Functional Expression of Brain Neuronal CB2 Cannabinoid Receptors Are Involved in the Effects of Drugs of Abuse and in Depression
Major depression and addiction are mental health problems associated with stressful events in life with high relapse and recurrence even after treatment. Many laboratories were not able to detect the presence of CB2 cannabinoid receptors (CB2‐Rs) in healthy brains, but CB2‐R expression has been demo...
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| Published in | Annals of the New York Academy of Sciences Vol. 1139; no. 1; pp. 434 - 449 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Malden, USA
Blackwell Publishing Inc
01.10.2008
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0077-8923 1749-6632 1749-6632 1930-6547 |
| DOI | 10.1196/annals.1432.036 |
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| Abstract | Major depression and addiction are mental health problems associated with stressful events in life with high relapse and recurrence even after treatment. Many laboratories were not able to detect the presence of CB2 cannabinoid receptors (CB2‐Rs) in healthy brains, but CB2‐R expression has been demonstrated in rat microglial cells and other brain‐associated cells during inflammation. Thus, neuronal expression of CB2‐Rs has been ambiguous and controversial, and its role in depression and substance abuse is unknown. In this study we tested the hypothesis that genetic variants of the CB2 gene might be associated with depression in a human population and that alteration in CB2 gene expression may be involved in the effects of abused substances, including opiates, cocaine, and ethanol, in rodents. Here we demonstrate that a high incidence of Q63R but not H316Y polymorphism in the CB2 gene was found in Japanese depressed subjects. CB2‐Rs and their gene transcripts are expressed in the brains of naïve mice and are modulated after exposure to stressors and administration of abused drugs. Mice that developed an alcohol preference had reduced CB2 gene expression, and chronic treatment with JWH015 a putative CB2‐R agonist, enhanced alcohol consumption in stressed but not in control mice. The direct intracerebroventricular microinjection of CB2 antisense oligonucleotide into the mouse brain reduced mouse aversions in the plus‐maze test, indicating the functional presence of CB2‐Rs in the brain that modifies behavior. Using electron microscopy we report the subcellular localization of CB2‐Rs that are mainly on postsynaptic elements in rodent brain. Our data demonstrate the functional expression of CB2‐Rs in the brain that may provide novel targets for the effects of cannabinoids in depression and substance abuse disorders beyond neuroimmunocannabinoid activity. |
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| AbstractList | Major depression and addiction are mental health problems associated with stressful events in life with high relapse and recurrence even after treatment. Many laboratories were not able to detect the presence of CB2 cannabinoid receptors (CB2-Rs) in healthy brains, but CB2-R expression has been demonstrated in rat microglial cells and other brain-associated cells during inflammation. Thus, neuronal expression of CB2-Rs has been ambiguous and controversial, and its role in depression and substance abuse is unknown. In this study we tested the hypothesis that genetic variants of the CB2 gene might be associated with depression in a human population and that alteration in CB2 gene expression may be involved in the effects of abused substances, including opiates, cocaine, and ethanol, in rodents. Here we demonstrate that a high incidence of Q63R but not H316Y polymorphism in the CB2 gene was found in Japanese depressed subjects. CB2-Rs and their gene transcripts are expressed in the brains of naïve mice and are modulated after exposure to stressors and administration of abused drugs. Mice that developed an alcohol preference had reduced CB2 gene expression, and chronic treatment with JWH015 a putative CB2-R agonist, enhanced alcohol consumption in stressed but not in control mice. The direct intracerebroventricular microinjection of CB2 antisense oligonucleotide into the mouse brain reduced mouse aversions in the plus-maze test, indicating the functional presence