB1 receptor"

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Soraya, hiva, Ruohollah Seddigh, Fatemeh Hadi, and Mohammad Faramarzi. "Chemical cannabis; The New Trend of addiction in Iran." Iranian Journal of Psychiatry and Clinical Psychology 28, no. 1 (April 20, 2022): 10. http://dx.doi.org/10.32598/ijpcp.28.1.4010.1.

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Synthetic cannabinoids (SC) are a heterogeneous group of substances with a high affinity for cannabinoid receptors. Unlike Δ9-tetrahydrocannabinol (THC), synthetic cannabinoids are incredibly potent, highly productive, have more affinity for the Cannabinoid receptor type 1 (CB1), and Cannabinoid receptor type 2 (CB2), and are designed to accelerate the effects of tetrahydrocannabinol. Also, there is experimental evidence that SCs acts on non-cannabinoid receptors, such as the 5-HT2B receptor or dopaminergic receptors. (1, 2).
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Walsh, Kenneth B., and Andrea E. Holmes. "Pharmacology of Minor Cannabinoids at the Cannabinoid CB1 Receptor: Isomer- and Ligand-Dependent Antagonism by Tetrahydrocannabivarin." Receptors 1, no. 1 (August 2, 2022): 3–12. http://dx.doi.org/10.3390/receptors1010002.

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(1) Background: In addition to the major phytocannabinoids, trans-Δ9-tetrahydrocannabinol (Δ9-THC) and cannabidiol (CBD), the cannabis plant (Cannabis sativa L.) synthesizes over 120 additional cannabinoids that are known as minor cannabinoids. These minor cannabinoids have been proposed to act as agonists and antagonists at numerous targets including cannabinoid type 1 (CB1) and type 2 (CB2) receptors, transient receptor potential (TRP) channels and others. The goal of the present study was to determine the agonist effects of the minor cannabinoids: cannabinol (CBN), cannabigerol (CBG), cannabichromene (CBC), cannabitriol (CBT) and cannabidivarin (CBDV) at the CB1 receptor. In addition, the CB1 receptor antagonist effects of Δ9-tetrahydrocannabivarin (Δ9-THCV) were compared with its isomer Δ8-tetrahydrocannabivarin (Δ8-THCV). (2) Methods: CB1 receptor activity was monitored by measuring cannabinoid activation of G protein-gated inward rectifier K+ (GIRK) channels in AtT20 pituitary cells using a membrane potential-sensitive fluorescent dye assay. (3) Results: When compared to the CB1 receptor full agonist WIN 55,212-2 and the partial agonist Δ9-THC, none of the minor cannabinoids caused a significant activation of Gi/GIRK channel signaling. However, Δ9-THCV and Δ8-THCV antagonized the effect of WIN 55,212-2 with half-maximal inhibitory concentrations (IC50s) of 434 nM and 757 nM, respectively. Δ9-THCV antagonism of the CB1 receptor was “ligand-dependent”; Δ9-THCV was more potent in inhibiting WIN 55,212-2 and 2-arachidonoylglycerol (2-AG) than Δ9-THC. (4) Conclusions: While none of the minor cannabinoids caused Gi/GIRK channel activation, Δ9-THCV antagonized the CB1 receptor in an isomer- and ligand-dependent manner.
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Li, Yong, and Jimok Kim. "CB2 Cannabinoid Receptor Knockout in Mice Impairs Contextual Long-Term Memory and Enhances Spatial Working Memory." Neural Plasticity 2016 (2016): 1–14. http://dx.doi.org/10.1155/2016/9817089.

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Neurocognitive effects of cannabinoids have been extensively studied with a focus on CB1 cannabinoid receptors because CB1 receptors have been considered the major cannabinoid receptor in the nervous system. However, recent discoveries of CB2 cannabinoid receptors in the brain demand accurate determination of whether and how CB2 receptors are involved in the cognitive effects of cannabinoids. CB2 cannabinoid receptors are primarily involved in immune functions, but also implicated in psychiatric disorders such as schizophrenia and depression. Here, we examined the effects of CB2 receptor knockout in mice on memory to determine the roles of CB2 receptors in modulating cognitive function. Behavioral assays revealed that hippocampus-dependent, long-term contextual fear memory was impaired whereas hippocampus-independent, cued fear memory was normal in CB2 receptor knockout mice. These mice also displayed enhanced spatial working memory when tested in a Y-maze. Motor activity and anxiety of CB2 receptor knockout mice were intact when assessed in an open field arena and an elevated zero maze. In contrast to the knockout of CB2 receptors, acute blockade of CB2 receptors by AM603 in C57BL/6J mice had no effect on memory, motor activity, or anxiety. Our results suggest that CB2 cannabinoid receptors play diverse roles in regulating memory depending on memory types and/or brain areas.
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SMALL-HOWARD, Andrea L., Lori M. N. SHIMODA, Chaker N. ADRA, and Helen TURNER. "Anti-inflammatory potential of CB1-mediated cAMP elevation in mast cells." Biochemical Journal 388, no. 2 (May 24, 2005): 465–73. http://dx.doi.org/10.1042/bj20041682.

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Cannabinoids are broadly immunosuppressive, and anti-inflammatory properties have been reported for certain marijuana constituents and endogenously produced cannabinoids. The CB2 cannabinoid receptor is an established constituent of immune system cells, and we have recently established that the CB1 cannabinoid receptor is expressed in mast cells. In the present study, we sought to define a role for CB1 in mast cells and to identify the signalling pathways that may mediate the suppressive effects of CB1 ligation on mast cell activation. Our results show that CB1 and CB2 mediate diametrically opposed effects on cAMP levels in mast cells. The observed long-term stimulation of cAMP levels by the Gαi/o-coupled CB1 is paradoxical, and our results indicate that it may be attributed to CB1-mediated transcriptional regulation of specific adenylate cyclase isoenzymes that exhibit superactivatable kinetics. Taken together, these results reveal the complexity in signalling of natively co-expressed cannabinoid receptors and suggest that some anti-inflammatory effects of CB1 ligands may be attributable to sustained cAMP elevation that, in turn, causes suppression of mast cell degranulation.
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Dobovišek, Luka, Fran Krstanović, Simona Borštnar, and Nataša Debeljak. "Cannabinoids and Hormone Receptor-Positive Breast Cancer Treatment." Cancers 12, no. 3 (February 25, 2020): 525. http://dx.doi.org/10.3390/cancers12030525.

