Brain Cannabinoid CB2 Receptor in Schizophrenia
Neural endocannabinoid function appears to be involved in schizophrenia. Two endocannabinoid receptors, CB1 and CB2, are found in the brain and elsewhere in the body. We investigated roles of CB2 in schizophrenia. An association study was performed between tag single nucleotide polymorphisms (SNPs)...
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| Published in | Biological psychiatry (1969) Vol. 67; no. 10; pp. 974 - 982 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
New York, NY
Elsevier Inc
15.05.2010
Elsevier |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0006-3223 1873-2402 1873-2402 |
| DOI | 10.1016/j.biopsych.2009.09.024 |
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| Abstract | Neural endocannabinoid function appears to be involved in schizophrenia. Two endocannabinoid receptors, CB1 and CB2, are found in the brain and elsewhere in the body. We investigated roles of CB2 in schizophrenia.
An association study was performed between tag single nucleotide polymorphisms (SNPs) in the
CNR2 gene encoding the CB2 receptor and schizophrenia in two independent case-control populations. Allelic differences of associated SNPs were analyzed in human postmortem brain tissues and in cultured cells. Prepulse inhibition and locomotor activity in C57BL/6JJmsSlc mice with CB2 receptor antagonist AM630 administration was examined.
The analysis in the first population revealed nominally significant associations between schizophrenia and two SNPs, and the associations were replicated in the second population. The R63 allele of rs2501432 (R63Q) (
p = .001), the C allele of rs12744386 (
p = .005) and the haplotype of the R63-C allele (
p = 5 × 10
−6) were significantly increased among 1920 patients with schizophrenia compared with 1920 control subjects in the combined population. A significantly lower response to CB2 ligands in cultured CHO cells transfected with the R63 allele compared with those with Q63, and significantly lower CB2 receptor mRNA and protein levels found in human brain with the CC and CT genotypes of rs12744386 compared with TT genotype were observed. AM630 exacerbated MK-801- or methamphetamine-induced disturbance of prepulse inhibition and hyperactivity in C57BL/6JJmsSlc mice.
These findings indicate an increased risk of schizophrenia for people with low CB2 receptor function. |
|---|---|
| AbstractList | Neural endocannabinoid function appears to be involved in schizophrenia. Two endocannabinoid receptors, CB1 and CB2, are found in the brain and elsewhere in the body. We investigated roles of CB2 in schizophrenia.BACKGROUNDNeural endocannabinoid function appears to be involved in schizophrenia. Two endocannabinoid receptors, CB1 and CB2, are found in the brain and elsewhere in the body. We investigated roles of CB2 in schizophrenia.An association study was performed between tag single nucleotide polymorphisms (SNPs) in the CNR2 gene encoding the CB2 receptor and schizophrenia in two independent case-control populations. Allelic differences of associated SNPs were analyzed in human postmortem brain tissues and in cultured cells. Prepulse inhibition and locomotor activity in C57BL/6JJmsSlc mice with CB2 receptor antagonist AM630 administration was examined.MATERIALS AND METHODSAn association study was performed between tag single nucleotide polymorphisms (SNPs) in the CNR2 gene encoding the CB2 receptor and schizophrenia in two independent case-control populations. Allelic differences of associated SNPs were analyzed in human postmortem brain tissues and in cultured cells. Prepulse inhibition and locomotor activity in C57BL/6JJmsSlc mice with CB2 receptor antagonist AM630 administration was examined.The analysis in the first population revealed nominally significant associations between schizophrenia and two SNPs, and the associations were replicated in the second population. The R63 allele of rs2501432 (R63Q) (p = .001), the C allele of rs12744386 (p = .005) and the haplotype of the R63-C allele (p = 5 x 10(-6)) were significantly increased among 1920 patients with schizophrenia compared with 1920 control subjects in the combined population. A significantly lower response to CB2 ligands in cultured CHO cells transfected with the R63 allele compared with those with Q63, and significantly lower CB2 receptor mRNA and protein levels found in human brain with the CC and CT genotypes of rs12744386 compared with TT genotype were observed. AM630 exacerbated MK-801- or methamphetamine-induced disturbance of prepulse inhibition and hyperactivity in C57BL/6JJmsSlc mice.RESULTSThe analysis in the first population revealed nominally significant associations between schizophrenia and two SNPs, and the associations were replicated in the second population. The R63 allele of rs2501432 (R63Q) (p = .001), the C allele of rs12744386 (p = .005) and the haplotype of the R63-C allele (p = 5 x 10(-6)) were