of CB2-Rs in the brain that modifies behavior. Using electron microscopy we report the subcellular localization of CB2-Rs that are mainly on postsynaptic elements in rodent brain. Our data demonstrate the functional expression of CB2-Rs in the brain that may provide novel targets for the effects of cannabinoids in depression and substance abuse disorders beyond neuroimmunocannabinoid activity.Major depression and addiction are mental health problems associated with stressful events in life with high relapse and recurrence even after treatment. Many laboratories were not able to detect the presence of CB2 cannabinoid receptors (CB2-Rs) in healthy brains, but CB2-R expression has been demonstrated in rat microglial cells and other brain-associated cells during inflammation. Thus, neuronal expression of CB2-Rs has been ambiguous and controversial, and its role in depression and substance abuse is unknown. In this study we tested the hypothesis that genetic variants of the CB2 gene might be associated with depression in a human population and that alteration in CB2 gene expression may be involved in the effects of abused substances, including opiates, cocaine, and ethanol, in rodents. Here we demonstrate that a high incidence of Q63R but not H316Y polymorphism in the CB2 gene was found in Japanese depressed subjects. CB2-Rs and their gene transcripts are expressed in the brains of naïve mice and are modulated after exposure to stressors and administration of abused drugs. Mice that developed an alcohol preference had reduced CB2 gene expression, and chronic treatment with JWH015 a putative CB2-R agonist, enhanced alcohol consumption in stressed but not in control mice. The direct intracerebroventricular microinjection of CB2 antisense oligonucleotide into the mouse brain reduced mouse aversions in the plus-maze test, indicating the functional presence of CB2-Rs in the brain that modifies behavior. Using electron microscopy we report the subcellular localization of CB2-Rs that are mainly on postsynaptic elements in rodent brain. Our data demonstrate the functional expression of CB2-Rs in the brain that may provide novel targets for the effects of cannabinoids in depression and substance abuse disorders beyond neuroimmunocannabinoid activity. Major depression and addiction are mental health problems associated with stressful events in life with high relapse and recurrence even after treatment. Many laboratories were not able to detect the presence of CB2 cannabinoid receptors (CB2-Rs) in healthy brains, but CB2-R expression has been demonstrated in rat microglial cells and other brain-associated cells during inflammation. Thus, neuronal expression of CB2-Rs has been ambiguous and controversial, and its role in depression and substance abuse is unknown. In this study we tested the hypothesis that genetic variants of the CB2 gene might be associated with depression in a human population and that alteration in CB2 gene expression may be involved in the effects of abused substances, including opiates, cocaine, and ethanol, in rodents. Here we demonstrate that a high incidence of Q63R but not H316Y polymorphism in the CB2 gene was found in Japanese depressed subjects. CB2-Rs and their gene transcripts are expressed in the brains of naive mice and are modulated after exposure to stressors and administration of abused drugs. Mice that developed an alcohol preference had reduced CB2 gene expression, and chronic treatment with JWH015 a putative CB2-R agonist, enhanced alcohol consumption in stressed but not in control mice. The direct intracerebroventricular microinjection of CB2 antisense oligonucleotide into the mouse brain reduced mouse aversions in the plus-maze test, indicating the functional presence of CB2-Rs in the brain that modifies behavior. Using electron microscopy we report the subcellular localization of CB2-Rs that are mainly on postsynaptic elements in rodent brain. Our data demonstrate the functional expression of CB2-Rs in the brain that may provide novel targets for the effects of cannabinoids in depression and substance abuse disorders beyond neuroimmunocannabinoid activity. Major depression and addiction are mental health problems associated with stressful events in life with high relapse and recurrence even after