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Breast cancer (BC) is the most common cancer in women worldwide. Approximately 70–80% of BCs express estrogen receptors (ER), which predict the response to endocrine therapy (ET), and are therefore hormone receptor-positive (HR+). Endogenous cannabinoids together with cannabinoid receptor 1 and 2 (CB1, CB2) constitute the basis of the endocannabinoid system. Interactions of cannabinoids with hypothalamic–pituitary–gonadal axis hormones are well documented, and two studies found a positive correlation between peak plasma endogenous cannabinoid anandamide with peak plasma 17β-estradiol, luteinizing hormone and follicle-stimulating hormone levels at ovulation in healthy premenopausal women. Do cannabinoids have an effect on HR+ BC? In this paper we review known and possible interactions between cannabinoids and specific HR+ BC treatments. In preclinical studies, CB1 and CB2 agonists (i.e., anandamide, THC) have been shown to inhibit the proliferation of ER positive BC cell lines. There is less evidence for antitumor cannabinoid action in HR+ BC in animal models and there are no clinical trials exploring the effects of cannabinoids on HR+ BC treatment outcomes. Two studies have shown that tamoxifen and several other selective estrogen receptor modulators (SERM) can act as inverse agonists on CB1 and CB2, an interaction with possible clinical consequences. In addition, cannabinoid action could interact with other commonly used endocrine and targeted therapies used in the treatment of HR+ BC.
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GÓMEZ DEL PULGAR, Teresa, Guillermo VELASCO, and Manuel GUZMÁN. "The CB1 cannabinoid receptor is coupled to the activation of protein kinase B/Akt." Biochemical Journal 347, no. 2 (April 10, 2000): 369–73. http://dx.doi.org/10.1042/bj3470369.

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Cannabinoids exert most of their effects in the central nervous system through the CB1 cannabinoid receptor. This G-protein-coupled receptor has been shown to be functionally coupled to inhibition of adenylate cyclase, modulation of ion channels and activation of extracellular-signal-regulated kinase. Using Chinese hamster ovary cells stably transfected with the CB1 receptor cDNA we show here that ∆9-tetrahydrocannabinol (THC), the major active component of marijuana, induces the activation of protein kinase B/Akt (PKB). This effect of THC was also exerted by the endogenous cannabinoid anandamide and the synthetic cannabinoids CP-55940 and HU-210, and was prevented by the selective CB1 antagonist SR141716. Pertussis toxin and wortmannin blocked the CB1 receptor-evoked activation of PKB, pointing to the sequential involvement of a Gi/Go protein and phosphoinositide 3ʹ-kinase. The functionality of the cannabinoid-induced stimulation of PKB was proved by the increased phosphorylation of glycogen synthase kinase-3 serine 21 observed in cannabinoid-treated cells and its prevention by SR141716 and wortmannin. Cannabinoids activated PKB in the human astrocytoma cell line U373 MG, which expresses the CB1 receptor, but not in the human promyelocytic cell line HL-60, which expresses the CB2 receptor. Data indicate that activation of PKB may be responsible for some of the effects of cannabinoids in cells expressing the CB1 receptor.
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Bow, Eric W., and John M. Rimoldi. "The Structure–Function Relationships of Classical Cannabinoids: CB1/CB2 Modulation." Perspectives in Medicinal Chemistry 8 (January 2016): PMC.S32171. http://dx.doi.org/10.4137/pmc.s32171.

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The cannabinoids are members of a deceptively simple class of terpenophenolic secondary metabolites isolated from Cannabis sativa highlighted by (-)-Δ 9 -tetrahydrocannabinol (THC), eliciting distinct pharmacological effects mediated largely by cannabinoid receptor (CB1 or CB2) signaling. Since the initial discovery of THC and related cannabinoids, synthetic and semisynthetic classical cannabinoid analogs have been evaluated to help define receptor binding modes and structure–CB1/CB2 functional activity relationships. This perspective will examine the classical cannabinoids, with particular emphasis on the structure–activity relationship of five regions: C3 side chain, phenolic hydroxyl, aromatic A-ring, pyran B-ring, and cyclohexenyl C-ring. Cumulative structure–activity relationship studies to date have helped define the critical structural elements required for potency and selectivity toward CB1 and CB2 and, more importantly, ushered the discovery and development of contemporary nonclassical cannabinoid modulators with enhanced physicochemical and pharmacological profiles.
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Zibolka, Juliane, Anja Wolf, Lisa Rieger, Candy Rothgänger, Anne Jörns, Beat Lutz, Andreas Zimmer, Faramarz Dehghani, and Ivonne Bazwinsky-Wutschke. "Influence of Cannabinoid Receptor Deficiency on Parameters Involved in Blood Glucose Regulation in Mice." International Journal of Molecular Sciences 21, no. 9 (April 30, 2020): 3168. http://dx.doi.org/10.3390/ijms21093168.

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Cannabinoids are known to influence hormone secretion of pancreatic islets via G protein-coupled cannabinoid receptor type 1 and 2 (CB1 and CB2). The present study was designed to further investigate the impact of cannabinoid receptors on the parameters involved in insulin secretion and blood glucose recognition. To this end, CB1 and CB2 receptor knockout mice (10–12 week old, both sexes) were characterised at basal state and compared to wild-type mice. The elimination of cannabinoid receptor signalling resulted in alterations of blood glucose concentrations, body weights and insulin levels. Changes were dependent on the deleted receptor type and on the sex. Analyses at mRNA and protein levels provided evidence for the impact of cannabinoid receptor deficiency on the glucose sensing apparatus in the pancreas. Both receptor knockout mouse lines showed decreased mRNA and protein amounts of glucose transporters Glut1 and Glut2, combined with alterations in immunostaining. In addition, pancreatic glucokinase expression was elevated and immunohistochemical labelling was modified in the pancreatic islets. Taken together, CB1 and CB2 signalling pathways seem to influence glucose sensing in β-cells by affecting glucose transporters and glucokinase. These alterations were more pronounced in CB2 knockout mice, resulting in higher blood glucose and lower plasma insulin levels.
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Černe, Katarina. "Toxicological properties of Δ9-tetrahydrocannabinol and cannabidiol." Archives of Industrial Hygiene and Toxicology 71, no. 1 (March 1, 2020): 1–11. http://dx.doi.org/10.2478/aiht-2020-71-3301.

