Brain Neuronal CB2 Cannabinoid Receptors in Drug Abuse and Depression: From Mice to Human Subjects
Addiction and major depression 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 cannabinoid CB2 receptors (CB2-Rs) in healthy brains, but there has been demonstration...
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| Published in | PloS one Vol. 3; no. 2; p. e1640 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Public Library of Science
20.02.2008
Public Library of Science (PLoS) |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1932-6203 1932-6203 |
| DOI | 10.1371/journal.pone.0001640 |
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| Abstract | Addiction and major depression 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 cannabinoid CB2 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. We report for the using electron microscopy 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. |
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| AbstractList | Background Addiction and major depression 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 cannabinoid CB2 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. Methodology/Principal Findings 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. We report for the using electron microscopy the sub cellular localization of CB2-Rs that are mainly on post-synaptic elements in rodent brain. Conclusions/Significance 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. Addiction and major depression 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 cannabinoid CB2 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. We report for the using electron microscopy 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. Addiction and major depression 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 cannabinoid CB2 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.BACKGROUNDAddiction and major depression 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 cannabinoid CB2 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. We report for the using electron microscopy the sub cellular localization of CB2-Rs that are mainly on post-synaptic elements in rodent brain.METHODOLOGY/PRINCIPAL FINDINGSIn 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. We report for the using electron microscopy 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.CONCLUSIONS/SIGNIFICANCEOur 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. Background Addiction and major depression 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 cannabinoid CB2 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. Methodology/Principal Findings 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. We report for the using electron microscopy the sub cellular localization of CB2-Rs that are mainly on post-synaptic elements in rodent brain. Conclusions/Significance 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. Addiction and major depression 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 cannabinoid CB2 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. We report for the using electron microscopy 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. |
| Audience | Academic |
| 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 Ishiguro, Hiroki Patel, Sejal Akinshola, B. Emmanuel Inada, Toshiya Teasenfitz, Lindsey Arinami, Tadao Tagliaferro, Patricia A. Onaivi, Emmanuel S. |
| AuthorAffiliation | 2 Molecular Neurobiology Branch, Intramural Research Program, National Institute on Drug Abuse (NID)-National Institutes of Health (NIH), Bethesda, Maryland, United States of America 1 Department of Biology, William Paterson University, Wayne, New Jersey, United States of America University of Sydney, Australia 7 Chiba Medical Center, Teikyo University, Ichihara, Chiba, Japan 6 Behavioral Neuroscience Branch, Intramural Research Program, National Institute on Drug Abuse (NID)-National Institutes of Health (NIH), Bethesda, Maryland, United States of America 3 Department of Medical Genetics, Institute of Basic Medical Sciences, University of Tsukuba, Japan 4 Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina 5 Department of Pharmacology, Howard University, Washington, D. C., United States of America |
| AuthorAffiliation_xml | – name: 2 Molecular Neurobiology Branch, Intramural Research Program, National Institute on Drug Abuse (NID)-National Institutes of Health (NIH), Bethesda, Maryland, United States of America – name: 3 Department of Medical Genetics, Institute of Basic Medical Sciences, University of Tsukuba, Japan – name: 6 Behavioral Neuroscience Branch, Intramural Research Program, National Institute on Drug Abuse (NID)-National Institutes of Health (NIH), Bethesda, Maryland, United States of America – name: 5 Department of Pharmacology, Howard University, Washington, D. C., United States of America – name: 4 Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina – name: University of Sydney, Australia – name: 1 Department of Biology, William Paterson University, Wayne, New Jersey, United States of America – name: 7 Chiba Medical Center, Teikyo University, Ichihara, Chiba, Japan |
| Author_xml | – sequence: 1 givenname: Emmanuel S. surname: Onaivi fullname: Onaivi, Emmanuel S. – sequence: 2 givenname: Hiroki surname: Ishiguro fullname: Ishiguro, Hiroki – sequence: 3 givenname: Jian-Ping surname: Gong fullname: Gong, Jian-Ping – sequence: 4 givenname: Sejal surname: Patel fullname: Patel, Sejal – sequence: 5 givenname: Paul A. surname: Meozzi fullname: Meozzi, Paul A. – sequence: 6 givenname: Lester surname: Myers fullname: Myers, Lester – sequence: 7 givenname: Alex surname: Perchuk fullname: Perchuk, Alex – sequence: 8 givenname: Zoila surname: Mora fullname: Mora, Zoila – sequence: 9 givenname: Patricia A. surname: Tagliaferro fullname: Tagliaferro, Patricia A. – sequence: 10 givenname: Eileen surname: Gardner fullname: Gardner, Eileen – sequence: 11 givenname: Alicia surname: Brusco fullname: Brusco, Alicia – sequence: 12 givenname: B. Emmanuel surname: Akinshola fullname: Akinshola, B. Emmanuel – sequence: 13 givenname: Bruce surname: Hope fullname: Hope, Bruce – sequence: 14 givenname: Javier surname: Lujilde fullname: Lujilde, Javier – sequence: 15 givenname: Toshiya surname: Inada fullname: Inada, Toshiya – sequence: 16 givenname: Shinya surname: Iwasaki fullname: Iwasaki, Shinya – sequence: 17 givenname: David surname: Macharia fullname: Macharia, David – sequence: 18 givenname: Lindsey surname: Teasenfitz fullname: Teasenfitz, Lindsey – sequence: 19 givenname: Tadao surname: Arinami fullname: Arinami, Tadao – sequence: 20 givenname: George R. surname: Uhl fullname: Uhl, George R. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/18286196$$D View this record in MEDLINE/PubMed |
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| Snippet | Addiction and major depression are mental health problems associated with stressful events in life with high relapse and reoccurrence even after treatment.... Background Addiction and major depression are mental health problems associated with stressful events in life with high relapse and reoccurrence even after... BACKGROUND: Addiction and major depression are mental health problems associated with stressful events in life with high relapse and reoccurrence even after... Background Addiction and major depression are mental health problems associated with stressful events in life with high relapse and reoccurrence even after... |
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| SubjectTerms | Adipocytes Alcohol Alcohol use Alcoholic beverages Animals Antisense oligonucleotides Autoimmune diseases Biology Brain Brain Chemistry Brain research Cannabinoid CB2 receptors Cocaine Depression (Mood disorder) Depressive Disorder - genetics Dopamine Drug abuse Drug therapy Drugs Electron microscopy Ethanol Gene expression Gene Expression Regulation - drug effects Gene polymorphism Genes Genetic diversity Genetic polymorphisms Genetic variance Genetics and Genomics/Animal Genetics Genetics and Genomics/Gene Function Haplotypes Health problems Human populations Humans Localization Mammals Marijuana Mental depression Mental disorders Mental health Mice Microglia Microglial cells Microinjection Narcotics Neurobiology Neurons Neurons - chemistry Neuroscience/Behavioral Neuroscience Neurosciences Opiates Opioids Osteoporosis Pharmacology Polymorphism Polymorphism, Genetic Receptor, Cannabinoid, CB2 - analysis Receptor, Cannabinoid, CB2 - genetics Receptors Rodentia Rodents Substance-Related Disorders - genetics |
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| Title | Brain Neuronal CB2 Cannabinoid Receptors in Drug Abuse and Depression: From Mice to Human Subjects |
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