significantly increased among 1920 patients with schizophrenia compared with 1920 control subjects in the combined population. A significantly lower response to CB2 ligands in cultured CHO cells transfected with the R63 allele compared with those with Q63, and significantly lower CB2 receptor mRNA and protein levels found in human brain with the CC and CT genotypes of rs12744386 compared with TT genotype were observed. AM630 exacerbated MK-801- or methamphetamine-induced disturbance of prepulse inhibition and hyperactivity in C57BL/6JJmsSlc mice.These findings indicate an increased risk of schizophrenia for people with low CB2 receptor function.CONCLUSIONSThese findings indicate an increased risk of schizophrenia for people with low CB2 receptor function. Neural endocannabinoid function appears to be involved in schizophrenia. Two endocannabinoid receptors, CB1 and CB2, are found in the brain and elsewhere in the body. We investigated roles of CB2 in schizophrenia. An association study was performed between tag single nucleotide polymorphisms (SNPs) in the CNR2 gene encoding the CB2 receptor and schizophrenia in two independent case-control populations. Allelic differences of associated SNPs were analyzed in human postmortem brain tissues and in cultured cells. Prepulse inhibition and locomotor activity in C57BL/6JJmsSlc mice with CB2 receptor antagonist AM630 administration was examined. The analysis in the first population revealed nominally significant associations between schizophrenia and two SNPs, and the associations were replicated in the second population. The R63 allele of rs2501432 (R63Q) ( p = .001), the C allele of rs12744386 ( p = .005) and the haplotype of the R63-C allele ( p = 5 × 10 −6) were significantly increased among 1920 patients with schizophrenia compared with 1920 control subjects in the combined population. A significantly lower response to CB2 ligands in cultured CHO cells transfected with the R63 allele compared with those with Q63, and significantly lower CB2 receptor mRNA and protein levels found in human brain with the CC and CT genotypes of rs12744386 compared with TT genotype were observed. AM630 exacerbated MK-801- or methamphetamine-induced disturbance of prepulse inhibition and hyperactivity in C57BL/6JJmsSlc mice. These findings indicate an increased risk of schizophrenia for people with low CB2 receptor function. Neural endocannabinoid function appears to be involved in schizophrenia. Two endocannabinoid receptors, CB1 and CB2, are found in the brain and elsewhere in the body. We investigated roles of CB2 in schizophrenia. Materials and Methods - An association study was performed between tag single nucleotide polymorphisms (SNPs) in the CNR2 gene encoding the CB2 receptor and schizophrenia in two independent case-control populations. Allelic differences of associated SNPs were analyzed in human postmortem brain tissues and in cultured cells. Prepulse inhibition and locomotor activity in C57BL/6JJmsSlc mice with CB2 receptor antagonist AM630 administration was examined. Results - The analysis in the first population revealed nominally significant associations between schizophrenia and two SNPs, and the associations were replicated in the second population. The R63 allele of rs2501432 (R63Q) (p = .001), the C allele of rs12744386 (p = .005) and the haplotype of the R63-C allele (p = 5 x 10 super(-6)) were significantly increased among 1920 patients with schizophrenia compared with 1920 control subjects in the combined population. A significantly lower response to CB2 ligands in cultured CHO cells transfected with the R63 allele compared with those with Q63, and significantly lower CB2 receptor mRNA and protein levels found in human brain with the CC and CT genotypes of rs12744386 compared with TT genotype were observed. AM630 exacerbated MK-801- or methamphetamine-induced disturbance of prepulse inhibition and hyperactivity in C57BL/6JJmsSlc mice. Conclusions - These findings indicate an increased risk of schizophrenia for people with low CB2 receptor function. Background Neural endocannabinoid function appears to be involved in schizophrenia. Two endocannabinoid receptors, CB1 and CB2, are found in the brain and elsewhere in the body. We investigated roles of CB2 in schizophrenia. Materials and Methods An association study was performed between tag single nucleotide polymorphisms (SNPs) in the CNR2 gene encoding the CB2 receptor and schizophrenia in two independent case-control populations. Allelic differences of associated SNPs were analyzed in human postmortem brain tissues and in cultured cells. Prepulse inhibition and locomotor activity in C57BL/6JJmsSlc mice with CB2 receptor antagonist AM630 administration was examined. Results The analysis in the first population revealed nominally significant associations between schizophrenia and two SNPs, and the associations were replicated in the second population. The R63 allele of