Modulation of brain β-endorphin concentration by the specific part of the Y chromosome in mice
Several studies in animal models suggest a possible effect of the specific part of the Y-chromosome (Y(NPAR)) on brain opioid, and more specifically on brain β-endorphin (BE). In humans, male prevalence is found in autistic disorder in which observation of abnormal peripheral or central BE levels ar...
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description | Several studies in animal models suggest a possible effect of the specific part of the Y-chromosome (Y(NPAR)) on brain opioid, and more specifically on brain β-endorphin (BE). In humans, male prevalence is found in autistic disorder in which observation of abnormal peripheral or central BE levels are also reported. This suggests gender differences in BE associated with genetic factors and more precisely with Y(NPAR).
Brain BE levels and plasma testosterone concentrations were measured in two highly inbred strains of mice, NZB/BlNJ (N) and CBA/HGnc (H), and their consomic strains for the Y(NPAR). An indirect effect of the Y(NPAR) on brain BE level via plasma testosterone was also tested by studying the correlation between brain BE concentration and plasma testosterone concentration in eleven highly inbred strains. There was a significant and major effect (P |
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Brain BE levels and plasma testosterone concentrations were measured in two highly inbred strains of mice, NZB/BlNJ (N) and CBA/HGnc (H), and their consomic strains for the Y(NPAR). An indirect effect of the Y(NPAR) on brain BE level via plasma testosterone was also tested by studying the correlation between brain BE concentration and plasma testosterone concentration in eleven highly inbred strains. There was a significant and major effect (P<0.0001) of the Y(NPAR) in interaction with the genetic background on brain BE levels. Effect size calculated using Cohen's procedure was large (56% of the total variance). The variations of BE levels were not correlated with plasma testosterone which was also dependent of the Y(NPAR).
The contribution of Y(NPAR) on brain BE concentration in interaction with the genetic background is the first demonstration of Y-chromosome mediated control of brain opioid. Given that none of the genes encompassed by the Y(NPAR) encodes for BE or its precursor, our results suggest a contribution of the sex-determining region (Sry, carried by Y(NPAR)) to brain BE concentration. Indeed, the transcription of the Melanocortin 2 receptor gene (Mc2R gene, identified as the proopiomelanocortin receptor gene) depends on the presence of Sry and BE is derived directly from proopiomelanocortin. The results shed light on the sex dependent differences in brain functioning and the role of Sry in the BE system might be related to the higher frequency of autistic disorder in males.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0016704</identifier><identifier>PMID: 21408198</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animal models ; Animals ; Autism ; Behavior ; Behavioral sciences ; beta -Endorphin ; beta-Endorphin - metabolism ; Biology ; Brain ; Brain - metabolism ; Chromosomes ; Endorphins ; Gender ; Gender aspects ; Gene expression ; Genetic factors ; Genetic Loci - genetics ; Genomes ; Humans ; Hypotheses ; Inbreeding ; Informatics ; Laboratories ; Male ; Males ; Mathematical analysis ; Medicine ; Melanocortin ; Mice ; Mice, Inbred Strains ; Mitochondrial DNA ; Opioids ; Phenols ; Plasma ; Proopiomelanocortin ; Rodents ; Sex ; Sex differences ; Studies ; Testosterone ; Testosterone - blood ; Transcription ; World Wide Web ; Y chromosome ; Y Chromosome - metabolism ; Y Chromosomes</subject><ispartof>PloS one, 2011-03, Vol.6 (3), p.e16704-e16704</ispartof><rights>2011 Botbol et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Botbol et al. 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c557t-f9520e01219a8b49924501d8538efc8740bf72376fc4bd4594b9a71781b2af573</citedby><cites>FETCH-LOGICAL-c557t-f9520e01219a8b49924501d8538efc8740bf72376fc4bd4594b9a71781b2af573</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3050789/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3050789/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2095,2914,23846,27903,27904,53769,53771,79346,79347</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21408198$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Chapouthier, Georges</contributor><creatorcontrib>Botbol, Michel</creatorcontrib><creatorcontrib>Roubertoux, Pierre L</creatorcontrib><creatorcontrib>Carlier, Michèle</creatorcontrib><creatorcontrib>Trabado, Séverine</creatorcontrib><creatorcontrib>Brailly-Tabard, Sylvie</creatorcontrib><creatorcontrib>Perez-Diaz, Fernando</creatorcontrib><creatorcontrib>Bonnot, Olivier</creatorcontrib><creatorcontrib>Bronsard, Guillaume</creatorcontrib><creatorcontrib>Tordjman, Sylvie</creatorcontrib><title>Modulation of brain β-endorphin concentration by the specific part of the Y chromosome in mice</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Several studies in animal models suggest a possible effect of the specific part of the Y-chromosome (Y(NPAR)) on brain opioid, and more specifically on brain β-endorphin (BE). In humans, male prevalence is found in autistic disorder in which observation of abnormal peripheral or central BE levels are also reported. This suggests gender differences in BE associated with genetic factors and more precisely with Y(NPAR).