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AbstractCannabis sativa L. contains more than 100 phytocannabinoids that can interact with cannabinoid receptors CB1 and CB2. None of the cannabinoid receptor ligands is entirely CB1- or CB2-specific. The effects of cannabinoids therefore differ not just because of different potency at cannabinoid receptors but also because they can interact with other non-CB1 and non-CB2 targets, such as TRPV1, GPR55, and GPR119. The most studied phytocannabinoid is Δ9-tetrahydrocannabinol (THC). THC is a partial agonist at both cannabinoid receptors, but its psychotomimetic effect is produced primarily via activation of the CB1 receptor, which is strongly expressed in the central nervous system, with the noteworthy exception of the brain stem. Although acute cognitive and other effects of THC are well known, the risk of irreversible neuropsychological effects of THC needs further research to elucidate the association. Unlike THC, phytocannabinoid cannabidiol (CBD) does not appear to have psychotomimetic effects but may interact with some of the effects of THC if taken concomitantly. CBD administered orally has recently undergone well-controlled clinical trials to assess its safety in the treatment of paediatric epilepsy syndromes. Their findings point to increased transaminase levels as a safety issue that calls for postmarketing surveillance for liver toxicity. The aim of this review is to summarise what is known about acute and chronic toxicological effects of both compounds and address the gaps in knowledge about the safety of exogenous cannabinoids that are still open.
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Barth, Francis, and Murielle Rinaldi-Carmona. "The Development of Cannabinoid Antagonists." Current Medicinal Chemistry 6, no. 8 (August 1999): 745–55. http://dx.doi.org/10.2174/0929867306666220401143808.

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The discovery of two distinct cannabinoid receptors (CB1 and C B 2 ) in the early 1990's has revived the research on cannabinoid antagonists. While the search for antagonists based on the structure of agonists (classical cannabinoids or aminoalkylindoles) appeared rather disappointing, the first potent cannabinoid antagonists were developed in a new chemical series: the diarylpyrazoles. Since its discovery in 1994, the selective CB1 antagonist SR 141716 has become a major pharmacological tool to elucidate the physiological role of the CB 1 cannabinoid receptor and its endogenous ligand. The selective CB2 antagonist SR 144528 is expected to play the same role for the CB2 receptors, while the recent development of cannabinoid antagonists belonging to other chemical series illustrates the interest of these compounds which are now considered as interesting therapeutic targets by many pharmaceutical companies.
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Dissertations / Theses on the topic "Cannabinoid CB1 receptor"

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Smith, Tricia. "Effects of Cannabinoid Receptor Interacting Protein (CRIP1a) on Cannabinoid Receptor (CB1) Function." VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/1977.

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EFFECTS OF CANNABINOID RECEPTOR INTERACTING PROTEIN (CRIP1a) ON CANNABINOID (CB1) RECEPTOR FUNCTION. By Tricia Hardt Smith, B.S., M.S. A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy at Virginia Commonwealth University Virginia Commonwealth University, 2009. Major Director: Dana E. Selley, Ph.D., Department of Pharmacology and Toxicology This dissertation examines modulation of cannabinoid CB1 receptor function by Cannabinoid Receptor Interacting Protein (CRIP1a), a novel protein that binds the C-terminus of CB1 receptors. In Human embryonic kidney cells expressing human CB1 receptors (hCB1-HEK) and hCB1-HEK cells stably co-expressing CRIP1a (hCB1-HEK-CRIP1a), quantitative immunoblotting revealed a CRIP1a/CB1 molar ratio of 5.4 and 0.37, respectively, with no difference in CB1 receptor expression. To test the hypothesis that CRIP1a modulates CB1 receptor signaling, G-protein and effector activity were examined with and without full, partial and inverse agonists. [35S]GTPgS binding, which measures G-protein-coupled receptor (GPCR)-mediated G-protein activation, showed that CRIP1a inhibited constitutive CB1 receptor activity, as indicated by the decreased effect of the inverse agonist SR141716A. CRIP1a also decreased CB1 receptor-mediated G-protein activation by high efficacy agonists, whereas moderate and low efficacy agonists were unaffected. In experiments varying Na+ concentration, CRIP1a decreased spontaneous G-protein activation at low Na+ concentrations, where spontaneous GPCR activity is highest. This effect was eliminated by pertussis toxin pre-treatment, indicating that CRIP1a only inhibits GPCR-mediated activity. To determine whether CRIP1a modulates receptor adaptation, hCB1-HEK (±CRIP1a) cells were pretreated with WIN or THC. Both ligands desensitized CB1 receptor-mediated G-protein activation, but desensitization was unaffected by CRIP1a. In contrast, CRIP1a attenuated downregulation of CB1 receptor binding sites by WIN, but not THC. Downstream, CRIP1a attenuated constitutive CB1 receptor-mediated inhibition of cAMP, as indicated by elimination of SR141716A-stimulated cAMP, without affecting agonist-induced cAMP inhibition. Constitutive inhibition was not due to endocannabinoids because LC-ESI-MS-MS did not detect endocannabinoids in hCB1-HEK (±CRIP1a) cells. To determine whether effects of CRIP1a were conserved among cell types, Chinese Hamster Ovary cells expressing CB1 receptors were stably co-transfected with CRIP1a, and had a CRIP1a/CB1 receptor molar ratio of 15 and 1900 with and without CRIP1a over-expression, respectively. In this model, CRIP1a inhibited constitutive CB1 receptor-mediated G-protein activity, but activation by agonists was enhanced, suggesting CRIP1a effects were dependent on stoichiometry of CRIP1a/CB1 receptor or cell type. Overall, these results indicate that CRIP1a decreases constitutive CB1 receptor activity, modulates agonist efficacy, and inhibits CB1 receptor downregulation, in a ligand- and cellular environment-dependent manner.
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Daigle, Tanya L. "Molecular mechanisms of CB1 cannabinoid receptor signaling and internalization /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/10527.