rs2501432 (R63Q) ( p = .001), the C allele of rs12744386 ( p = .005) and the haplotype of the R63-C allele ( p = 5 × 10−6 ) were significantly increased among 1920 patients with schizophrenia compared with 1920 control subjects in the combined population. A significantly lower response to CB2 ligands in cultured CHO cells transfected with the R63 allele compared with those with Q63, and significantly lower CB2 receptor mRNA and protein levels found in human brain with the CC and CT genotypes of rs12744386 compared with TT genotype were observed. AM630 exacerbated MK-801- or methamphetamine-induced disturbance of prepulse inhibition and hyperactivity in C57BL/6JJmsSlc mice. Conclusions These findings indicate an increased risk of schizophrenia for people with low CB2 receptor function. Neural endocannabinoid function appears to be involved in schizophrenia. Two endocannabinoid receptors, CB1 and CB2, are found in the brain and elsewhere in the body. We investigated roles of CB2 in schizophrenia. An association study was performed between tag single nucleotide polymorphisms (SNPs) in the CNR2 gene encoding the CB2 receptor and schizophrenia in two independent case-control populations. Allelic differences of associated SNPs were analyzed in human postmortem brain tissues and in cultured cells. Prepulse inhibition and locomotor activity in C57BL/6JJmsSlc mice with CB2 receptor antagonist AM630 administration was examined. The analysis in the first population revealed nominally significant associations between schizophrenia and two SNPs, and the associations were replicated in the second population. The R63 allele of rs2501432 (R63Q) (p = .001), the C allele of rs12744386 (p = .005) and the haplotype of the R63-C allele (p = 5 x 10(-6)) were significantly increased among 1920 patients with schizophrenia compared with 1920 control subjects in the combined population. A significantly lower response to CB2 ligands in cultured CHO cells transfected with the R63 allele compared with those with Q63, and significantly lower CB2 receptor mRNA and protein levels found in human brain with the CC and CT genotypes of rs12744386 compared with TT genotype were observed. AM630 exacerbated MK-801- or methamphetamine-induced disturbance of prepulse inhibition and hyperactivity in C57BL/6JJmsSlc mice. These findings indicate an increased risk of schizophrenia for people with low CB2 receptor function. |
| Author | Arai, Makoto Kakita, Akiyoshi Ishikawa, Maya Iritani, Shyuji Takahashi, Makoto Ozaki, Norio Koga, Minori Watanabe, Yuichiro Suzuki, Yoshimi Ishiguro, Hiroki Takahashi, Hitoshi Someya, Toshiyuki Ujike, Hiroshi Kunugi, Hiroshi Inada, Toshiya Morikawa, Miyuki Arinami, Tadao Itokawa, Masanari Nawa, Hiroyuki Ohashi, Jun Sasaki, Tsukasa Imai, Keiko Niizato, Kazuhiro Horiuchi, Yasue Iwata, Nakao Naka, Izumi Onaivi, Emmanuel S. |
| Author_xml | – sequence: 1 givenname: Hiroki surname: Ishiguro fullname: Ishiguro, Hiroki email: hishigur@md.tsukuba.ac.jp organization: Department of Medical Genetics, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan – sequence: 2 givenname: Yasue surname: Horiuchi fullname: Horiuchi, Yasue organization: Department of Medical Genetics, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan – sequence: 3 givenname: Maya surname: Ishikawa fullname: Ishikawa, Maya organization: Department of Medical Genetics, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan – sequence: 4 givenname: Minori surname: Koga fullname: Koga, Minori organization: Department of Medical Genetics, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan – sequence: 5 givenname: Keiko surname: Imai fullname: Imai, Keiko organization: Department of Medical Genetics, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan – sequence: 6 givenname: Yoshimi surname: Suzuki fullname: Suzuki, Yoshimi organization: Department of Medical Genetics, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan – sequence: 7 givenname: Miyuki surname: Morikawa fullname: Morikawa, Miyuki organization: Department of Medical Genetics, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan – sequence: 8 givenname: Toshiya surname: Inada fullname: Inada, Toshiya organization: Seiwa Hospital, Institute of Neuropsychiatry, Tokyo, Japan – sequence: 9 givenname: Yuichiro surname: Watanabe fullname: Watanabe, Yuichiro organization: Department of Psychiatry, Niigata University, Graduate School of Medical and Dental Sciences, Niigata, Japan – sequence: 10 givenname: Makoto surname: Takahashi fullname: Takahashi, Makoto organization: Department of Psychiatry, Niigata University, Graduate School of Medical and Dental Sciences, Niigata, Japan – sequence: 11 givenname: Toshiyuki surname: Someya fullname: Someya, Toshiyuki organization: Department of Psychiatry, Niigata University, Graduate School of Medical and Dental Sciences, Niigata, Japan – sequence: 12 givenname: Hiroshi surname: Ujike fullname: Ujike, Hiroshi