Loading…
Enriched environment impacts trimethylthiazoline-induced anxiety-related behavior and immediate early gene expression: critical role of Crhr1
It has been shown previously (Sotnikov et al., ) that mice selectively inbred for high anxiety‐related behavior (HAB) vs. low anxiety‐related behavior in the elevated plus maze differentially respond to trimethylthiazoline (TMT), a synthetic fox fecal odor. However, less is known about whether envir...
Saved in:
Published in: | The European journal of neuroscience 2014-08, Vol.40 (4), p.2691-2700 |
---|---|
Main Authors: | , , , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
cited_by | |
---|---|
cites | |
container_end_page | 2700 |
container_issue | 4 |
container_start_page | 2691 |
container_title | The European journal of neuroscience |
container_volume | 40 |
creator | Sotnikov, S. V. Chekmareva, N. Y. Schmid, B. Harbich, D. Malik, V. Bauer, S. Kuehne, C. Markt, P. O. Deussing, J. M. Schmidt, M. V. Landgraf, R. |
description | It has been shown previously (Sotnikov et al., ) that mice selectively inbred for high anxiety‐related behavior (HAB) vs. low anxiety‐related behavior in the elevated plus maze differentially respond to trimethylthiazoline (TMT), a synthetic fox fecal odor. However, less is known about whether environmental factors can rescue these extreme phenotypes. Here, we found that an enriched environment (EE) provided during early adolescence induced anxiolytic effects in HAB (HAB‐EE) mice, rescuing their strong avoidance behavior induced by TMT. In a series of experiments, the contribution of maternal, juvenile and adolescent behavior to the anxiolytic effects elicited by EE was investigated. At the molecular level, using c‐fos expression mapping, we found that the activity of the medial and basolateral amygdala was significantly reduced in HAB‐EE mice after TMT exposure. We further analysed the expression of Crhr1, as its amount in the amygdala has been reported to be important for the regulation of anxiety‐related behavior after EE. Indeed, in situ hybridisation indicated significantly decreased Crhr1 expression in the basolateral and central amygdala of HAB‐EE mice. To further test the involvement of Crhr1 in TMT‐induced avoidance, we exposed conditional glutamatergic‐specific Crhr1‐knockout mice to the odor. The behavioral response of Crhr1‐knockout mice mimicked that of HAB‐EE mice, and c‐fos expression in the amygdala after TMT exposure was significantly lower compared with controls, thereby further supporting a critical involvement of Crhr1 in environmentally‐induced anxiolysis. Altogether, our results indicate that EE can rescue strong avoidance of TMT by HAB mice with Crhr1 expression in the amygdala being critically involved.
High anxiety‐related behavior mice housed in enriched environment displayed reduced TMT avoidance, which is potentially mediated via decreased amygdala activity as indicated by lower c‐fos expression. Lower Crhr1 expression in the amygdala of enriched mice is likely to be critically involved in this phenomenon. Indeed, Crhr1 glutamatergic‐specific knock‐out mice showed decreased TMT avoidance and c‐fos expression in the amygdala compared to wild type. |
doi_str_mv | 10.1111/ejn.12624 |
format | article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_1566822318</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1566822318</sourcerecordid><originalsourceid>FETCH-LOGICAL-i4554-c6f3ec8223027c9f6ab31158c157cd66664381a9ce56c9ebed379b1cc72ab8913</originalsourceid><addsrcrecordid>eNpFkc9u1DAQxi0EokvhwAugXJC4pLXj2HG4odX2H1GrIhDcLMeZEBfHWWxv2fQd-s643aXMxTOe33zSzIfQW4KPSIpjuHFHpOBF-QwtSMlxXjMunqMFrhnNBeE_DtCrEG4wxoKX7CU6KEpRYkzEAt2vnDd6gC4Dd2v85EZwMTPjWukYsujNCHGYbRyMupuscZAb12104pXbGohz7sGqmOoWBnVrJp8aXRIYoTPpPwPl7Zz9BJfS7dpDCGZyHzPtTTRa2cxPFrKpz5Z-8OQ1etErG-DN_j1E305WX5dneXN1er781OSmZKzMNe8paFEUFBeVrnuuWkoIE5qwSnc8RUkFUbUGxnUNLXS0qluidVWoVtSEHqIPO921n35vIEQ5mqDBWuVg2gRJGOcP8kQk9N0e3bRpJ7lOJ1F-lv9OmID3e0CFtFDvldMm_OdExSkpaOKOd9wfY2F-6hMsHzyUyUP56KFcXVw-Jmki302YEGH7NKH8L8krWjH5_fJUXn9u6ovmSyNP6F9UaKBW</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1566822318</pqid></control><display><type>article</type><title>Enriched environment impacts trimethylthiazoline-induced anxiety-related behavior and immediate early gene expression: critical role of Crhr1</title><source>Wiley</source><creator>Sotnikov, S. V. ; Chekmareva, N. Y. ; Schmid, B. ; Harbich, D. ; Malik, V. ; Bauer, S. ; Kuehne, C. ; Markt, P. O. ; Deussing, J. M. ; Schmidt, M. V. ; Landgraf, R.