Fetal male masculinization in control and prenatally stressed rats
The present experiments were designed to test the hypothesis that males in utero masculinize the development of other males. This effect was examined during fetal development in males from control and prenatally stressed rats. A code identified the number of cervical‐flanking males between the targe...
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Veröffentlicht in: | Developmental psychobiology 1989-11, Vol.22 (7), p.707-716 |
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description | The present experiments were designed to test the hypothesis that males in utero masculinize the development of other males. This effect was examined during fetal development in males from control and prenatally stressed rats. A code identified the number of cervical‐flanking males between the target male and the cervical end of the uterus. The male parameters morphology (anogenital distance) and body, adrenal, and testis weights were recorded on the eighteenth and twentieth gestational days and categorized by the cervical‐flanking male classificantion. At Day 18, control fetuses with two cervical‐flanking males in utero displayed significantly greater anogenital distance values than did males with no cervical‐flanking male. At Day 20, control fetuses with two cervical‐flanking males had testicular weights significantly greater than those of fetuses with one or zero cervical positioned male. Prenatal stress markedly impaired male fetal development, at gestational Days 18 and 20 while suppressing the cervical‐flanking male effect. These results confirm and extend previous data that indicate: (a) prenatal stress disrupts normal fetal development, resulting in long‐term changes; and (b) androgens via a cervical‐flanking blood‐flow mechanism influence littermate morphology and sexual development during the prenatal period. Our findings also demonstrate that a general masculinizing effect could not be made across the measured male parameters since the effect of males positioned at the cervical‐flanking region in utero appears to be dependent upon maternal sources of variance. Finally, androgens prenatally have an apparent positive interaction with somatic growth. |
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D. ; Fleming, D. E. ; Rhees, R. W.</creator><creatorcontrib>Lephart, E. D. ; Fleming, D. E. ; Rhees, R. W.</creatorcontrib><description>The present experiments were designed to test the hypothesis that males in utero masculinize the development of other males. This effect was examined during fetal development in males from control and prenatally stressed rats. A code identified the number of cervical‐flanking males between the target male and the cervical end of the uterus. The male parameters morphology (anogenital distance) and body, adrenal, and testis weights were recorded on the eighteenth and twentieth gestational days and categorized by the cervical‐flanking male classificantion. At Day 18, control fetuses with two cervical‐flanking males in utero displayed significantly greater anogenital distance values than did males with no cervical‐flanking male. At Day 20, control fetuses with two cervical‐flanking males had testicular weights significantly greater than those of fetuses with one or zero cervical positioned male. Prenatal stress markedly impaired male fetal development, at gestational Days 18 and 20 while suppressing the cervical‐flanking male effect. These results confirm and extend previous data that indicate: (a) prenatal stress disrupts normal fetal development, resulting in long‐term changes; and (b) androgens via a cervical‐flanking blood‐flow mechanism influence littermate morphology and sexual development during the prenatal period. Our findings also demonstrate that a general masculinizing effect could not be made across the measured male parameters since the effect of males positioned at the cervical‐flanking region in utero appears to be dependent upon maternal sources of variance. Finally, androgens prenatally have an apparent positive interaction with somatic growth.</description><identifier>ISSN: 0012-1630</identifier><identifier>EISSN: 1098-2302</identifier><identifier>DOI: 10.1002/dev.420220705</identifier><identifier>PMID: 2553513</identifier><identifier>CODEN: DEPBA5</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Adrenocorticotropic Hormone ; Analysis of Variance ; Androgens - physiology ; Animals ; Behavioral psychophysiology ; Biological and medical sciences ; Embryonic and Fetal Development - physiology ; Female ; Fundamental and applied biological sciences. Psychology ; Male ; Miscellaneous ; Organ Size ; Pregnancy ; Pregnancy, Animal - blood ; Psychology. Psychoanalysis. Psychiatry ; Psychology. Psychophysiology ; Rats ; Rats, Inbred Strains ; Sex Differentiation ; Stress, Physiological - blood ; Stress, Physiological - chemically induced ; Stress, Physiological - complications ; Testis - anatomy & histology ; Testis - metabolism</subject><ispartof>Developmental psychobiology, 1989-11, Vol.22 (7), p.707-716</ispartof><rights>Copyright © 1989 John Wiley & Sons, Inc.