Prolonged c-Jun expression in the basolateral amygdala following bulbectomy: possible implications for antidepressant activity and time of onset
Olfactory bulbectomy is a well established animal model of depression. Neurochemical and behavioral alterations observed following olfactory bulbectomy, are due, in part, to the neurodegeneration of specific brain structures. Amygdaloid dysfunction in particular, is known to play a substantial role...
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Veröffentlicht in: | Brain research. Molecular brain research. 2000-03, Vol.76 (1), p.7-17 |
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description | Olfactory bulbectomy is a well established animal model of depression. Neurochemical and behavioral alterations observed following olfactory bulbectomy, are due, in part, to the neurodegeneration of specific brain structures. Amygdaloid dysfunction in particular, is known to play a substantial role in the syndrome of the olfactory bulbectomized rat. The present study examined both short- and long-term alterations in immediate early gene expression, tyrosine hydroxylase and serotonin immunoreactivity, and classical silver staining, following olfactory bulbectomy in the basolateral amygdala. The results indicated no consistent change in Fos expression observed over the experimental period. Following bulbectomy, long term (up to 64 days post-lesion) Jun expression, not coincident with silver staining, was observed in the basolateral nucleus. The basolateral nucleus was also intensely immunoreactive for serotonin at this timepoint post-bulbectomy. Thus, following bulbectomy long term alterations in Jun expression occurs in the serotonin rich basolateral amygdala. As a site of action for antidepressant compounds, alterations at the immediate early gene level in this region may have implications both for the model, and antidepressant drug action therein. |
doi_str_mv | 10.1016/S0169-328X(99)00326-5 |
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Neurochemical and behavioral alterations observed following olfactory bulbectomy, are due, in part, to the neurodegeneration of specific brain structures. Amygdaloid dysfunction in particular, is known to play a substantial role in the syndrome of the olfactory bulbectomized rat. The present study examined both short- and long-term alterations in immediate early gene expression, tyrosine hydroxylase and serotonin immunoreactivity, and classical silver staining, following olfactory bulbectomy in the basolateral amygdala. The results indicated no consistent change in Fos expression observed over the experimental period. Following bulbectomy, long term (up to 64 days post-lesion) Jun expression, not coincident with silver staining, was observed in the basolateral nucleus. The basolateral nucleus was also intensely immunoreactive for serotonin at this timepoint post-bulbectomy. Thus, following bulbectomy long term alterations in Jun expression occurs in the serotonin rich basolateral amygdala. As a site of action for antidepressant compounds, alterations at the immediate early gene level in this region may have implications both for the model, and antidepressant drug action therein.</description><identifier>ISSN: 0169-328X</identifier><identifier>EISSN: 1872-6941</identifier><identifier>DOI: 10.1016/S0169-328X(99)00326-5</identifier><identifier>PMID: 10719210</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Adult and adolescent clinical studies ; Amygdala ; Amygdala - metabolism ; Animals ; Biological and medical sciences ; Degeneration ; Depression ; Depression - metabolism ; Disease Models, Animal ; Immediate early gene Jun ; Immediate-Early Proteins - metabolism ; Immunohistochemistry ; Male ; Medical sciences ; Model of depression ; Mood disorders ; Olfactory Bulb - physiology ; Olfactory bulbectomy ; Plasticity ; Proto-Oncogene Proteins c-fos - metabolism ; Proto-Oncogene Proteins c-jun - metabolism ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Rats ; Rats, Wistar ; Serotonergic reinnervation ; Serotonin - metabolism ; Silver Staining ; Time Factors ; Tyrosine 3-Monooxygenase - metabolism</subject><ispartof>Brain research. Molecular brain research., 2000-03, Vol.76 (1), p.7-17</ispartof><rights>2000 Elsevier Science B.V.