organization: Department of Neuropsychiatry, Okayama University, Graduate School of Medicine, Dentistry & Pharmaceutical Sciences, Shikata-cho, Okayama, Japan – sequence: 13 givenname: Nakao surname: Iwata fullname: Iwata, Nakao organization: Department of Psychiatry, Fujita Health University School of Medicine, Toyoake, Aichi, Japan – sequence: 14 givenname: Norio surname: Ozaki fullname: Ozaki, Norio organization: Department of Psychiatry, School of Medicine, Nagoya University, Nagoya, Aichi, Japan – sequence: 15 givenname: Emmanuel S. surname: Onaivi fullname: Onaivi, Emmanuel S. organization: Department of Biology, William Paterson University, Wayne, New Jersey – sequence: 16 givenname: Hiroshi surname: Kunugi fullname: Kunugi, Hiroshi organization: National Center of Neurology and Psychiatry, Tokyo, Japan – sequence: 17 givenname: Tsukasa surname: Sasaki fullname: Sasaki, Tsukasa organization: Health Service Center, University of Tokyo, Tokyo, Japan – sequence: 18 givenname: Masanari surname: Itokawa fullname: Itokawa, Masanari organization: Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Kawaguchi-shi, Saitama, Japan – sequence: 19 givenname: Makoto surname: Arai fullname: Arai, Makoto organization: Department of Schizophrenia Research, Tokyo Institute of Psychiatry, Tokyo, Japan – sequence: 20 givenname: Kazuhiro surname: Niizato fullname: Niizato, Kazuhiro organization: Tokyo Metropolitan Matsuzawa Hospital, Department of Psychiatry, Tokyo, Japan – sequence: 21 givenname: Shyuji surname: Iritani fullname: Iritani, Shyuji organization: Tokyo Metropolitan Matsuzawa Hospital, Department of Psychiatry, Tokyo, Japan – sequence: 22 givenname: Izumi surname: Naka fullname: Naka, Izumi organization: Department of Human Genetics, Graduate School of Medicine, University of Tokyo, Tokyo, Japan – sequence: 23 givenname: Jun surname: Ohashi fullname: Ohashi, Jun organization: Department of Genome Epidemiology, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan – sequence: 24 givenname: Akiyoshi surname: Kakita fullname: Kakita, Akiyoshi organization: Brain Research Institute, Niigata University, Niigata, Japan – sequence: 25 givenname: Hitoshi surname: Takahashi fullname: Takahashi, Hitoshi organization: Brain Research Institute, Niigata University, Niigata, Japan – sequence: 26 givenname: Hiroyuki surname: Nawa fullname: Nawa, Hiroyuki organization: Brain Research Institute, Niigata University, Niigata, Japan – sequence: 27 givenname: Tadao surname: Arinami fullname: Arinami, Tadao organization: Department of Medical Genetics, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan |
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| Copyright | 2010 Society of Biological Psychiatry Society of Biological Psychiatry 2015 INIST-CNRS Copyright 2010 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved. |
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| Keywords | MK-801 mouse Association G protein coupled receptor gene methamphetamine cannabinoid postmortem brain schizophrenia cAMP Amphetamine derivatives Psychotropic Central nervous system Metamfetamine Schizophrenia Glutamate receptor Cannabinoid Genetic determinism Encephalon Psychosis Gene Cannabinoid receptor Genetics Drug of abuse Antagonist G protein Biological receptor CNS stimulant Dizocilpine Rodentia Postmortem Cyclic AMP Neuroprotective agent CB2 cannabinoid receptor Sympathomimetic Vertebrata Mammalia Mouse Animal NMDA receptor |
| Language | English |
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| Snippet | Neural endocannabinoid function appears to be involved in schizophrenia. Two endocannabinoid receptors, CB1 and CB2, are found in the brain and elsewhere in... Background Neural endocannabinoid function appears to be involved in schizophrenia. Two endocannabinoid receptors, CB1 and CB2, are found in the brain and... |
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| SubjectTerms | Adult and adolescent clinical studies Animals Association Biological and medical sciences Brain - metabolism cAMP cannabinoid Case-Control Studies CHO Cells Cricetinae Cricetulus Cyclic AMP - metabolism G protein coupled receptor gene Gene Expression Regulation Genetic Predisposition to Disease Humans Indoles - pharmacology Medical sciences methamphetamine Mice Mice, Inbred C57BL MK-801 Motor Activity - drug effects mouse Neuropharmacology Pharmacology. Drug treatments Polymorphism, Single Nucleotide postmortem brain Psychiatry Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease) Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Psychopharmacology Psychoses Receptor, Cannabinoid, CB2 - antagonists & inhibitors Receptor, Cannabinoid, CB2 - genetics Receptor, Cannabinoid, CB2 - metabolism Reflex, Startle - drug effects Schizophrenia Schizophrenia - genetics Schizophrenia - metabolism |
| Title | Brain Cannabinoid CB2 Receptor in Schizophrenia |
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