</creator><creatorcontrib>Sotnikov, S. V. ; Chekmareva, N. Y. ; Schmid, B. ; Harbich, D. ; Malik, V. ; Bauer, S. ; Kuehne, C. ; Markt, P. O. ; Deussing, J. M. ; Schmidt, M. V. ; Landgraf, R.</creatorcontrib><description>It has been shown previously (Sotnikov et al., ) that mice selectively inbred for high anxiety‐related behavior (HAB) vs. low anxiety‐related behavior in the elevated plus maze differentially respond to trimethylthiazoline (TMT), a synthetic fox fecal odor. However, less is known about whether environmental factors can rescue these extreme phenotypes. Here, we found that an enriched environment (EE) provided during early adolescence induced anxiolytic effects in HAB (HAB‐EE) mice, rescuing their strong avoidance behavior induced by TMT. In a series of experiments, the contribution of maternal, juvenile and adolescent behavior to the anxiolytic effects elicited by EE was investigated. At the molecular level, using c‐fos expression mapping, we found that the activity of the medial and basolateral amygdala was significantly reduced in HAB‐EE mice after TMT exposure. We further analysed the expression of Crhr1, as its amount in the amygdala has been reported to be important for the regulation of anxiety‐related behavior after EE. Indeed, in situ hybridisation indicated significantly decreased Crhr1 expression in the basolateral and central amygdala of HAB‐EE mice. To further test the involvement of Crhr1 in TMT‐induced avoidance, we exposed conditional glutamatergic‐specific Crhr1‐knockout mice to the odor. The behavioral response of Crhr1‐knockout mice mimicked that of HAB‐EE mice, and c‐fos expression in the amygdala after TMT exposure was significantly lower compared with controls, thereby further supporting a critical involvement of Crhr1 in environmentally‐induced anxiolysis. Altogether, our results indicate that EE can rescue strong avoidance of TMT by HAB mice with Crhr1 expression in the amygdala being critically involved.
High anxiety‐related behavior mice housed in enriched environment displayed reduced TMT avoidance, which is potentially mediated via decreased amygdala activity as indicated by lower c‐fos expression. Lower Crhr1 expression in the amygdala of enriched mice is likely to be critically involved in this phenomenon. Indeed, Crhr1 glutamatergic‐specific knock‐out mice showed decreased TMT avoidance and c‐fos expression in the amygdala compared to wild type.</description><identifier>ISSN: 0953-816X</identifier><identifier>EISSN: 1460-9568</identifier><identifier>DOI: 10.1111/ejn.12624</identifier><identifier>PMID: 24840018</identifier><language>eng</language><publisher>Oxford: Blackwell Publishing Ltd</publisher><subject>amygdala ; Amygdala - metabolism ; Animals ; Anxiety - chemically induced ; Anxiety - genetics ; Anxiety - metabolism ; avoidance ; Brain - metabolism ; Crhr1-knockout mice ; Environment, Controlled ; Genes, Immediate-Early ; high anxiety-related behavior ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Motor Activity ; Proto-Oncogene Proteins c-fos - metabolism ; Receptors, Corticotropin-Releasing Hormone - genetics ; Receptors, Corticotropin-Releasing Hormone - metabolism ; Thiazoles - toxicity ; trimethylthiazoline</subject><ispartof>The European journal of neuroscience, 2014-08, Vol.40 (4), p.2691-2700</ispartof><rights>2014 Federation of European Neuroscience Societies and John Wiley & Sons Ltd</rights><rights>2015 INIST-CNRS</rights><rights>2014 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=28763123$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24840018$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sotnikov, S. V.