Dopamine attenuates ethanol-induced neuroapoptosis in the developing rat retina via the cAMP/PKA pathway
Apoptosis has been identified as the primary cause of fetal alcohol spectrum disorder (FASD), and the development of methods to prevent and treat FASD have been based on the mechanisms of alcohol-induced apoptosis. The present study aimed to explore the effects of dopamine on alcohol-induced neurona...
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| Veröffentlicht in: | Molecular medicine reports 2017-08, Vol.16 (2), p.1982-1990 |
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| container_end_page | 1990 |
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| creator | Han, Junde Gao, Lingqi Dong, Jing Wang, Yingtian Zhang, Mazhong Zheng, Jijian |
| description | Apoptosis has been identified as the primary cause of fetal alcohol spectrum disorder (FASD), and the development of methods to prevent and treat FASD have been based on the mechanisms of alcohol-induced apoptosis. The present study aimed to explore the effects of dopamine on alcohol-induced neuronal apoptosis using whole-mount cultures of rat retinas (postnatal day 7). Retinas were initially incubated with ethanol (100, 200 or 500 mM), and in subsequent analyses retinas were co-incubated with ethanol (200 mM) and dopamine (10 µM). In addition, several antagonists and inhibitors were used, including a D1 dopamine receptor (D1R) antagonist (SCH23390; 10 µM), a D2R antagonist (raclopride; 40 µM), an adenosine A2A receptor (AA2AR) antagonist (SCH58261; 100 nM), an adenylyl cyclase (AC) inhibitor (SQ22536; 100 µM) and a PKA inhibitor (H-89; 1 µM). The results demonstrated that exposure increased neuroapoptosis in the retinal ganglion cell layer (GCL) in a dose-dependent manner. Dopamine treatment significantly attenuated ethanol-induced neuronal apoptosis. D1R, D2R and AA2AR antagonists partially inhibited the protective effects of dopamine against ethanol-induced apoptosis; similar results were observed with AC and PKA inhibitor treatments. In summary, the present study demonstrated that dopamine treatment may be able to attenuate alcohol-induced neuroapoptosis in the developing rat retina by activating D1R, D2R and AA2AR, and by upregulating cyclic AMP/protein kinase A signaling. |
| doi_str_mv | 10.3892/mmr.2017.6823 |
| format | Article |
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The present study aimed to explore the effects of dopamine on alcohol-induced neuronal apoptosis using whole-mount cultures of rat retinas (postnatal day 7). Retinas were initially incubated with ethanol (100, 200 or 500 mM), and in subsequent analyses retinas were co-incubated with ethanol (200 mM) and dopamine (10 µM). In addition, several antagonists and inhibitors were used, including a D1 dopamine receptor (D1R) antagonist (SCH23390; 10 µM), a D2R antagonist (raclopride; 40 µM), an adenosine A2A receptor (AA2AR) antagonist (SCH58261; 100 nM), an adenylyl cyclase (AC) inhibitor (SQ22536; 100 µM) and a PKA inhibitor (H-89; 1 µM). The results demonstrated that exposure increased neuroapoptosis in the retinal ganglion cell layer (GCL) in a dose-dependent manner. Dopamine treatment significantly attenuated ethanol-induced neuronal apoptosis. D1R, D2R and AA2AR antagonists partially inhibited the protective effects of dopamine against ethanol-induced apoptosis; similar results were observed with AC and PKA inhibitor treatments. In summary, the present study demonstrated that dopamine treatment may be able to attenuate alcohol-induced neuroapoptosis in the developing rat retina by activating D1R, D2R and AA2AR, and by upregulating cyclic AMP/protein kinase A signaling.