</rights><rights>1990 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4035-ba3ee4e96272207530e191b3669d9d6c0ca843e0e2df3c9cd19c1f99105814e83</citedby><cites>FETCH-LOGICAL-c4035-ba3ee4e96272207530e191b3669d9d6c0ca843e0e2df3c9cd19c1f99105814e83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fdev.420220705$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fdev.420220705$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,27923,27924,45573,45574</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=6742236$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2553513$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lephart, E. D.</creatorcontrib><creatorcontrib>Fleming, D. E.</creatorcontrib><creatorcontrib>Rhees, R. W.</creatorcontrib><title>Fetal male masculinization in control and prenatally stressed rats</title><title>Developmental psychobiology</title><addtitle>Dev. Psychobiol</addtitle><description>The present experiments were designed to test the hypothesis that males in utero masculinize the development of other males. This effect was examined during fetal development in males from control and prenatally stressed rats. A code identified the number of cervical‐flanking males between the target male and the cervical end of the uterus. The male parameters morphology (anogenital distance) and body, adrenal, and testis weights were recorded on the eighteenth and twentieth gestational days and categorized by the cervical‐flanking male classificantion. At Day 18, control fetuses with two cervical‐flanking males in utero displayed significantly greater anogenital distance values than did males with no cervical‐flanking male. At Day 20, control fetuses with two cervical‐flanking males had testicular weights significantly greater than those of fetuses with one or zero cervical positioned male. Prenatal stress markedly impaired male fetal development, at gestational Days 18 and 20 while suppressing the cervical‐flanking male effect. These results confirm and extend previous data that indicate: (a) prenatal stress disrupts normal fetal development, resulting in long‐term changes; and (b) androgens via a cervical‐flanking blood‐flow mechanism influence littermate morphology and sexual development during the prenatal period. Our findings also demonstrate that a general masculinizing effect could not be made across the measured male parameters since the effect of males positioned at the cervical‐flanking region in utero appears to be dependent upon maternal sources of variance. Finally, androgens prenatally have an apparent positive interaction with somatic growth.</description><subject>Adrenocorticotropic Hormone</subject><subject>Analysis of Variance</subject><subject>Androgens - physiology</subject><subject>Animals</subject><subject>Behavioral psychophysiology</subject><subject>Biological and medical sciences</subject><subject>Embryonic and Fetal Development - physiology</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Male</subject><subject>Miscellaneous</subject><subject>Organ Size</subject><subject>Pregnancy</subject><subject>Pregnancy, Animal - blood</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychology. Psychophysiology</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Sex Differentiation</subject><subject>Stress, Physiological - blood</subject><subject>Stress, Physiological - chemically induced</subject><subject>Stress, Physiological - complications</subject><subject>Testis - anatomy & histology</subject><subject>Testis - metabolism</subject><issn>0012-1630</issn><issn>1098-2302</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1989</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kDtPwzAURi0EglIYGZEyILbAtZ048cijLSAEDDxGy3VuJIObFDsFyq_HqFHFxGLLusff_XQIOaBwQgHYaYUfJxkDxqCAfIMMKMgyZRzYJhkAUJZSwWGH7IbwGp80K4ttss3ynOeUD8j5GDvtkpl2GI9gFs429lt3tm0S2ySmbTrfukQ3VTL32OgIu2USOo8hYJV43YU9slVrF3C_v4fkaTx6vLhKb-8n1xdnt6nJgOfpVHPEDKVgxW_XnANSSadcCFnJShgwusw4ArKq5kaaikpDaykp5CXNsORDcrzKnfv2fYGhUzMbDDqnG2wXQRWSlayMu4YkXYHGtyF4rNXc25n2S0VB_TpT0ZlaO4v8YR-8mM6wWtO9pDg_6udRkHa1142xYY2JImOMi4gVK-zTOlz-v1Ndjp7_FugL29Dh1_qn9m8xnBe5ermbqAcxLrMbJpTgP1GKkjs</recordid><startdate>198911</startdate><enddate>198911</enddate><creator>Lephart, E. D.