treatment. Many laboratories were not able to detect the presence of CB2 cannabinoid receptors (CB2‐Rs) in healthy brains, but CB2‐R expression has been demonstrated in rat microglial cells and other brain‐associated cells during inflammation. Thus, neuronal expression of CB2‐Rs has been ambiguous and controversial, and its role in depression and substance abuse is unknown. In this study we tested the hypothesis that genetic variants of the CB2 gene might be associated with depression in a human population and that alteration in CB2 gene expression may be involved in the effects of abused substances, including opiates, cocaine, and ethanol, in rodents. Here we demonstrate that a high incidence of Q63R but not H316Y polymorphism in the CB2 gene was found in Japanese depressed subjects. CB2‐Rs and their gene transcripts are expressed in the brains of naïve mice and are modulated after exposure to stressors and administration of abused drugs. Mice that developed an alcohol preference had reduced CB2 gene expression, and chronic treatment with JWH015 a putative CB2‐R agonist, enhanced alcohol consumption in stressed but not in control mice. The direct intracerebroventricular microinjection of CB2 antisense oligonucleotide into the mouse brain reduced mouse aversions in the plus‐maze test, indicating the functional presence of CB2‐Rs in the brain that modifies behavior. Using electron microscopy we report the subcellular localization of CB2‐Rs that are mainly on postsynaptic elements in rodent brain. Our data demonstrate the functional expression of CB2‐Rs in the brain that may provide novel targets for the effects of cannabinoids in depression and substance abuse disorders beyond neuroimmunocannabinoid activity. Major depression and addiction are mental health problems associated with stressful events in life with high relapse and reoccurrence even after treatment. Many laboratories were not able to detect the presence of CB2 cannabinoid receptors (CB2-Rs) in healthy brains, but there has been demonstration of CB2-R expression in rat microglial cells and other brain associated cells during inflammation. Therefore, neuronal expression of CB2-Rs had been ambiguous and controversial and its role in depression and substance abuse is unknown. In this study we tested the hypothesis that genetic variants of CB2 gene might be associated with depression in a human population and that alteration in CB2 gene expression may be involved in the effects of abused substances including opiates, cocaine and ethanol in rodents. Here we demonstrate that a high incidence of (Q63R) but not (H316Y) polymorphism in the CB2 gene was found in Japanese depressed subjects. CB2-Rs and their gene transcripts are expressed in the brains of naïve mice and are modulated following exposure to stressors and administration of abused drugs. Mice that developed alcohol preference had reduced CB2 gene expression and chronic treatment with JWH015 a putative CB2-R agonist, enhanced alcohol consumption in stressed but not in control mice. The direct intracerebroventricular microinjection of CB2 anti-sense oligonucleotide into the mouse brain reduced mouse aversions in the plus-maze test, indicating the functional presence of CB2-Rs in the brain that modifies behavior. Using electron microscopy we report the sub cellular localization of CB2-Rs that are mainly on post-synaptic elements in rodent brain. Our data demonstrate the functional expression of CB2-Rs in brain that may provide novel targets for the effects of cannabinoids in depression and substance abuse disorders beyond neuro-immunocannabinoid activity. Major depression and addiction are mental health problems associated with stressful events in life with high relapse and recurrence even after treatment. Many laboratories were not able to detect the presence of CB2 cannabinoid receptors (CB2‐Rs) in healthy brains, but CB2‐R expression has been demonstrated in rat microglial cells and other brain‐associated cells during inflammation. Thus, neuronal expression of CB2‐Rs has been ambiguous and controversial, and its role in depression and substance abuse is unknown. In this study we tested the hypothesis that genetic variants of the CB2 gene might be associated with depression in a human population and that alteration in CB2 gene