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Slaughter, Kimari. "Synthesis and Development of Potential CB1 Receptor Neutral Antagonists." ScholarWorks@UNO, 2012. http://scholarworks.uno.edu/td/1483.

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Cannabis and its derivatives have been used for both medicinal and recreational purposes. The study of this plant led to the discovery of over 60 cannabinoids, found exclusively in cannabis, that contribute to the behavioral effects of cannabis use, the most common is delta-9-tetrahydrocannabinol. Cannabinoid receptors function to increase activity in the mesolimbic dopamine reward system. Dopamine is a neurotransmitter that plays a major role in addition and its regulation plays a crucial role in mental and physical well-being. There is evidence that CB1 receptors are important to the reinforcing effects and the development of physical dependence on opiate drugs. Studies have shown that increased levels of dopamine are consistent with addiction while reduced levels lead to a decline in recreational use. The goal of this research is to design, synthesize and develop potential CB1 receptors that exhibit a neutral cannabinoid antagonist pharmacological profile.
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Horswill, James G. "Pharmacological characterisation of a novel cannabinoid CB1 receptor allosteric modulator." Thesis, University of Reading, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.541953.

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Grim, Travis. "Synthetic cannabinoids versus delta-9-tetrahydrocannabinol: abuse-related consequences of enhanced efficacy at the cannabinoid 1 receptor." VCU Scholars Compass, 2015. http://scholarscompass.vcu.edu/etd/4039.

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In the past ten years, synthetic cannabinoids (SC) have emerged as drugs of abuse. Unlike D9-tetrahydrocannabinol (THC), many SCs are associated with serious health complications and death. One way in which THC and SCs differ lies with their enhanced potency and efficacy at the CB1 receptor. No current methods exist to measure efficacy at the CB1 receptor in vivo, and the abuse-related properties of SC cannabinoids are not well explored. Here, we utilized CB1 wild type (WT), heterozygous (HET), and knockout (KO) mice. By employing CB1 ligands which differ in efficacy we have developed a method to explore the relationship between efficacy and the ability to produce cannabimimetic (catalepsy, hypothermia, and antinociception) effects when CB1 expression was reduced by half. Additionally, the intracranial self-stimulation procedure (ICSS) was utilized to investigate the effects of enhanced efficacy at CB1 upon reward processes using representative SC CP55,940. As predicted, the potency shift between WT and HET mice inversely correlated with the efficacy of the test drug for both hypothermia and antinociception, but not catalepsy. This efficacy stratification was correlated with the agonist-stimulated [35S]GTPgS binding assay, demonstrating this model as an effective tool to ascertain in vivo efficacy differences at CB1. In ICSS, CP55,940 elicited only rate-decreasing effects acutely, although tolerance developed following repeated dosing, with no evidence for spontaneous or rimonabant-precipitated withdrawal. Together, these data indicate that highly efficacious cannabinoid ligands require few receptors to produce cannabimimetic effects, and that the model provides an effective means to quickly ascertain differences in efficacy.
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Wing, Victoria Caroline. "The role of the cannabinoid CB1 receptor subtype in nicotine dependence." Thesis, University of Newcastle Upon Tyne, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.500924.

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Tobacco smoking, considered an addiction to nicotine, is a worldwide health problem but limited effective pharmacotherapies are available. Nicotine acts on nicotinic acetylcholine receptors in the brain thus interacting with a range of neurotransmitter systems of which the mesocorticolimbic dopamine system is considered crucial for drug dependence. The endocannabinoid system has also been implicated in nicotine dependence and the cannabinoid CB1 receptor antagonist rimonabant has shown efficacy as a smoking cessation aid. This thesis aimed to further examine the role of CBl receptors in the motivational properties of nicotine, both positive and negative.
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Marcu, Jahan Phillip. "Novel Insights into CB1 Receptor Signaling and the Anabolic Role of Cannabinoid Receptors in Bone." Diss., Temple University Libraries, 2013. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/233543.

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Cell Biology
Ph.D.
Activation of the CB1 receptor is modulated by aspartate residue D2.63176 in transmembrane helix (TMH) II. Interestingly, D2.63 does not affect the affinity for ligand binding at the CB1 receptor. Studies in class A GPCRs have suggested an ionic interaction between residues of TMHII and VII. In this report, modeling studies identified residue K373, in the extracellular (EC)-3 loop, in charged interactions with D2.63. We investigated this possibility by performing reciprocal mutations and biochemical studies. D2.63176A, K373A, D2.63176A-K373A, and the reciprocal mutant with the interacting residues juxtaposed, D2.63176K-K373D were characterized using radioligand binding and guanosine 5'-3-O-(thio)triphosphate functional assays. None of the mutations resulted in a significant change in the binding affinity of CP55,940 or SR141716A. Computational results indicate that the D2.63176-K373 ionic interaction strongly influences the conformation(s) of the EC-3 loop, providing a structure-based rationale for the importance of the EC-3 loop to signal transduction in CB1. Specifically, the putative ionic interaction results in the EC-3 loop pulling over the top (extracellular side) of the receptor; this EC-3 loop conformation may serve protective and mechanistic roles. These results suggest that the ionic interaction between D2.63176 and K373 is crucial for CB1 signal transduction. This work may help to aide drug design efforts for the effective treatment of different diseases. The cannabinoid receptors of osteoblasts may represent a target for the treatment of bone disorders such as osteoporosis. Our research demonstrates that cannabinoids can affect important signaling molecules in osteoblasts. In MC3T3-E1 osteoblastic cells, the CB1 antagonist, AM251, has been reported to induce increases in Runx2 mRNA, mineralized bone nodule formation, and activation of signaling molecules such as ERK and AKT (Wu et al., 2011). Studies from our lab characterizing mice in which both CB1 and CB2 receptors were inactivated by homologous recombination have demonstrated increased bone mass coupled with enhanced osteoblast differentiation of bone marrow stromal cells in culture (manuscript in preparation). We explored the effect of antagonizing CB1 and CB2 cannabinoid receptors in osteoblastic cells to gain insights into molecular pathways that may help to explain the effects of the endocannabinoid system (ECS) in bone development. Our data was generated by running time course experiments with MC3T3-E1 cells under the influence of SR141716A, SR144528 or both in combination. The cells were harvested with a lysis buffer at specific time points and analyzed by western blot analysis. Quantification of protein activation was calculated using LiCor imaging equipment and software. Within 15 minutes, treatment with the CB1 receptor antagonist SR141716A resulted in several fold increases in pERK, pSMAD158, and pAKT. SR144528, a CB2 receptor antagonist, caused increases in pERK and pSMAD158, but not pAKT. When both antagonists were applied together, pERK and pSMAD158 levels increased, while pAKT signaling was diminished compared to SR141716A alone. The finding that cannabinoid receptor antagonists alter the activity of the SMAD158 complex is a novel finding, which suggests that cannabinoids can influence bone morphogenic signaling pathways, and therefore play a significant role in osteoblast differentiation and function.
Temple University--Theses
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Feliszek, Monika [Verfasser]. "Age-dependent cannabinoid CB1 receptor plasticity and search for histamine H4 receptors in the brain / Monika Feliszek." Bonn : Universitäts- und Landesbibliothek Bonn, 2016. http://d-nb.info/1119888875/34.