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2017.6823</identifier><identifier>PMID: 28656313</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Adenosine ; Alcohol ; Animals ; Apoptosis ; Apoptosis - drug effects ; Brain research ; Care and treatment ; Cell culture ; Chemical properties ; cyclic adenosine monophosphate/protein kinase A ; Cyclic AMP ; Cyclic AMP - metabolism ; Cyclic AMP-Dependent Protein Kinases - metabolism ; Development and progression ; Diagnosis ; Dopamine ; Dopamine - pharmacology ; Dopamine D1 receptors ; Dopamine D2 receptors ; Ethanol ; Ethanol - toxicity ; Fetal alcohol syndrome ; Ganglion cells ; Kinases ; Laboratory animals ; neuronal apoptosis ; Neurons - drug effects ; Neurons - metabolism ; Neurons - pathology ; Neuroprotective Agents - pharmacology ; Pharmaceutical industry ; Prevention ; Protein kinase A ; Raclopride ; Rats, Sprague-Dawley ; Receptors, Dopamine - metabolism ; Retina ; Retina - pathology ; retina ganglion cell ; Retinal Ganglion Cells - drug effects ; Retinal Ganglion Cells - metabolism ; Rodents ; Signal transduction ; Studies</subject><ispartof>Molecular medicine reports, 2017-08, Vol.16 (2), p.1982-1990</ispartof><rights>Copyright: © Han et al.</rights><rights>COPYRIGHT 2017 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><rights>Copyright: © Han et al. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c514t-29ed7c7eab8e57b177b48f020ba0a9e71d99a8571b42e71a3b6000d3612931193</citedby><cites>FETCH-LOGICAL-c514t-29ed7c7eab8e57b177b48f020ba0a9e71d99a8571b42e71a3b6000d3612931193</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,777,781,882,5556,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28656313$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Han, Junde</creatorcontrib><creatorcontrib>Gao, Lingqi</creatorcontrib><creatorcontrib>Dong, Jing</creatorcontrib><creatorcontrib>Wang, Yingtian</creatorcontrib><creatorcontrib>Zhang, Mazhong</creatorcontrib><creatorcontrib>Zheng, Jijian</creatorcontrib><title>Dopamine attenuates ethanol-induced neuroapoptosis in the developing rat retina via the cAMP/PKA pathway</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Apoptosis has been identified as the primary cause of fetal alcohol spectrum disorder (FASD), and the development of methods to prevent and treat FASD have been based on the mechanisms of alcohol-induced apoptosis. The present study aimed to explore the effects of dopamine on alcohol-induced neuronal apoptosis using whole-mount cultures of rat retinas (postnatal day 7). Retinas were initially incubated with ethanol (100, 200 or 500 mM), and in subsequent analyses retinas were co-incubated with ethanol (200 mM) and dopamine (10 µM). In addition, several antagonists and inhibitors were used, including a D1 dopamine receptor (D1R) antagonist (SCH23390; 10 µM), a D2R antagonist (raclopride; 40 µM), an adenosine A2A receptor (AA2AR) antagonist (SCH58261; 100 nM), an adenylyl cyclase (AC) inhibitor (SQ22536; 100 µM) and a PKA inhibitor (H-89; 1 µM). The results demonstrated that exposure increased neuroapoptosis in the retinal ganglion cell layer (GCL) in a dose-dependent manner. Dopamine treatment significantly attenuated ethanol-induced neuronal apoptosis. D1R, D2R and AA2AR antagonists partially inhibited the protective effects of dopamine against ethanol-induced apoptosis; similar results were observed with AC and PKA inhibitor treatments. In summary, the present study demonstrated that dopamine treatment may be able to attenuate alcohol-induced neuroapoptosis in the developing rat retina by activating D1R, D2R and AA2AR, and by upregulating cyclic AMP/protein kinase A signaling.