expression may be involved in the effects of abused substances, including opiates, cocaine, and ethanol, in rodents. Here we demonstrate that a high incidence of Q63R but not H316Y polymorphism in the CB2 gene was found in Japanese depressed subjects. CB2‐Rs and their gene transcripts are expressed in the brains of naïve mice and are modulated after exposure to stressors and administration of abused drugs. Mice that developed an alcohol preference had reduced CB2 gene expression, and chronic treatment with JWH015 a putative CB2‐R agonist, enhanced alcohol consumption in stressed but not in control mice. The direct intracerebroventricular microinjection of CB2 antisense oligonucleotide into the mouse brain reduced mouse aversions in the plus‐maze test, indicating the functional presence of CB2‐Rs in the brain that modifies behavior. Using electron microscopy we report the subcellular localization of CB2‐Rs that are mainly on postsynaptic elements in rodent brain. Our data demonstrate the functional expression of CB2‐Rs in the brain that may provide novel targets for the effects of cannabinoids in depression and substance abuse disorders beyond neuroimmunocannabinoid activity. |
| Author | Hope, Bruce Gong, Jian-Ping Brusco, Alicia Uhl, George R. Perchuk, Alex Gardner, Eileen Iwasaki, Shinya Mora, Zoila Macharia, David Meozzi, Paul A. Myers, Lester Lujilde, Javier Chirwa, Sanika S. Liu, Qing-Rong Ishiguro, Hiroki Patel, Sejal Akinshola, B. Emmanuel Inada, Toshiya Teasenfitz, Lindsey Arinami, Tadao Tagliaferro, Patricia A. Onaivi, Emmanuel S. |
| AuthorAffiliation | 6 Department of Biomedical Sciences, Meharry Medical College, Nashville, TN USA 8 Chiba Medical Center, Teikyo University, Anesaki, Ichihara, Chiba, Japan 4 Facultad de Medicina. Universidad de Buenos Aires, Argentina 5 Department of Pharmacology, Howard University, USA 3 Department of Medical Genetics, Institute of Basic Medical Sciences, University of Tsukuba, Japan 7 Behavioral Neuroscience Branch, Intramural Research Program, NIDA-NIH, USA 1 Department of Biology, William Paterson University, USA 2 Molecular Neurobiology Branch, Intramural Research Program, NIDA-NIH, USA |
| AuthorAffiliation_xml | – name: 2 Molecular Neurobiology Branch, Intramural Research Program, NIDA-NIH, USA – name: 5 Department of Pharmacology, Howard University, USA – name: 3 Department of Medical Genetics, Institute of Basic Medical Sciences, University of Tsukuba, Japan – name: 1 Department of Biology, William Paterson University, USA – name: 6 Department of Biomedical Sciences, Meharry Medical College, Nashville, TN USA – name: 8 Chiba Medical Center, Teikyo University, Anesaki, Ichihara, Chiba, Japan – name: 7 Behavioral Neuroscience Branch, Intramural Research Program, NIDA-NIH, USA – name: 4 Facultad de Medicina. Universidad de Buenos Aires, Argentina |
| Author_xml | – sequence: 1 givenname: Emmanuel S. surname: Onaivi fullname: Onaivi, Emmanuel S. organization: Department of Biology, William Paterson University, Wayne, New Jersey, USA – sequence: 2 givenname: Hiroki surname: Ishiguro fullname: Ishiguro, Hiroki organization: Molecular Neurobiology Branch, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland, USA – sequence: 3 givenname: Jian-Ping surname: Gong fullname: Gong, Jian-Ping organization: Molecular Neurobiology Branch, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland, USA – sequence: 4 givenname: Sejal surname: Patel fullname: Patel, Sejal organization: Department of Biology, William Paterson University, Wayne, New Jersey, USA – sequence: 5 givenname: Paul A. surname: Meozzi fullname: Meozzi, Paul A. organization: Department of Biology, William Paterson University, Wayne, New Jersey, USA – sequence: 6 givenname: Lester surname: Myers fullname: Myers, Lester organization: Department of Biology, William Paterson University, Wayne, New Jersey, USA – sequence: 7 givenname: Alex surname: Perchuk fullname: Perchuk, Alex organization: Department of Biology, William Paterson University, Wayne, New Jersey, USA – sequence: 8 givenname: Zoila surname: Mora fullname: Mora, Zoila organization: Department of Biology, William Paterson University, Wayne, New Jersey, USA – sequence: 9 givenname: Patricia A. surname: Tagliaferro fullname: Tagliaferro, Patricia