</rights><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c516t-a19ea623b1acd57ff0a46bc1299e26aed9e4adaea01c30ab996f11dcb7a93c733</citedby><cites>FETCH-LOGICAL-c516t-a19ea623b1acd57ff0a46bc1299e26aed9e4adaea01c30ab996f11dcb7a93c733</cites></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=1319251$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10719210$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wrynn, Aileen S</creatorcontrib><creatorcontrib>Sebens, Jantiena B</creatorcontrib><creatorcontrib>Koch, Tineke</creatorcontrib><creatorcontrib>Leonard, Brian E</creatorcontrib><creatorcontrib>Korf, Jakob</creatorcontrib><title>Prolonged c-Jun expression in the basolateral amygdala following bulbectomy: possible implications for antidepressant activity and time of onset</title><title>Brain research. Molecular brain research.</title><addtitle>Brain Res Mol Brain Res</addtitle><description>Olfactory bulbectomy is a well established animal model of depression. Neurochemical and behavioral alterations observed following olfactory bulbectomy, are due, in part, to the neurodegeneration of specific brain structures. Amygdaloid dysfunction in particular, is known to play a substantial role in the syndrome of the olfactory bulbectomized rat. The present study examined both short- and long-term alterations in immediate early gene expression, tyrosine hydroxylase and serotonin immunoreactivity, and classical silver staining, following olfactory bulbectomy in the basolateral amygdala. The results indicated no consistent change in Fos expression observed over the experimental period. Following bulbectomy, long term (up to 64 days post-lesion) Jun expression, not coincident with silver staining, was observed in the basolateral nucleus. The basolateral nucleus was also intensely immunoreactive for serotonin at this timepoint post-bulbectomy. Thus, following bulbectomy long term alterations in Jun expression occurs in the serotonin rich basolateral amygdala. As a site of action for antidepressant compounds, alterations at the immediate early gene level in this region may have implications both for the model, and antidepressant drug action therein.</description><subject>Adult and adolescent clinical studies</subject><subject>Amygdala</subject><subject>Amygdala - metabolism</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Degeneration</subject><subject>Depression</subject><subject>Depression - metabolism</subject><subject>Disease Models, Animal</subject><subject>Immediate early gene Jun</subject><subject>Immediate-Early Proteins - metabolism</subject><subject>Immunohistochemistry</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Model of depression</subject><subject>Mood disorders</subject><subject>Olfactory Bulb - physiology</subject><subject>Olfactory bulbectomy</subject><subject>Plasticity</subject><subject>Proto-Oncogene Proteins c-fos - metabolism</subject><subject>Proto-Oncogene Proteins c-jun - metabolism</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Serotonergic reinnervation</subject><subject>Serotonin - metabolism</subject><subject>Silver Staining</subject><subject>Time Factors</subject><subject>Tyrosine 3-Monooxygenase - metabolism</subject><issn>0169-328X</issn><issn>1872-6941</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc2KFDEURoMoTs_oIyhZiIyL0tyqrkrHjcjgLwMKKrgLt5JbbSRVKZPUaL-Fj2ymu1F3s0lCON-XcA9jD0A8BQHds09lUVVTb76eK_VEiKbuqvYWW8FG1lWn1nCbrf4iJ-w0pe9CCNgA3GUnICSoGsSK_f4Ygw_Tliw31ftl4vRrjpSSCxN3E8_fiPeYgsdMET3Hcbe16JEPwfvw001b3i--J5PDuHvO51CSvSfuxtk7g7nUpMJGjlN2lvbV5cjRZHfl8q7cW57dSDwMvLCU77E7A_pE94_7Gfvy-tXni7fV5Yc37y5eXlamhS5XCIqwq5se0NhWDoPAddcbqJWiukOyitZokVCAaQT2SnUDgDW9RNUY2TRn7PGhd47hx0Ip69ElQ97jRGFJWgolQcLNIMhW1GupCtgeQBPLGCINeo5uxLjTIPS1M713pq-FaKX03pluS-7h8YGlH8n-lzpIKsCjI4DJoB8iTsalf1xTsBYK9uKAURnblaOok3E0GbIuFkHaBnfDT_4AkXC4Hg</recordid><startdate>20000310</startdate><enddate>20000310</enddate><creator>Wrynn, Aileen S</creator><creator>Sebens, Jantiena B</creator><creator>Koch, Tineke</creator><creator>Leonard, Brian E</creator><creator>Korf, Jakob</creator><general>Elsevier B.V</general><general>Elsevier</general><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>7TK</scope><scope>7X8</scope></search><sort><creationdate>20000310</creationdate><title>Prolonged c-Jun expression in the basolateral amygdala following bulbectomy: possible implications for antidepressant activity and time of onset</title><author>Wrynn, Aileen S ; Sebens, Jantiena B ; Koch, Tineke ; Leonard, Brian E ; Korf, Jakob</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c516t-a19ea623b1acd57ff0a46bc1299e26aed9e4adaea01c30ab996f11dcb7a93c733</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Adult and adolescent clinical studies</topic><topic>Amygdala</topic><topic>Amygdala - metabolism</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Degeneration</topic><topic>Depression</topic><topic>Depression - metabolism</topic><topic>Disease Models, Animal</topic><topic>Immediate early gene Jun</topic><topic>Immediate-Early Proteins - metabolism</topic><topic>Immunohistochemistry</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Model of depression</topic><topic>Mood disorders</topic><topic>Olfactory Bulb - physiology</topic><topic>Olfactory bulbectomy</topic><topic>Plasticity</topic><topic>Proto-Oncogene Proteins c-fos - metabolism</topic><topic>Proto-Oncogene Proteins c-jun - metabolism</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Serotonergic reinnervation</topic><topic>Serotonin - metabolism</topic><topic>Silver Staining</topic><topic>Time Factors</topic><topic>Tyrosine 3-Monooxygenase - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wrynn, Aileen S</creatorcontrib><creatorcontrib>Sebens, Jantiena B</creatorcontrib><creatorcontrib>Koch, Tineke</creatorcontrib><creatorcontrib>Leonard, Brian E</creatorcontrib><creatorcontrib>Korf, Jakob</creatorcontrib><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>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Brain research. Molecular brain research.</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wrynn, Aileen S</au><au>Sebens, Jantiena B</au><au>Koch, Tineke</au><au>Leonard, Brian E</au><au>Korf, Jakob</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Prolonged c-Jun expression in the basolateral amygdala following bulbectomy: possible implications for antidepressant activity and time of onset</atitle><jtitle>Brain research. Molecular brain research.</jtitle><addtitle>Brain Res Mol Brain Res</addtitle><date>2000-03-10</date><risdate>2000</risdate><volume>76</volume><issue>1</issue><spage>7</spage><epage>17</epage><pages>7-17</pages><issn>0169-328X</issn><eissn>1872-6941</eissn><abstract>Olfactory bulbectomy is a well established animal model of depression. Neurochemical and behavioral alterations observed following olfactory bulbectomy, are due, in part, to the neurodegeneration of specific brain structures. Amygdaloid dysfunction in particular, is known to play a substantial role in the syndrome of the olfactory bulbectomized rat. The present study examined both short- and long-term alterations in immediate early gene expression, tyrosine hydroxylase and serotonin immunoreactivity, and classical silver staining, following olfactory bulbectomy in the basolateral amygdala. The results indicated no consistent change in Fos expression observed over the experimental period. Following bulbectomy, long term (up to 64 days post-lesion) Jun expression, not coincident with silver staining, was observed in the basolateral nucleus. The basolateral nucleus was also intensely immunoreactive for serotonin at this timepoint post-bulbectomy. Thus, following bulbectomy long term alterations in Jun expression occurs in the serotonin rich basolateral amygdala. As a site of action for antidepressant compounds, alterations at the immediate early gene level in this region may have implications both for the model, and antidepressant drug action therein.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>10719210</pmid><doi>10.1016/S0169-328X(99)00326-5</doi><tpages>11</tpages></addata></record> |
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subjects | Adult and adolescent clinical studies Amygdala Amygdala - metabolism Animals Biological and medical sciences Degeneration Depression Depression - metabolism Disease Models, Animal Immediate early gene Jun Immediate-Early Proteins - metabolism Immunohistochemistry Male Medical sciences Model of depression Mood disorders Olfactory Bulb - physiology Olfactory bulbectomy Plasticity Proto-Oncogene Proteins c-fos - metabolism Proto-Oncogene Proteins c-jun - metabolism Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Rats Rats, Wistar Serotonergic reinnervation Serotonin - metabolism Silver Staining Time Factors Tyrosine 3-Monooxygenase - metabolism |
title | Prolonged c-Jun expression in the basolateral amygdala following bulbectomy: possible implications for antidepressant activity and time of onset |
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