Unpredictable Chronic Stress Alters Adenosine Metabolism in Zebrafish Brain
Stress is considered a risk factor for several human disorders. Despite the broad knowledge of stress responses in mammals, data on the relationship between unpredictable chronic stress (UCS) and its effects on purinergic signaling are limited. ATP hydrolysis by ectonucleotidases is an important sou...
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| Veröffentlicht in: | Molecular neurobiology 2016-05, Vol.53 (4), p.2518-2528 |
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| creator | Zimmermann, F. F. Altenhofen, S. Kist, L. W. Leite, C. E. Bogo, M. R. Cognato, G. P. Bonan, C. D. |
| description | Stress is considered a risk factor for several human disorders. Despite the broad knowledge of stress responses in mammals, data on the relationship between unpredictable chronic stress (UCS) and its effects on purinergic signaling are limited. ATP hydrolysis by ectonucleotidases is an important source of adenosine, and adenosine deaminase (ADA) contributes to the control of the nucleoside concentrations. Considering that some stress models could affect signaling systems, the objective of this study was to investigate whether UCS alters ectonucleotidase and ADA pathway in zebrafish brain. Additionally, we analyzed ATP metabolism as well as
ada1
,
ada2.1
,
ada2.2
,
adaL
, and
adaasi
gene expression in zebrafish brain. Our results have demonstrated that UCS did not alter ectonucleotidase and soluble ADA activities. However, ecto-ADA activity was significantly decreased (26.8 %) in brain membranes of animals exposed to UCS when compared to the control group. Quantitative reverse transcription PCR (RT-PCR) analysis did not show significant changes on ADA gene expression after the UCS exposure. The brain ATP metabolism showed a marked increase in adenosine levels (ADO) in animals exposed to UCS. These data suggest an increase on extracellular adenosine levels in zebrafish brain. Since this nucleoside has neuromodulatory and anxiolytic effects, changes in adenosine levels could play a role in counteracting the stress, which could be related to a compensatory mechanism in order to restore the homeostasis. |
| doi_str_mv | 10.1007/s12035-015-9270-7 |
| format | Article |
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ada1
,
ada2.1
,
ada2.2
,
adaL
, and
adaasi
gene expression in zebrafish brain. Our results have demonstrated that UCS did not alter ectonucleotidase and soluble ADA activities. However, ecto-ADA activity was significantly decreased (26.8 %) in brain membranes of animals exposed to UCS when compared to the control group. Quantitative reverse transcription PCR (RT-PCR) analysis did not show significant changes on ADA gene expression after the UCS exposure. The brain ATP metabolism showed a marked increase in adenosine levels (ADO) in animals exposed to UCS. These data suggest an increase on extracellular adenosine levels in zebrafish brain. Since this nucleoside has neuromodulatory and anxiolytic effects, changes in adenosine levels could play a role in counteracting the stress, which could be related to a compensatory mechanism in order to restore the homeostasis.</description><identifier>ISSN: 0893-7648</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-015-9270-7</identifier><identifier>PMID: 26081145</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Adenosine ; Adenosine - metabolism ; Adenosine Deaminase - genetics ; Adenosine Deaminase - metabolism ; Adenosine Triphosphatases - metabolism ; Adenosine Triphosphate - metabolism ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Brain - metabolism ; Brain - pathology ; Cell Biology ; Chronic Disease ; Danio rerio ; Enzyme Assays ; Extracellular Space - metabolism ; Gene expression ; Gene Expression Regulation ; Homeostasis ; Hormones ; Hydrolysis ; Male ; Metabolism ; Nervous system ; Neurobiology ; Neurology ; Neurosciences ; Physiology ; Stress ; Stress response ; Stress, Psychological - metabolism ; Zebrafish - metabolism</subject><ispartof>Molecular neurobiology, 2016-05, Vol.53 (4), p.2518-2528</ispartof><rights>Springer Science+Business Media New York 2015</rights><rights>Springer Science+Business Media New York 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c514t-c54185aa07114b0d14cecaa67f59f1346b7e6fddfb9ac0f544a27cf83823e7ec3</citedby><cites>FETCH-LOGICAL-c514t-c54185aa07114b0d14cecaa67f59f1346b7e6fddfb9ac0f544a27cf83823e7ec3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12035-015-9270-7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12035-015-9270-7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26081145$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zimmermann, F. F.</creatorcontrib><creatorcontrib>Altenhofen, S.</creatorcontrib><creatorcontrib>Kist, L. W.</creatorcontrib><creatorcontrib>Leite, C. E.</creatorcontrib><creatorcontrib>Bogo, M. R.</creatorcontrib><creatorcontrib>Cognato, G. P.</creatorcontrib><creatorcontrib>Bonan, C. D.</creatorcontrib><title>Unpredictable Chronic Stress Alters Adenosine Metabolism in Zebrafish Brain</title><title>Molecular neurobiology</title><addtitle>Mol Neurobiol</addtitle><addtitle>Mol Neurobiol</addtitle><description>Stress is considered a risk factor for several human disorders. Despite the broad knowledge of stress responses in mammals, data on the relationship between unpredictable chronic stress (UCS) and its effects on purinergic signaling are limited. ATP hydrolysis by ectonucleotidases is an important source of adenosine, and adenosine deaminase (ADA) contributes to the control of the nucleoside concentrations. Considering that some stress models could affect signaling systems, the objective of this study was to investigate whether UCS alters ectonucleotidase and ADA pathway in zebrafish brain. Additionally, we analyzed ATP metabolism as well as