</creatorcontrib><creatorcontrib>Chekmareva, N. Y.</creatorcontrib><creatorcontrib>Schmid, B.</creatorcontrib><creatorcontrib>Harbich, D.</creatorcontrib><creatorcontrib>Malik, V.</creatorcontrib><creatorcontrib>Bauer, S.</creatorcontrib><creatorcontrib>Kuehne, C.</creatorcontrib><creatorcontrib>Markt, P. O.</creatorcontrib><creatorcontrib>Deussing, J. M.</creatorcontrib><creatorcontrib>Schmidt, M. V.</creatorcontrib><creatorcontrib>Landgraf, R.</creatorcontrib><title>Enriched environment impacts trimethylthiazoline-induced anxiety-related behavior and immediate early gene expression: critical role of Crhr1</title><title>The European journal of neuroscience</title><addtitle>Eur J Neurosci</addtitle><description>It has been shown previously (Sotnikov et al., ) that mice selectively inbred for high anxiety‐related behavior (HAB) vs. low anxiety‐related behavior in the elevated plus maze differentially respond to trimethylthiazoline (TMT), a synthetic fox fecal odor. However, less is known about whether environmental factors can rescue these extreme phenotypes. Here, we found that an enriched environment (EE) provided during early adolescence induced anxiolytic effects in HAB (HAB‐EE) mice, rescuing their strong avoidance behavior induced by TMT. In a series of experiments, the contribution of maternal, juvenile and adolescent behavior to the anxiolytic effects elicited by EE was investigated. At the molecular level, using c‐fos expression mapping, we found that the activity of the medial and basolateral amygdala was significantly reduced in HAB‐EE mice after TMT exposure. We further analysed the expression of Crhr1, as its amount in the amygdala has been reported to be important for the regulation of anxiety‐related behavior after EE. Indeed, in situ hybridisation indicated significantly decreased Crhr1 expression in the basolateral and central amygdala of HAB‐EE mice. To further test the involvement of Crhr1 in TMT‐induced avoidance, we exposed conditional glutamatergic‐specific Crhr1‐knockout mice to the odor. The behavioral response of Crhr1‐knockout mice mimicked that of HAB‐EE mice, and c‐fos expression in the amygdala after TMT exposure was significantly lower compared with controls, thereby further supporting a critical involvement of Crhr1 in environmentally‐induced anxiolysis. Altogether, our results indicate that EE can rescue strong avoidance of TMT by HAB mice with Crhr1 expression in the amygdala being critically involved.
High anxiety‐related behavior mice housed in enriched environment displayed reduced TMT avoidance, which is potentially mediated via decreased amygdala activity as indicated by lower c‐fos expression. Lower Crhr1 expression in the amygdala of enriched mice is likely to be critically involved in this phenomenon. Indeed, Crhr1 glutamatergic‐specific knock‐out mice showed decreased TMT avoidance and c‐fos expression in the amygdala compared to wild type.</description><subject>amygdala</subject><subject>Amygdala - metabolism</subject><subject>Animals</subject><subject>Anxiety - chemically induced</subject><subject>Anxiety - genetics</subject><subject>Anxiety - metabolism</subject><subject>avoidance</subject><subject>Brain - metabolism</subject><subject>Crhr1-knockout mice</subject><subject>Environment, Controlled</subject><subject>Genes, Immediate-Early</subject><subject>high anxiety-related behavior</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Motor Activity</subject><subject>Proto-Oncogene Proteins c-fos - metabolism</subject><subject>Receptors, Corticotropin-Releasing Hormone - genetics</subject><subject>Receptors, Corticotropin-Releasing Hormone - metabolism</subject><subject>Thiazoles - toxicity</subject><subject>trimethylthiazoline</subject><issn>0953-816X</issn><issn>1460-9568</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><recordid>eNpFkc9u1DAQxi0EokvhwAugXJC4pLXj2HG4odX2H1GrIhDcLMeZEBfHWWxv2fQd-s643aXMxTOe33zSzIfQW4KPSIpjuHFHpOBF-QwtSMlxXjMunqMFrhnNBeE_DtCrEG4wxoKX7CU6KEpRYkzEAt2vnDd6gC4Dd2v85EZwMTPjWukYsujNCHGYbRyMupuscZAb12104pXbGohz7sGqmOoWBnVrJp8aXRIYoTPpPwPl7Zz9BJfS7dpDCGZyHzPtTTRa2cxPFrKpz5Z-8OQ1etErG-DN_j1E305WX5dneXN1er781OSmZKzMNe8paFEUFBeVrnuuWkoIE5qwSnc8RUkFUbUGxnUNLXS0qluidVWoVtSEHqIPO921n35vIEQ5mqDBWuVg2gRJGOcP8kQk9N0e3bRpJ7lOJ1F-lv9OmID3e0CFtFDvldMm_OdExSkpaOKOd9wfY2F-6hMsHzyUyUP56KFcXVw-Jmki302YEGH7NKH8L8krWjH5_fJUXn9u6ovmSyNP6F9UaKBW</recordid><startdate>201408</startdate><enddate>201408</enddate><creator>Sotnikov, S. V.</creator><creator>Chekmareva, N. Y.</creator><creator>Schmid, B.</creator><creator>Harbich, D.</creator><creator>Malik, V.</creator><creator>Bauer, S.</creator><creator>Kuehne, C.</creator><creator>Markt, P. O.</creator><creator>Deussing, J. M.</creator><creator>Schmidt, M. V.</creator><creator>Landgraf, R.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</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>7X8</scope></search><sort><creationdate>201408</creationdate><title>Enriched environment impacts trimethylthiazoline-induced anxiety-related behavior and immediate early gene expression: critical role of Crhr1</title><author>Sotnikov, S. V. ; Chekmareva, N. Y. ; Schmid, B. ; Harbich, D. ; Malik, V. ; Bauer, S. ; Kuehne, C. ; Markt, P. O. ; Deussing, J. M. ; Schmidt, M. V. ; Landgraf, R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-i4554-c6f3ec8223027c9f6ab31158c157cd66664381a9ce56c9ebed379b1cc72ab8913</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>amygdala</topic><topic>Amygdala - metabolism</topic><topic>Animals</topic><topic>Anxiety - chemically induced</topic><topic>Anxiety - genetics</topic><topic>Anxiety - metabolism</topic><topic>avoidance</topic><topic>Brain - metabolism</topic><topic>Crhr1-knockout mice</topic><topic>Environment, Controlled</topic><topic>Genes, Immediate-Early</topic><topic>high anxiety-related behavior</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Motor Activity</topic><topic>Proto-Oncogene Proteins c-fos - metabolism</topic><topic>Receptors, Corticotropin-Releasing Hormone - genetics</topic><topic>Receptors, Corticotropin-Releasing Hormone - metabolism</topic><topic>Thiazoles - toxicity</topic><topic>trimethylthiazoline</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sotnikov, S. V.</creatorcontrib><creatorcontrib>Chekmareva, N. Y.</creatorcontrib><creatorcontrib>Schmid, B.</creatorcontrib><creatorcontrib>Harbich, D.</creatorcontrib><creatorcontrib>Malik, V.</creatorcontrib><creatorcontrib>Bauer, S.</creatorcontrib><creatorcontrib>Kuehne, C.</creatorcontrib><creatorcontrib>Markt, P. O.</creatorcontrib><creatorcontrib>Deussing, J. M.</creatorcontrib><creatorcontrib>Schmidt, M. V.</creatorcontrib><creatorcontrib>Landgraf, R.</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>MEDLINE - Academic</collection><jtitle>The European journal of neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sotnikov, S. V.</au><au>Chekmareva, N. Y.</au><au>Schmid, B.</au><au>Harbich, D.</au><au>Malik, V.</au><au>Bauer, S.</au><au>Kuehne, C.</au><au>Markt, P. O.</au><au>Deussing, J. M.</au><au>Schmidt, M. V.</au><au>Landgraf, R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Enriched environment impacts trimethylthiazoline-induced anxiety-related behavior and immediate early gene expression: critical role of Crhr1</atitle><jtitle>The European journal of neuroscience</jtitle><addtitle>Eur J Neurosci</addtitle><date>2014-08</date><risdate>2014</risdate><volume>40</volume><issue>4</issue><spage>2691</spage><epage>2700</epage><pages>2691-2700</pages><issn>0953-816X</issn><eissn>1460-9568</eissn><abstract>It has been shown previously (Sotnikov et al., ) that mice selectively inbred for high anxiety‐related behavior (HAB) vs. low anxiety‐related behavior in the elevated plus maze differentially respond to trimethylthiazoline (TMT), a synthetic fox fecal odor. However, less is known about whether environmental factors can rescue these extreme phenotypes. Here, we found that an enriched environment (EE) provided during early adolescence induced anxiolytic effects in HAB (HAB‐EE) mice, rescuing their strong avoidance behavior induced by TMT. In a series of experiments, the contribution of maternal, juvenile and adolescent behavior to the anxiolytic effects elicited by EE was investigated. At the molecular level, using c‐fos expression mapping, we found that the activity of the medial and basolateral amygdala was significantly reduced in HAB‐EE mice after TMT exposure. We further analysed the expression of Crhr1, as its amount in the amygdala has been reported to be important for the regulation of anxiety‐related behavior after EE. Indeed, in situ hybridisation indicated significantly decreased Crhr1 expression in the basolateral and central amygdala of HAB‐EE mice. To further test the involvement of Crhr1 in TMT‐induced avoidance, we exposed conditional glutamatergic‐specific Crhr1‐knockout mice to the odor. The behavioral response of Crhr1‐knockout mice mimicked that of HAB‐EE mice, and c‐fos expression in the amygdala after TMT exposure was significantly lower compared with controls, thereby further supporting a critical involvement of Crhr1 in environmentally‐induced anxiolysis. Altogether, our results indicate that EE can rescue strong avoidance of TMT by HAB mice with Crhr1 expression in the amygdala being critically involved.
High anxiety‐related behavior mice housed in enriched environment displayed reduced TMT avoidance, which is potentially mediated via decreased amygdala activity as indicated by lower c‐fos expression. Lower Crhr1 expression in the amygdala of enriched mice is likely to be critically involved in this phenomenon. Indeed, Crhr1 glutamatergic‐specific knock‐out mice showed decreased TMT avoidance and c‐fos expression in the amygdala compared to wild type.</abstract><cop>Oxford</cop><pub>Blackwell Publishing Ltd</pub><pmid>24840018</pmid><doi>10.1111/ejn.12624</doi><tpages>10</tpages></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0953-816X |
ispartof | The European journal of neuroscience, 2014-08, Vol.40 (4), p.2691-2700 |
issn | 0953-816X 1460-9568 |
language | eng |
recordid | cdi_proquest_miscellaneous_1566822318 |
source | Wiley |
subjects | amygdala Amygdala - metabolism Animals Anxiety - chemically induced Anxiety - genetics Anxiety - metabolism avoidance Brain - metabolism Crhr1-knockout mice Environment, Controlled Genes, Immediate-Early high anxiety-related behavior Male Mice Mice, Inbred C57BL Mice, Knockout Motor Activity Proto-Oncogene Proteins c-fos - metabolism Receptors, Corticotropin-Releasing Hormone - genetics Receptors, Corticotropin-Releasing Hormone - metabolism Thiazoles - toxicity trimethylthiazoline |
title | Enriched environment impacts trimethylthiazoline-induced anxiety-related behavior and immediate early gene expression: critical role of Crhr1 |
url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-25T19%3A18%3A03IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Enriched%20environment%20impacts%20trimethylthiazoline-induced%20anxiety-related%20behavior%20and%20immediate%20early%20gene%20expression:%20critical%20role%20of%20Crhr1&rft.jtitle=The%20European%20journal%20of%20neuroscience&rft.au=Sotnikov,%20S.%20V.&rft.date=2014-08&rft.volume=40&rft.issue=4&rft.spage=2691&rft.epage=2700&rft.pages=2691-2700&rft.issn=0953-816X&rft.eissn=1460-9568&rft_id=info:doi/10.1111/ejn.12624&rft_dat=%3Cproquest_pubme%3E1566822318%3C/proquest_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-i4554-c6f3ec8223027c9f6ab31158c157cd66664381a9ce56c9ebed379b1cc72ab8913%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=1566822318&rft_id=info:pmid/24840018&rfr_iscdi=true |