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Jacob, Wolfgang. "Role of the Cannabinoid Receptor Type 1 (CB1) in Synaptic Plasticity, Memory and Emotionality." Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-72307.

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Marsicano, Giovanni. "Physiological role of the cannabinoid receptor 1 (CB1) in the murine central nervous system." Thesis, Open University, 2001. http://oro.open.ac.uk/58198/.

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The cannabinoid system is involved in many functions of mammalian brain, such as learning and memory, pain perception and 'locomotion. The "brain type" cannabinoid receptor CB 1 is one of the key elements of the cannabinoid system. In this Thesis, some aspects of the neurobiology of mouse CB 1 are described. CB 1 mRNA distribution was analysed by single and double in situ hybridization (ISH), revealing the expression of the receptor in specific neuronal subpopulations. This expression pattern suggests many putative functional cross-talks between the cannabinoid system and other signalling molecules in the brain, such as glutamate, GABA, cholecystokinin and nitric oxide (NO). The putative functional interactions of the cannabinoid system with the NO pathway was studied by pharmacological treatment of neuronal NO synthase (nNOS) mutant mice with the CBI agonist A9-tetrahydrocannabinol (A9-THC). The results showed that nNOS is necessary for some central effects of A9-THC. Moreover, ISH analysis revealed. that nNOS-deficient mice contain levels of CBI lower than normal in selected brain regions. A "conditional" targeting approach was developed to gain insights into the specific functions of CB 1 in mouse brain. By gene targeting experiments, two mutant lines were obtained. The "Flox CB 1" mouse line, containing the whole open reading frame of CB I flanked by two loxP sites will be the key tool for the generation of mouse mutants with a spatiotemporal-restricted deletion of CB I. The "CBN" mice, carrying a "null" mutation of CB 1, were used for a study aimed to clarify some aspects of the in vitro neuroprotective activity of cannabinoids and, in particular, the involvement of CB 1. In vitro oxidative stress assays were performed on cell lines and on primary neuronal cultures derived from homozygous CBN/CBN mice and wild type littermates. The results indicate a differential protective activity of cannabinoids on cell lines and primary cultures. However, CBI does not appear to be involved in the in vitro leuroprotective effects of cannabinoids.
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Books on the topic "Cannabinoid CB1 receptor"

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Desroches, Julie. Peripheral analgesia involves cannabinoid receptors. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0034.

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This landmark paper by Agarwal and colleagues was published in 2007, when the exact contribution of the activation of the cannabinoid type 1 receptor (CB1) receptors expressed on the peripheral terminals of nociceptors in pain modulation was still uncertain. At that time, while it was clearly demonstrated that the central nervous system (CNS) was involved in the antinociceptive effects induced by the activation of the CB1 receptor, many strains of mice in which the gene encoding the CB1 receptor was deleted by conditional mutagenesis were used to study the specific role of these receptors in pain. Creating an ingenious model of genetically modified mice with a conditional deletion of the CB1 receptor gene exclusively in the peripheral nociceptors, Agarwal and colleagues were the first to unequivocally demonstrate the major role of this receptor in the control of pain at the peripheral level. In fact, these mutant mice lacking CB1 receptors only in sensory neurons (those expressing the sodium channel Nav1.8) have been designed to highlight that CB1 receptors on nociceptors, and not those within the CNS, constitute an important target for mediating local or systemic (but not intrathecal) cannabinoid analgesia. Overall, they have clarified the anatomical locus of cannabinoid-induced analgesia, highlighted the potential significance of peripheral CB1-mediated cannabinoid analgesia, and revealed important insights into how the peripheral endocannabinoid system works in controlling both inflammatory pain and neuropathic pain.
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Abood, Mary E., and Thomas Gamage. The cloning and characterization of the cannabinoid type 1 receptor. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0025.

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The cloning and characterization of the first cannabinoid receptor (now known as the cannabinoid type 1 (CB1) receptor) by Matsuda et al. in the landmark paper discussed in this chapter was a seminal discovery in 1990. While the analgesic properties of marijuana had been known for thousands of years, the mechanisms through which marijuana produces analgesia were not understood. The identification and functional characterization of the CB1 receptor led to the discovery of an endogenous cannabinoid system (the endocannabinoid system), which has now been shown to be important not only for acute and chronic pain states, but also for a whole host of physiological and pathophysiological disorders.
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Abood, Mary E., Nephi Stella, and Roger G. Sorensen. EndoCANNABINOIDS: Actions at Non-CB1/CB2 Cannabinoid Receptors. Springer London, Limited, 2012.