ada1
,
ada2.1
,
ada2.2
,
adaL
, and
adaasi
gene expression in zebrafish brain. Our results have demonstrated that UCS did not alter ectonucleotidase and soluble ADA activities. However, ecto-ADA activity was significantly decreased (26.8 %) in brain membranes of animals exposed to UCS when compared to the control group. Quantitative reverse transcription PCR (RT-PCR) analysis did not show significant changes on ADA gene expression after the UCS exposure. The brain ATP metabolism showed a marked increase in adenosine levels (ADO) in animals exposed to UCS. These data suggest an increase on extracellular adenosine levels in zebrafish brain. Since this nucleoside has neuromodulatory and anxiolytic effects, changes in adenosine levels could play a role in counteracting the stress, which could be related to a compensatory mechanism in order to restore the homeostasis.</description><subject>Adenosine</subject><subject>Adenosine - metabolism</subject><subject>Adenosine Deaminase - genetics</subject><subject>Adenosine Deaminase - metabolism</subject><subject>Adenosine Triphosphatases - metabolism</subject><subject>Adenosine Triphosphate - metabolism</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Cell Biology</subject><subject>Chronic Disease</subject><subject>Danio rerio</subject><subject>Enzyme Assays</subject><subject>Extracellular Space - metabolism</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Homeostasis</subject><subject>Hormones</subject><subject>Hydrolysis</subject><subject>Male</subject><subject>Metabolism</subject><subject>Nervous system</subject><subject>Neurobiology</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Physiology</subject><subject>Stress</subject><subject>Stress response</subject><subject>Stress, Psychological - metabolism</subject><subject>Zebrafish - metabolism</subject><issn>0893-7648</issn><issn>1559-1182</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kD1PxDAMhiMEguPjB7CgSiwshThNmnSEE18CxAAsLFGaOhDUS4-kN_DvyekAISQWe_Dj19ZDyD7QY6BUniRgtBIlBVE2TNJSrpEJCNGUAIqtkwlVTVXKmqstsp3SG6WMAZWbZIvVVAFwMSE3T2EesfN2NG2PxfQ1DsHb4mGMmFJx2o8Yc-swDMkHLO4wc0Pv06zwoXjGNhrn02txFo0Pu2TDmT7h3lffIU8X54_Tq_L2_vJ6enpbWgF8zJWDEsZQmV9oaQfcojWmlk40DipetxJr13WubYylTnBumLROVYpVKNFWO-RolTuPw_sC06hnPlnsexNwWCQNUglWKQ51Rg__oG_DIob8XaakkpRLJjMFK8rGIaWITs-jn5n4oYHqpWm9Mq2zab00rZc7B1_Ji3aG3c_Gt9oMsBWQ8ii8YPx1-t_UT-LCiEU</recordid><startdate>20160501</startdate><enddate>20160501</enddate><creator>Zimmermann, F. 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F. ; Altenhofen, S. ; Kist, L. W. ; Leite, C. E. ; Bogo, M. R. ; Cognato, G. P. ; Bonan, C. 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F.</au><au>Altenhofen, S.</au><au>Kist, L. W.</au><au>Leite, C. E.</au><au>Bogo, M. R.</au><au>Cognato, G. P.</au><au>Bonan, C. D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Unpredictable Chronic Stress Alters Adenosine Metabolism in Zebrafish Brain</atitle><jtitle>Molecular neurobiology</jtitle><stitle>Mol Neurobiol</stitle><addtitle>Mol Neurobiol</addtitle><date>2016-05-01</date><risdate>2016</risdate><volume>53</volume><issue>4</issue><spage>2518</spage><epage>2528</epage><pages>2518-2528</pages><issn>0893-7648</issn><eissn>1559-1182</eissn><abstract>Stress is considered a risk factor for several human disorders. Despite the broad knowledge of stress responses in mammals, data on the relationship between unpredictable chronic stress (UCS) and its effects on purinergic signaling are limited. ATP hydrolysis by ectonucleotidases is an important source of adenosine, and adenosine deaminase (ADA) contributes to the control of the nucleoside concentrations. Considering that some stress models could affect signaling systems, the objective of this study was to investigate whether UCS alters ectonucleotidase and ADA pathway in zebrafish brain. Additionally, we analyzed ATP metabolism as well as
ada1
,
ada2.1
,
ada2.2
,
adaL
, and
adaasi
gene expression in zebrafish brain. Our results have demonstrated that UCS did not alter ectonucleotidase and soluble ADA activities. However, ecto-ADA activity was significantly decreased (26.8 %) in brain membranes of animals exposed to UCS when compared to the control group. Quantitative reverse transcription PCR (RT-PCR) analysis did not show significant changes on ADA gene expression after the UCS exposure. The brain ATP metabolism showed a marked increase in adenosine levels (ADO) in animals exposed to UCS. These data suggest an increase on extracellular adenosine levels in zebrafish brain. Since this nucleoside has neuromodulatory and anxiolytic effects, changes in adenosine levels could play a role in counteracting the stress, which could be related to a compensatory mechanism in order to restore the homeostasis.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>26081145</pmid><doi>10.1007/s12035-015-9270-7</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenosine Adenosine - metabolism Adenosine Deaminase - genetics Adenosine Deaminase - metabolism Adenosine Triphosphatases - metabolism Adenosine Triphosphate - metabolism Animals Biomedical and Life Sciences Biomedicine Brain - metabolism Brain - pathology Cell Biology Chronic Disease Danio rerio Enzyme Assays Extracellular Space - metabolism Gene expression Gene Expression Regulation Homeostasis Hormones Hydrolysis Male Metabolism Nervous system Neurobiology Neurology Neurosciences Physiology Stress Stress response Stress, Psychological - metabolism Zebrafish - metabolism |
| title | Unpredictable Chronic Stress Alters Adenosine Metabolism in Zebrafish Brain |
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