A. organization: Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina – sequence: 10 givenname: Eileen surname: Gardner fullname: Gardner, Eileen organization: Department of Biology, William Paterson University, Wayne, New Jersey, USA – sequence: 11 givenname: Alicia surname: Brusco fullname: Brusco, Alicia organization: Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina – sequence: 12 givenname: B. Emmanuel surname: Akinshola fullname: Akinshola, B. Emmanuel organization: Department of Pharmacology, Howard University, Washington, D.C., USA – sequence: 13 givenname: Qing-Rong surname: Liu fullname: Liu, Qing-Rong organization: Molecular Neurobiology Branch, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland, USA – sequence: 14 givenname: Sanika S. surname: Chirwa fullname: Chirwa, Sanika S. organization: Department of Biomedical Sciences, Meharry Medical College, Nashville, Tennessee, USA – sequence: 15 givenname: Bruce surname: Hope fullname: Hope, Bruce organization: Behavioral Neuroscience Branch, Intramural Research Program, NIDA-NIH, Baltimore, Maryland, USA – sequence: 16 givenname: Javier surname: Lujilde fullname: Lujilde, Javier organization: Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina – sequence: 17 givenname: Toshiya surname: Inada fullname: Inada, Toshiya organization: Chiba Medical Center, Teikyo University, Anesaki, Ichihara, Chiba, Japan – sequence: 18 givenname: Shinya surname: Iwasaki fullname: Iwasaki, Shinya organization: Molecular Neurobiology Branch, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland, USA – sequence: 19 givenname: David surname: Macharia fullname: Macharia, David organization: Department of Biology, William Paterson University, Wayne, New Jersey, USA – sequence: 20 givenname: Lindsey surname: Teasenfitz fullname: Teasenfitz, Lindsey organization: Department of Biology, William Paterson University, Wayne, New Jersey, USA – sequence: 21 givenname: Tadao surname: Arinami fullname: Arinami, Tadao organization: Molecular Neurobiology Branch, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland, USA – sequence: 22 givenname: George R. surname: Uhl fullname: Uhl, George R. organization: Molecular Neurobiology Branch, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/18991891$$D View this record in MEDLINE/PubMed |
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| References | Ehrhart, J. et al . 2005. Stimulation of cannabinoid receptor 2 (CB2) suppresses microglial activation. J. Neuroinflammation 2: 29-42. Onaivi, E.S., V. Di Marzo & T. Sugiura. 2005. Endocannabinoids: The Brain and Body's Marijuana and Beyond. p. 563. CRC. Boca Raton , FL . Ishiguro, H. et al . 2006. Involvement of cannabinoid CB2 receptor in alcohol preference in mice and alcoholism in humans. Pharmacogenomics J. 7: 380-385. Benito, C. et al . 2005. A glial endogenous cannabinoid system is upregulated in the brains of macaques with simian immunodeficiency virus-induced encephalitis. J. Neurosci. 25: 2530-2536. Pickel, V.M. et al . 2006. Targeting dopamine D2 and cannabinoid-1 (CB1) receptors in rat nucleus accumbens. J. Comp. Neurol. 495: 299-313. Manzanares, J. et al . 2004. Role of endocannabinoid system in mental diseases. Neurotox Res. 6: 213-224. Ibrahim, M.M. et al . 2003. Activation of CB2 cannabinoid receptors by AM1241 inhibits experimental neuropathic pain: pain inhibition by receptors not present in the CNS. Proc. Natl. Acad. Sci. USA 100: 10529-10533. Zhong, L. et al . 2005. CB2 cannabinoid receptors in trabecular meshwork cells mediate JWH015-induced enhancement of aqueous humor outflow facility. Invest. Ophthalmol. Vis. Sci. 46: 1988-1992. Benito, C. et al . 2003. Cannabinoid CB2 receptors and fatty acid amide hydrolase are selectively overexpressed in neuritic plaque-associated glia in Alzheimer's disease brains. J. Neurosci. 23: 11136-11141. Beltramo, M. et al. (2006. CB2 receptor-mediated antihyperalgesia: possible direct involvement of neural mechanisms. Eur. J. Neurosci. 23: 1530-1538. Degenhardt, L. et al . 2001. Alcohol, cannabis and tobacco use among Australians: a comparison of their associations with other drug use and use disorders, affective and anxiety disorders, and psychosis. Addiction 96: 1603-1614. Galiegue, S. et al . 