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Abood, Mary E., Roger G. Sorensen, and Nephi Stella. endoCANNABINOIDS: Actions at Non-CB1/CB2 Cannabinoid Receptors. Springer, 2012.

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Abood, Mary E., Nephi Stella, and Roger G. Sorensen. EndoCANNABINOIDS: Actions at Non-CB1/CB2 Cannabinoid Receptors. Springer New York, 2014.

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Iversen, Leslie. The Pharmacology of Delta-9-Tetrahydrocannabinol (THC). Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190846848.003.0002.

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The 19th century was a great era for plant chemistry. Many complex drug molecules, known as alkaloids, were isolated and identified from plants. This chapter discusses the history of the discovery of delta-9-tetrahyrocannabinol (THC) as the psychoactive substance in cannabis products and also the discovery of the cannabinoid receptors CB-1 and CB-2 in the body and brain. The mechanism of action of cannabinoids on such receptors to inhibit neurotransmitter release or other actions is also discussed. In addition, various methods for the ingestion of cannabis, such as smoking and vaping, are reviewed. Synthetic agonists and antagonists at cannabinoid receptors and the proliferation of synthetic agonists as novel psychoactive agents are also discussed.
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Rodriguez, Emma. Cannabinoid CB1: A Study of Morphological Levels and Distribution of MRNA and CB1 Receptors. Independently Published, 2019.

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Iversen, Leslie. Peripheral and Central Effects of THC. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190846848.003.0003.

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Although there is currently only limited knowledge of how activation of the CB-1 receptor in brain leads to the many actions of THC, some general features of cannabinoid control mechanisms are emerging. This chapter discusses THC in relation to the inhibition of neurotransmitter release, cardiovascular effects, effects on motility and pain, and behavioral models including the “Billy Martin tetrad.” It also discusses human laboratory models, including studies on learning and memory. A key effect of cannabis is intoxication, and the subjective effects of cannabis are reported in detail. Finally, the value of animal behavior studies is discussed, including discriminative stimulus effects, effects on cognition, and anti-anxiety effects.
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Book chapters on the topic "Cannabinoid CB1 receptor"

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Rech, Glenn R., and Samer N. Narouze. "Cannabinoid Receptor 1 (CB1)." In Cannabinoids and Pain, 47–54. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-69186-8_7.

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Zhang, Yanan, Herbert H. Seltzman, Marcus Brackeen, and Brian F. Thomas. "Structure–Activity Relationships and Conformational Freedom of CB1 Receptor Antagonists and Inverse Agonists." In The Cannabinoid Receptors, 95–119. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-503-9_4.

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Katona, István. "Endocannabinoid Receptors: CNS Localization of the CB1 Cannabinoid Receptor." In Behavioral Neurobiology of the Endocannabinoid System, 65–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-88955-7_3.

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Salamone, John D., Kelly Sink, Kristen N. Segovia, Patrick A. Randall, Peter J. McLaughlin, V. Kiran Vemuri, and Alexandros Makriyannis. "Cannabinoid Cb1 Receptor Antagonists/Inverse Agonists and Food-Seeking Behavior." In Handbook of Behavior, Food and Nutrition, 441–56. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-92271-3_29.

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Iliopoulos-Tsoutsouvas, Christos, Markos-Orestis Georgiadis, Lipin Ji, Spyros P. Nikas, and Alexandros Makriyannis. "Chapter 3. Natural Compounds and Synthetic Drugs to Target Type-1 Cannabinoid (CB1) Receptor." In Drug Discovery, 48–88. Cambridge: Royal Society of Chemistry, 2020. http://dx.doi.org/10.1039/9781839160752-00048.

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Pertwee, Roger G. "CB1 and CB2 Receptor Pharmacology." In Cannabinoids and the Brain, 91–99. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-74349-3_7.

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Pertwee, Roger G., and Adèle Thomas. "Therapeutic Applications for Agents that Act at CB1 and CB2 Receptors." In The Cannabinoid Receptors, 361–92. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-503-9_13.

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Antinori, Silvia, and Liana Fattore. "How CB1 Receptor Activity and Distribution Contribute to Make the Male and Female Brain Different Toward Cannabinoid-Induced Effects." In Endocannabinoids and Lipid Mediators in Brain Functions, 27–51. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57371-7_2.

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Wiley, Jenny L., and Billy R. Martin. "Preclinical Pharmacological and Brain Bioassay Systems for CB1 Cannabinoid Receptors." In The Cannabinoid Receptors, 329–60. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-503-9_12.

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Thomas, Brian F., Yanan Zhang, Marcus Brackeen, Kevin M. Page, S. Wayne Mascarella, and Herbert H. Seltzman. "Conformational Characteristics of the Interaction of SR141716A with the CB1 Cannabinoid Receptor as Determined Through the Use of Conformationally Constrained Analogs." In Drug Addiction, 707–18. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-76678-2_41.

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Conference papers on the topic "Cannabinoid CB1 receptor"

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Espinosa-Bustos, C., C. F. Lagos, J. Romero-Parra, J. Mella-Raipán, H. Pessoa- Mahana, G. Recabarren-Gajardo, and C. D. Pessoa-Mahana. "Synthesis and Docking of new (2-(2,5-dimethoxyphenyl)-1Hbenzo[ d]imidazol-1-yl)(aryl)methanone derivatives designed as novel cannabinoid CB1 receptor antagonists." In 14th Brazilian Meeting on Organic Synthesis. São Paulo: Editora Edgard Blücher, 2013. http://dx.doi.org/10.5151/chempro-14bmos-r0169-1.

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Elói, Daniel Vinicius, Daniel Lopes Marques de Araújo, Gabriela Fonseca Marçal, Luana Soares Vargas, Matheus Garcia Ribeiro, and Nicollas Nunes Rabelo. "Canabinoids as a therapeutic alternative in refractory epilepsy." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.554.