</creator><creator>Fleming, D. E.</creator><creator>Rhees, R. W.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>198911</creationdate><title>Fetal male masculinization in control and prenatally stressed rats</title><author>Lephart, E. D. ; Fleming, D. E. ; Rhees, R. W.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4035-ba3ee4e96272207530e191b3669d9d6c0ca843e0e2df3c9cd19c1f99105814e83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1989</creationdate><topic>Adrenocorticotropic Hormone</topic><topic>Analysis of Variance</topic><topic>Androgens - physiology</topic><topic>Animals</topic><topic>Behavioral psychophysiology</topic><topic>Biological and medical sciences</topic><topic>Embryonic and Fetal Development - physiology</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Male</topic><topic>Miscellaneous</topic><topic>Organ Size</topic><topic>Pregnancy</topic><topic>Pregnancy, Animal - blood</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychology. Psychophysiology</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Sex Differentiation</topic><topic>Stress, Physiological - blood</topic><topic>Stress, Physiological - chemically induced</topic><topic>Stress, Physiological - complications</topic><topic>Testis - anatomy & histology</topic><topic>Testis - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lephart, E. D.</creatorcontrib><creatorcontrib>Fleming, D. E.</creatorcontrib><creatorcontrib>Rhees, R. W.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Developmental psychobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lephart, E. D.</au><au>Fleming, D. E.</au><au>Rhees, R. W.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fetal male masculinization in control and prenatally stressed rats</atitle><jtitle>Developmental psychobiology</jtitle><addtitle>Dev. Psychobiol</addtitle><date>1989-11</date><risdate>1989</risdate><volume>22</volume><issue>7</issue><spage>707</spage><epage>716</epage><pages>707-716</pages><issn>0012-1630</issn><eissn>1098-2302</eissn><coden>DEPBA5</coden><abstract>The present experiments were designed to test the hypothesis that males in utero masculinize the development of other males. This effect was examined during fetal development in males from control and prenatally stressed rats. A code identified the number of cervical‐flanking males between the target male and the cervical end of the uterus. The male parameters morphology (anogenital distance) and body, adrenal, and testis weights were recorded on the eighteenth and twentieth gestational days and categorized by the cervical‐flanking male classificantion. At Day 18, control fetuses with two cervical‐flanking males in utero displayed significantly greater anogenital distance values than did males with no cervical‐flanking male. At Day 20, control fetuses with two cervical‐flanking males had testicular weights significantly greater than those of fetuses with one or zero cervical positioned male. Prenatal stress markedly impaired male fetal development, at gestational Days 18 and 20 while suppressing the cervical‐flanking male effect. These results confirm and extend previous data that indicate: (a) prenatal stress disrupts normal fetal development, resulting in long‐term changes; and (b) androgens via a cervical‐flanking blood‐flow mechanism influence littermate morphology and sexual development during the prenatal period. Our findings also demonstrate that a general masculinizing effect could not be made across the measured male parameters since the effect of males positioned at the cervical‐flanking region in utero appears to be dependent upon maternal sources of variance. Finally, androgens prenatally have an apparent positive interaction with somatic growth.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>2553513</pmid><doi>10.1002/dev.420220705</doi><tpages>10</tpages></addata></record> |
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subjects | Adrenocorticotropic Hormone Analysis of Variance Androgens - physiology Animals Behavioral psychophysiology Biological and medical sciences Embryonic and Fetal Development - physiology Female Fundamental and applied biological sciences. Psychology Male Miscellaneous Organ Size Pregnancy Pregnancy, Animal - blood Psychology. Psychoanalysis. Psychiatry Psychology. Psychophysiology Rats Rats, Inbred Strains Sex Differentiation Stress, Physiological - blood Stress, Physiological - chemically induced Stress, Physiological - complications Testis - anatomy & histology Testis - metabolism |
title | Fetal male masculinization in control and prenatally stressed rats |
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