1995. Expression of central and peripheral cannabinoid receptors in human immune tissues and leukocyte subpopulations. Eur. J. Biochem. 232: 54-61. Onaivi, E.S. et al . 2006. Methods to study the behavioral effects and expression of CB2 cannabinoid receptor and its gene transcripts in the chronic mild stress model of depression. Methods Mol. Med. 123: 291-298. Griffin, G. et al . 1999. Evaluation of the cannabinoid CB2 receptor-selective antagonist, SR144528: further evidence for cannabinoid CB2 receptor absence in the rat central nervous system. Eur. J. Pharmacol. 377: 117-125. Golech, S.A. et al . 2004. Human brain endothelium: coexpression and function of vanilloid and endocannabinoid receptors. Brain Res. Mol. Brain Res. 132: 87-92. Volkow, N.D. & T.K. Li. 2005. Drugs and alcohol: treating and preventing abuse, addiction and their medical consequences. Pharmacol. Ther. 108: 3-17. Nunez, E. et al . 2004. Cannabinoid CB2 receptors are expressed by perivascular microglial cells in the human brain: an immunohistochemical study. Synapse 53: 208-213. Willner, P. 2005. Chronic mild stress (CMS) revisited: consistency and behavioural-neurobiological concordance in the effects of CMS. Neuropsychobiology 52: 90-110. Ashton, J.C. et al . 2006. Expression of the cannabinoid CB2 receptor in the rat cerebellum: an immunohistochemical study. Neurosci. Lett. 396: 113-116. Nieri, P. et al . 2003. CB1- and CB2-cannabinoid receptor-independent lipolysis induced by WIN 55, 212-2 in male rat adipocytes. Naunyn Schmiedebergs Arch. Pharmacol. 368: 352-359. Buckley, N.E. et al . 2000. Immunomodulation by cannabinoids is absent in mice deficient for the cannabinoid CB(2) receptor. Eur. J. Pharmacol. 396: 141-149. Sheng, W.S. et al . 2005. Synthetic cannabinoid WIN55, 212-2 inhibits generation of inflammatory mediators by IL-1beta-stimulated human astrocytes. Glia 49: 211-219. Onaivi, E.S. et al . 1990. Pharmacological characterization of cannabinoids in the elevated plus maze. J. Pharmacol. Exp. Ther. 253: 1002-1009. Reynolds, E.S. 1963. The use of lead citrate at high pH as an electron-opaque stain in electron microscopy. J. Cell Biol. 17: 208-212. Zhang, P.W. et al . 2004. Human cannabinoid receptor 1: 5′ exons, candidate regulatory regions, polymorphisms, haplotypes and association with polysubstance abuse. Mol. Psychiatry 9: 916-931. Bovasso, G.B. 2001. Cannabis abuse as a risk factor for depressive symptoms. Am. J. Psychiatry 158: 2033-2037. Patton, G.C. et al . 2002. Cannabis use and mental health in young people: cohort study. BMJ 325: 1195-1198. Paxinos, G. & C. Watson. 2005. The Rat Brain in Stereotaxic Coordinates. p. xiii [166]. Elsevier. Amsterdam . Sipe, J.C. et al . 2005. Reduced endocannabinoid immune modulation by a common cannabinoid 2 (CB2) receptor gene polymorphism: possible risk for autoimmune disorders. J. Leukoc. Biol. 78: 231-238. Van Sickle, M.D. et al . 2005. Identification and functional characterization of brainstem cannabinoid CB2 receptors. Science 310: 329-332. Munro, S. et al . 1993. Molecular characterization of a peripheral receptor for cannabinoids. Nature 365: 61-65. Vinod, K.Y. & B.L. Hungund. 2006. Role of the endocannabinoid system in depression and suicide. Trends Pharmacol. Sci. 27: 539-545. Valenzano, K.J. et al . 2005. Pharmacological and pharmacokinetic characterization of the cannabinoid receptor 2 agonist, GW405833, utilizing rodent models of acute and chronic pain, anxiety, ataxia and catalepsy. Neuropharmacology 48: 658-672. Gong, J.P. et al . 2006. Cannabinoid CB2 receptors: immunohistochemical localization in rat brain. Brain Res. 1071: 10-23. Karsak, M. et al . 2005. Cannabinoid receptor type 2 gene is associated with human osteoporosis. Hum. Mol. Genet. 14: 3389-3396. 2005; 310 2004; 9 2006; 7 2004; 6 2006; 396 2006; 495 2005 2000; 396 1995; 232 2005; 48 2005; 49 1993; 365 2005; 46 2005; 25 2004; 132 2004; 53 2006; 23 2006; 27 2005; 52 2005; 108 2002; 325 1999; 377 2005; 2 2003; 368 1990; 253 2003; 100 2006; 123 1963; 17 2001; 96 2001; 158 2005; 78 2003; 23 2006; 1071 2005; 14 e_1_2_7_5_2 e_1_2_7_4_2 e_1_2_7_3_2 e_1_2_7_2_2 e_1_2_7_9_2 e_1_2_7_8_2 e_1_2_7_7_2 e_1_2_7_6_2 e_1_2_7_18_2 e_1_2_7_17_2 e_1_2_7_16_2 e_1_2_7_15_2 e_1_2_7_14_2 e_1_2_7_13_2 e_1_2_7_12_2 e_1_2_7_11_2 e_1_2_7_10_2 e_1_2_7_27_2 e_1_2_7_28_2 Onaivi E.S. (e_1_2_7_26_2) 1990; 253 e_1_2_7_29_2 Paxinos G. (e_1_2_7_22_2) 2005 e_1_2_7_25_2 e_1_2_7_24_2 e_1_2_7_30_2 e_1_2_7_23_2 e_1_2_7_31_2 e_1_2_7_32_2 e_1_2_7_21_2 e_1_2_7_33_2 e_1_2_7_20_2 e_1_2_7_34_2 e_1_2_7_35_2 e_1_2_7_36_2 Onaivi E.S. (e_1_2_7_19_2) 2006; 123 |