</description><subject>Adenosine</subject><subject>Alcohol</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Brain research</subject><subject>Care and treatment</subject><subject>Cell culture</subject><subject>Chemical properties</subject><subject>cyclic adenosine monophosphate/protein kinase A</subject><subject>Cyclic AMP</subject><subject>Cyclic AMP - metabolism</subject><subject>Cyclic AMP-Dependent Protein Kinases - metabolism</subject><subject>Development and progression</subject><subject>Diagnosis</subject><subject>Dopamine</subject><subject>Dopamine - pharmacology</subject><subject>Dopamine D1 receptors</subject><subject>Dopamine D2 receptors</subject><subject>Ethanol</subject><subject>Ethanol - toxicity</subject><subject>Fetal alcohol syndrome</subject><subject>Ganglion cells</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>neuronal apoptosis</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Neurons - pathology</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Pharmaceutical industry</subject><subject>Prevention</subject><subject>Protein kinase A</subject><subject>Raclopride</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Dopamine - metabolism</subject><subject>Retina</subject><subject>Retina - pathology</subject><subject>retina ganglion cell</subject><subject>Retinal Ganglion Cells - drug effects</subject><subject>Retinal Ganglion Cells - metabolism</subject><subject>Rodents</subject><subject>Signal transduction</subject><subject>Studies</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</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>eNptkk1v1DAQhiMEoqVw5IoicSiXbP0Rx_EFaVUoIIroAc7WJJlsXCV2sJ1F_fd4u8tCEfLBHs8zrz2jN8teUrLitWIX0-RXjFC5qmrGH2WnVCpacELKx4czU0qeZM9CuCWkEkyop9kJqytRccpPs-Gdm2EyFnOIEe0CEUOOcQDrxsLYbmmxyy0u3sHs5uiCCbmxeRww73CLo5uN3eQeYu4xGgv51sB9tl1_ubm4-bzOZ4jDT7h7nj3pYQz44rCfZd-v3n-7_Fhcf_3w6XJ9XbSCljH9FjvZSoSmRiEbKmVT1j1hpAECCiXtlIJaSNqULEXAm4oQ0vGKMsUpVfwse7vXnZdmwq5FGz2MevZmAn-nHRj9MGPNoDduq4WoqFJ1EnhzEPDux4Ih6smEFscRLLolaKpoKWoqBUvo63_QW7d4m9pLVJVGLbhUf6gNjKiN7V16t92J6rUgJS9pKatErf5DpdXhZFpnsTfp_kFBsS9ovQvBY3_skRK9s4ZO1tA7a-idNRL_6u_BHOnfXkjA-R4IM9jOdC4cmaRU0KogrKAqaf0CfAnBBA</recordid><startdate>20170801</startdate><enddate>20170801</enddate><creator>Han, Junde</creator><creator>Gao, Lingqi</creator><creator>Dong, Jing</creator><creator>Wang, Yingtian</creator><creator>Zhang, Mazhong</creator><creator>Zheng, Jijian</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170801</creationdate><title>Dopamine attenuates ethanol-induced neuroapoptosis in the developing rat retina via the cAMP/PKA pathway</title><author>Han, Junde ; Gao, Lingqi ; Dong, Jing ; Wang, Yingtian ; Zhang, Mazhong ; Zheng, Jijian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c514t-29ed7c7eab8e57b177b48f020ba0a9e71d99a8571b42e71a3b6000d3612931193</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adenosine</topic><topic>Alcohol</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Brain research</topic><topic>Care and treatment</topic><topic>Cell culture</topic><topic>Chemical properties</topic><topic>cyclic adenosine monophosphate/protein kinase A</topic><topic>Cyclic AMP</topic><topic>Cyclic AMP - metabolism</topic><topic>Cyclic AMP-Dependent Protein Kinases - metabolism</topic><topic>Development and progression</topic><topic>Diagnosis</topic><topic>Dopamine</topic><topic>Dopamine - pharmacology</topic><topic>Dopamine D1 receptors</topic><topic>Dopamine D2 receptors</topic><topic>Ethanol</topic><topic>Ethanol - toxicity</topic><topic>Fetal alcohol syndrome</topic><topic>Ganglion cells</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>neuronal apoptosis</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Neurons - pathology</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Pharmaceutical industry</topic><topic>Prevention</topic><topic>Protein