Brain BE levels and plasma testosterone concentrations were measured in two highly inbred strains of mice, NZB/BlNJ (N) and CBA/HGnc (H), and their consomic strains for the Y(NPAR). An indirect effect of the Y(NPAR) on brain BE level via plasma testosterone was also tested by studying the correlation between brain BE concentration and plasma testosterone concentration in eleven highly inbred strains. There was a significant and major effect (P<0.0001) of the Y(NPAR) in interaction with the genetic background on brain BE levels. Effect size calculated using Cohen's procedure was large (56% of the total variance). The variations of BE levels were not correlated with plasma testosterone which was also dependent of the Y(NPAR).
The contribution of Y(NPAR) on brain BE concentration in interaction with the genetic background is the first demonstration of Y-chromosome mediated control of brain opioid. Given that none of the genes encompassed by the Y(NPAR) encodes for BE or its precursor, our results suggest a contribution of the sex-determining region (Sry, carried by Y(NPAR)) to brain BE concentration. Indeed, the transcription of the Melanocortin 2 receptor gene (Mc2R gene, identified as the proopiomelanocortin receptor gene) depends on the presence of Sry and BE is derived directly from proopiomelanocortin. The results shed light on the sex dependent differences in brain functioning and the role of Sry in the BE system might be related to the higher frequency of autistic disorder in males.</description><subject>Animal models</subject><subject>Animals</subject><subject>Autism</subject><subject>Behavior</subject><subject>Behavioral sciences</subject><subject>beta -Endorphin</subject><subject>beta-Endorphin - metabolism</subject><subject>Biology</subject><subject>Brain</subject><subject>Brain - metabolism</subject><subject>Chromosomes</subject><subject>Endorphins</subject><subject>Gender</subject><subject>Gender aspects</subject><subject>Gene expression</subject><subject>Genetic factors</subject><subject>Genetic Loci - genetics</subject><subject>Genomes</subject><subject>Humans</subject><subject>Hypotheses</subject><subject>Inbreeding</subject><subject>Informatics</subject><subject>Laboratories</subject><subject>Male</subject><subject>Males</subject><subject>Mathematical analysis</subject><subject>Medicine</subject><subject>Melanocortin</subject><subject>Mice</subject><subject>Mice, Inbred Strains</subject><subject>Mitochondrial DNA</subject><subject>Opioids</subject><subject>Phenols</subject><subject>Plasma</subject><subject>Proopiomelanocortin</subject><subject>Rodents</subject><subject>Sex</subject><subject>Sex differences</subject><subject>Studies</subject><subject>Testosterone</subject><subject>Testosterone - 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In humans, male prevalence is found in autistic disorder in which observation of abnormal peripheral or central BE levels are also reported. This suggests gender differences in BE associated with genetic factors and more precisely with Y(NPAR).
Brain BE levels and plasma testosterone concentrations were measured in two highly inbred strains of mice, NZB/BlNJ (N) and CBA/HGnc (H), and their consomic strains for the Y(NPAR). An indirect effect of the Y(NPAR) on brain BE level via plasma testosterone was also tested by studying the correlation between brain BE concentration and plasma testosterone concentration in eleven highly inbred strains. There was a significant and major effect (P<0.0001) of the Y(NPAR) in interaction with the genetic background on brain BE levels. Effect size calculated using Cohen's procedure was large (56% of the total variance). The variations of BE levels were not correlated with plasma testosterone which was also dependent of the Y(NPAR).
The contribution of Y(NPAR) on brain BE concentration in interaction with the genetic background is the first demonstration of Y-chromosome mediated control of brain opioid. Given that none of the genes encompassed by the Y(NPAR) encodes for BE or its precursor, our results suggest a contribution of the sex-determining region (Sry, carried by Y(NPAR)) to brain BE concentration. Indeed, the transcription of the Melanocortin 2 receptor gene (Mc2R gene, identified as the proopiomelanocortin receptor gene) depends on the presence of Sry and BE is derived directly from proopiomelanocortin. The results shed light on the sex dependent differences in brain functioning and the role of Sry in the BE system might be related to the higher frequency of autistic disorder in males.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>21408198</pmid><doi>10.1371/journal.pone.0016704</doi><oa>free_for_read</oa></addata></record> |
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source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
subjects | Animal models Animals Autism Behavior Behavioral sciences beta -Endorphin beta-Endorphin - metabolism Biology Brain Brain - metabolism Chromosomes Endorphins Gender Gender aspects Gene expression Genetic factors Genetic Loci - genetics Genomes Humans Hypotheses Inbreeding Informatics Laboratories Male Males Mathematical analysis Medicine Melanocortin Mice Mice, Inbred Strains Mitochondrial DNA Opioids Phenols Plasma Proopiomelanocortin Rodents Sex Sex differences Studies Testosterone Testosterone - blood Transcription World Wide Web Y chromosome Y Chromosome - metabolism Y Chromosomes |
title | Modulation of brain β-endorphin concentration by the specific part of the Y chromosome in mice |
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