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Psychiatry – volume: 23 start-page: 1530 year: 2006 end-page: 1538 article-title: CB2 receptor‐mediated antihyperalgesia: possible direct involvement of neural mechanisms publication-title: Eur. J. Neurosci. – volume: 6 start-page: 213 year: 2004 end-page: 224 article-title: Role of endocannabinoid system in mental diseases publication-title: Neurotox Res. – volume: 53 start-page: 208 year: 2004 end-page: 213 article-title: Cannabinoid CB2 receptors are expressed by perivascular microglial cells in the human brain: an immunohistochemical study publication-title: Synapse – volume: 25 start-page: 2530 year: 2005 end-page: 2536 article-title: A glial endogenous cannabinoid system is upregulated in the brains of macaques with simian immunodeficiency virus‐induced encephalitis publication-title: J. Neurosci. – volume: 123 start-page: 291 year: 2006 end-page: 298 article-title: Methods to study the behavioral effects and expression of CB2 cannabinoid receptor and its gene transcripts in the chronic mild stress model of depression publication-title: Methods Mol. Med. – volume: 96 start-page: 1603 year: 2001 end-page: 1614 article-title: Alcohol, cannabis and tobacco use among Australians: a comparison of their associations with other drug use and use disorders, affective and anxiety disorders, and psychosis publication-title: Addiction – volume: 132 start-page: 87 year: 2004 end-page: 92 article-title: Human brain endothelium: coexpression and function of vanilloid and endocannabinoid receptors publication-title: Brain Res. Mol. Brain Res. – volume: 377 start-page: 117 year: 1999 end-page: 125 article-title: Evaluation of the cannabinoid CB2 receptor‐selective antagonist, SR144528: further evidence for cannabinoid CB2 receptor absence in the rat central nervous system publication-title: Eur. J. Pharmacol. – volume: 310 start-page: 329 year: 2005 end-page: 332 article-title: Identification and functional characterization of brainstem cannabinoid CB2 receptors publication-title: Science – volume: 396 start-page: 113 year: 2006 end-page: 116 article-title: Expression of the cannabinoid CB2 receptor in the rat cerebellum: an immunohistochemical study publication-title: Neurosci. Lett. – volume: 7 start-page: 380 year: 2006 end-page: 385 article-title: Involvement of cannabinoid CB2 receptor in alcohol preference in mice and alcoholism in humans publication-title: Pharmacogenomics J. – volume: 46 start-page: 1988 year: 2005 end-page: 1992 article-title: CB2 cannabinoid receptors in trabecular meshwork cells mediate JWH015‐induced enhancement of aqueous humor outflow facility publication-title: Invest. Ophthalmol. Vis. Sci. – volume: 49 start-page: 211 year: 2005 end-page: 219 article-title: Synthetic cannabinoid WIN55, 212‐2 inhibits generation of inflammatory mediators by IL‐1beta‐stimulated human astrocytes publication-title: Glia – volume: 100 start-page: 10529 year: 2003 end-page: 10533 article-title: Activation of CB2 cannabinoid receptors by AM1241 inhibits experimental neuropathic pain: pain inhibition by receptors not present in the CNS publication-title: Proc. Natl. Acad. Sci. 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| SubjectTerms | anhedonia Animals Asian People - genetics Behavior, Animal - physiology brain Brain - cytology Brain - metabolism chronic mild stress depression Depression - genetics Depression - physiopathology drug abuse electron micrograph Female Humans Male Mice Mice, Inbred Strains Mice, Knockout Motor Activity - physiology neuronal CB2 cannabinoid receptors Oligonucleotides, Antisense - genetics Oligonucleotides, Antisense - metabolism Polymorphism, Genetic Rats Rats, Sprague-Dawley Receptor, Cannabinoid, CB2 - genetics Receptor, Cannabinoid, CB2 - metabolism Stress, Psychological - metabolism Substance-Related Disorders - genetics |
| Title | Functional Expression of Brain Neuronal CB2 Cannabinoid Receptors Are Involved in the Effects of Drugs of Abuse and in Depression |
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