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Introduction: Epilepsy is characterized by abnormal electrical discharges in the brain that generate neuronal hyperexcitability and hypersynchrony. In the last years, pharmacological strategies have been efficient in the control of epileptic seizures of approximately 80% of patients, however, there are still refractory cases. Objective: To elucidate new forms of epilepsy treatment with cannabinoids. Design: Systematic Review performed at Centro Universitário Atenas – Paracatu – Minas Gerais. Methods: Literature review performed in the SciELO and PubMed databases, with the following terms: epilepsy and cannabidiol. Five papers, published from 2017 to 2020, written in English or Portuguese, were selected. Review: Epileptic seizures affect conscience, motor, sensory, and cognitive functions. The treatment with available antiepileptic drugs does not display a complete therapeutic efficiency, as it is still observed the presence of refractory patients. In this context, the cannabidiol (CBD), by interfering in the information flow between neurons, acts therapeutically preventing overload. In the central nervous system, CBD acts in the CB1 receptors, present in GABAergic inhibitory neurons and glutamatergic excitatory neurons. Evidence from an electronic research performed in 2015, with 117 parents of children with refractory epilepsy that used cannabidiol, displayed that seizures were reduced by 85%, including 14% with total suppression. Conclusion: The studies show that CBD, by acting with specific neuronal receptors, decreases cerebral hyperexcitability. Therefore, this therapeutic alternative may improve the physical and emotional well-being of refractory epileptics.
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Gabrielli, Ângelo, Camila Sousa Bragunce Alves, Bruna Oliveira Bicalho, and Débora Pimenta Alves. "Benefits and Challenges of Cannabis Use in the Treatment of Refractory Epilepsy." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.239.

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Introduction: Refractory epilepsy (RE) is a disease that causes continuous and debilitating seizures. Due to the ineffectiveness of antiepileptic therapies, there is a growing interest in drugs made with cannabidiol (CBD), a substance extracted from Cannabis. Objective: To point out benefits and challenges of the use of CBD in the treatment of RE. Methods: Literature review performed at PubMed, with the descriptors Epilepsy, Drug Therapy and Cannabis. Results: It is suggested that CBD is mediated by cannabinoid receptors coupled to protein G, by blockade of NMDA receptors, by GABAergic modulation, glutamatergic synapses and / or mechanisms involving noncannabinoid receptors. CBD can also oppose the actions of exogenous and endogenous cannabinoid agonists, due to the negative allosteric modulation. The benefits of CBD are: great therapeutic diversity, safety and tolerability, rare and mild side effects, low risk of drug interactions, and milder cognitive effects, when compared to other antiepileptic drugs. Despite the benefits, CBD has adverse effects such as drowsiness, appetite reduction, diarrhea, increased activity of liver enzymes and interaction with substances metabolized by cytochrome P450. Still, the inefficient regulation generates variation in the composition of the marketed drugs, which can lead to Δ9 - tetrahydrocannabinol (THC) intoxication. Conclusions: Thus, it is essential that the scientific community remains open to investigate the effects of CBD, given the advantages of its use for treating RE.
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Sabater García, Luz María, Verónica Alarcón Ortiz, Alejandra Carrillo Llamas, Pablo García Verdú, and María Ángeles de Haro Rivas. "Síndrome hiperemético cannabinoide: A propósito de un caso clínico." In 22° Congreso de la Sociedad Española de Patología Dual (SEPD) 2020. SEPD, 2020. http://dx.doi.org/10.17579/sepd2020p085.

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- Objetivo: Actualizar la evidencia científica disponible en relación con el Síndrome hiperemético producido por el consumo crónico de cannabis a propósito de un caso clínico. - Material y métodos: Se ha llevado a cabo una revisión sistemática entre las principales fuentes de literatura científica y se han empleado los programas Selene y Ágora Plus para recopilar los diferentes datos médicos del caso (Palabras clave: “hyperemesis”, “Cannabis”, “THC”, “cannabinoid”). - Resultados: * Exposición de caso clínico (tabla en póster). * Etiología: Se piensa que el uso prolongado de cannabis conduciría a una regulación a la baja de los receptores CB1, causando un efecto pro-emético. También sería posible una acumulación de metabolitos por déficit de función enzimática y que la activación de CB1 altere el eje hipotálamo-hipófisis. * Epidemiología: 6% de los pacientes que consultan por vómitos cíclicos, 83% varones, edad media: 28.3 años. Consumo diario: 7,5 cigarrillos. Consumo antes del primer episodio agudo: 5,5 años. * Clínica: El único criterio obligatorio para el diagnóstico es el consumo prolongado de cannabis. Hay una serie de criterios mayores y menores descritos (tabla en póster). * Diagnóstico diferencial (tabla en póster). * Tratamiento: En fase aguda, de soporte. Otros tratamientos con cierta efectividad: Capsaicina tópica, haloperidol, propranolol, lorazepam. Inhibidores de la bomba de protones también pueden estar indicados. El remedio más efectivo en la fase aguda siguen siendo los baños de agua caliente. * Pronóstico: El único tratamiento efectivo para prevenir la reincidencia es el cese completo del consumo de cannabis. Los síntomas se resuelven espontáneamente en los días posteriores al cese de la sustancia. - Conclusiones: Clínica de episodios de vómitos incoercibles junto a baños calientes compulsivos en consumidores crónicos de cannabis. Retraso diagnóstico de más de 6 años. Diagnóstico diferencial es muy amplio y ha de incluir entidades muy variadas.
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"PV-006 - REVISIÓN SISTEMÁTICA PSICOSIS DUAL." In 24 CONGRESO DE LA SOCIEDAD ESPAÑOLA DE PATOLOGÍA DUAL. SEPD, 2022. http://dx.doi.org/10.17579/abstractbooksepd2022.pv006.

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Resumen: El sistema dopaminérgico participa en la recompensa cerebral en el trastorno por uso de sustancias (TUS). En la transición a la dependencia la prominencia del incentivo y los cambios neuroadaptivos en distintos sistemas de neurotransmisión son importantes. La excitabilidad cerebral y la hiperreactividad al estrés promueven un estado emocional negativo e hipodopaminergia prefrontal. La psicosis dual está presente en el 30-50% de trastornos psicóticos. La teoría de la vulnerabilidad compartida se propone como hipótesis explicativa. Objetivos: revisión sistemática de la neurobiología de la psicosis dual y un estudio descriptivo en una muestra hospitalaria. Metodología: revisión de 30 estudios publicados desde 2005 en las bases de datos Pubmed y Google Scholar. Resultados: en la psicosis dual las conductas de autoadministración son más compulsivas, objetivándose mayor aplanamiento de la liberación de dopamina ante estímulos condicionados. La actividad dopaminérgica puede disminuir un 80% en la dependencia crónica. La elevación de glutamato influye en la hiperexcitabilidad cerebral, encontrándose una correlación positiva con el craving. La hiperreactividad al estrés y el agonismo kappa opioide de la dinorfina, también promueve el estado aversivo, influyendo en el proceso de recaída junto a amígdala extendida. La actividad del receptor endocannabinoide CB1, modulador de la homeostasis del glutamato y dopamina, disminuye 17% la actividad en la abstinencia prolongada. El agonismo CB1R ha mostrado resultados positivos. En ambos trastornos se observa la influencia también de algunos neuropéptidos que participan en procesos degradativos y regulación del ritmo circadiano. El estudio descriptivo de una muestra hospitalaria, encuentra una prevalencia del 51% de psicosis dual. Los diagnósticos duales más frecuentes son la dependencia de cannabinoides (34%), múltiples drogas (25%), alcohol (23%) y anfetaminas (16%). Limitaciones: heterogeneidad de los estudios. Conclusiones: los resultados muestran alteraciones comunes en la psicosis dual, siendo necesario continuar investigando la interacción bidireccional.
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"PV-125 - HIPEREMESIS CANNABINOIDE. DUCHAS CALIENTES COMPULSIVAS EN PACIENTE CONSUMIDOR CRÓNICO DE CANNABIS. A PROPÓSITO DE UN CASO." In 24 CONGRESO DE LA SOCIEDAD ESPAÑOLA DE PATOLOGÍA DUAL. SEPD, 2022. http://dx.doi.org/10.17579/abstractbooksepd2022.pv125.

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Objetivos: Se establecen como objetivos presentar la evolución de un paciente varón de 28 años con diagnóstico de Esquizofrenia y trastorno por consumo de cannabis que ingresa en la Unidad de Hospitalización Breve de Psiquiatría (UHB). Asimismo, se establece el objetivo de revisar la bibliografía disponible relacionada con la mejoría sintomática de la ansiedad a través de un número elevado de duchas calientes en pacientes consumidores de cannabis. Material y métodos: Se desarrolla el caso clínico de un varón de 28 años que ingresa en la UHB de Psiquiatría por episodio psicótico en el contexto de consumo crónico de cannabis que solicita ducharse con agua caliente más de 10 veces al día para mejoría ansiolítica. Se decide realizar una búsqueda bibliográfica en PubMed acerca de duchas calientes en pacientes con consumo de cannabis con las palabras clave “hot showers” y “cannabis”. Resultados y conclusiones: la búsqueda en PubMed arroja 23 resultados en los últimos 10 años, poniendo de manifiesto la escasa bibliografía acerca de este tema. Se describe una posible desregulación del eje hipotálamo hipofisario adrenal (HHA) en consumidores crónicos de cannabis debido a la desregulación del sistema endocannabinoide, encargado de regular el termostato del hipotálamo a través de receptores como CB1 y TRPV1 (vanilloide/capsaicina). Se ha descrito que niveles elevados de tetrahidrocannabinol (THC) tienen una función proemética (frente a la mejoría de la emesis con niveles bajos de THC) y también de hipotermia; el estrés y la hiporexia pueden aumentar los niveles de THC (reintoxicación). De esta forma, la sintomatología emética, la ansiedad y la regulación térmica estarían relacionadas con los niveles de THC. Las duchas calientes podrían aliviar los síntomas de hiperemesis y de ansiedad relacionados con el consumo de THC a través de los receptores TRPV1 en el hipotálamo,así como el posible uso de cremas con capsaicina.
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Abdalla, J., J. K. Park, N. J. Coffey, C. N. Zawatsky, T. Yokoyama, T. Jourdan, G. Godlewski, et al. "Deletion of Cannabinoid 1 Receptor (CB1R) in Myeloid Cells Prevents Lung Inflammation and Neutrophil Infiltration in Bleomycin-Induced Pulmonary Fibrosis in Mice." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2387.

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Zawatsky, C., J. K. Park, N. J. Coffey, T. Yokoyama, T. Jourdan, G. Godlewski, W. A. Gahl, M. C. V. Malicdan, G. Kunos, and R. Cinar. "Activation of Cannabinoid 1 Receptor (CB1R) in Myeloid Cells Induces Lymphocyte Infiltration in Lung Via Regulating CXCL13 in Bleomycin-Induced Pulmonary Fibrosis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2391.

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Cinar, R., M. R. Iyer, J. K. Park, C. N. Zawatsky, N. J. Coffey, S. P. Bodine, J. Abdalla, et al. "MRI-1867, Dual Target Cannabinoid Receptor 1 (CB1R) and Inducible Nitric Oxide Synthase (iNOS) Inhibitor, for Effective Anti-Fibrotic Therapy for Hermansky-Pudlak Syndrome Pulmonary Fibrosis in Pale Ear Mic." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1198.

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Cinar, R., N. J. Coffey, S. Bodine, J. K. Park, M. R. Iyer, B. R. Gochuico, W. A. Gahl, M. C. V. Malicdan, and G. Kunos. "Effective Anti-Fibrotic Therapy for Hermansky-Pudlak Syndrome Pulmonary Fibrosis in Pale Ear Mice Using a Hybrid Inhibitor of Cannabinoid Receptor 1 (CB1R) and Inducible Nitric Oxide Synthase (iNOS), MRI-1867." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1227.

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Reports on the topic "Cannabinoid CB1 receptor"

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Lazarov, Nikolai E., Dimitrinka Y. Atanasova, Angel D. Dandov, and Nikolay D. Dimitrov. Anandamide-induced Expression of CB1 Cannabinoid Receptors in the Rat Mesencephalic Trigeminal Nucleus after Short-term Thermal Stress. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, September 2018. http://dx.doi.org/10.7546/crabs.2018.09.16.

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