kinase A</topic><topic>Raclopride</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Dopamine - metabolism</topic><topic>Retina</topic><topic>Retina - pathology</topic><topic>retina ganglion cell</topic><topic>Retinal Ganglion Cells - drug effects</topic><topic>Retinal Ganglion Cells - metabolism</topic><topic>Rodents</topic><topic>Signal transduction</topic><topic>Studies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Han, Junde</creatorcontrib><creatorcontrib>Gao, Lingqi</creatorcontrib><creatorcontrib>Dong, Jing</creatorcontrib><creatorcontrib>Wang, Yingtian</creatorcontrib><creatorcontrib>Zhang, Mazhong</creatorcontrib><creatorcontrib>Zheng, Jijian</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Han, Junde</au><au>Gao, Lingqi</au><au>Dong, Jing</au><au>Wang, Yingtian</au><au>Zhang, Mazhong</au><au>Zheng, Jijian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dopamine attenuates ethanol-induced neuroapoptosis in the developing rat retina via the cAMP/PKA pathway</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2017-08-01</date><risdate>2017</risdate><volume>16</volume><issue>2</issue><spage>1982</spage><epage>1990</epage><pages>1982-1990</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Apoptosis has been identified as the primary cause of fetal alcohol spectrum disorder (FASD), and the development of methods to prevent and treat FASD have been based on the mechanisms of alcohol-induced apoptosis. The present study aimed to explore the effects of dopamine on alcohol-induced neuronal apoptosis using whole-mount cultures of rat retinas (postnatal day 7). Retinas were initially incubated with ethanol (100, 200 or 500 mM), and in subsequent analyses retinas were co-incubated with ethanol (200 mM) and dopamine (10 µM). In addition, several antagonists and inhibitors were used, including a D1 dopamine receptor (D1R) antagonist (SCH23390; 10 µM), a D2R antagonist (raclopride; 40 µM), an adenosine A2A receptor (AA2AR) antagonist (SCH58261; 100 nM), an adenylyl cyclase (AC) inhibitor (SQ22536; 100 µM) and a PKA inhibitor (H-89; 1 µM). The results demonstrated that exposure increased neuroapoptosis in the retinal ganglion cell layer (GCL) in a dose-dependent manner. Dopamine treatment significantly attenuated ethanol-induced neuronal apoptosis. D1R, D2R and AA2AR antagonists partially inhibited the protective effects of dopamine against ethanol-induced apoptosis; similar results were observed with AC and PKA inhibitor treatments. In summary, the present study demonstrated that dopamine treatment may be able to attenuate alcohol-induced neuroapoptosis in the developing rat retina by activating D1R, D2R and AA2AR, and by upregulating cyclic AMP/protein kinase A signaling.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>28656313</pmid><doi>10.3892/mmr.2017.6823</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Adenosine Alcohol Animals Apoptosis Apoptosis - drug effects Brain research Care and treatment Cell culture Chemical properties cyclic adenosine monophosphate/protein kinase A Cyclic AMP Cyclic AMP - metabolism Cyclic AMP-Dependent Protein Kinases - metabolism Development and progression Diagnosis Dopamine Dopamine - pharmacology Dopamine D1 receptors Dopamine D2 receptors Ethanol Ethanol - toxicity Fetal alcohol syndrome Ganglion cells Kinases Laboratory animals neuronal apoptosis Neurons - drug effects Neurons - metabolism Neurons - pathology Neuroprotective Agents - pharmacology Pharmaceutical industry Prevention Protein kinase A Raclopride Rats, Sprague-Dawley Receptors, Dopamine - metabolism Retina Retina - pathology retina ganglion cell Retinal Ganglion Cells - drug effects Retinal Ganglion Cells - metabolism Rodents Signal transduction Studies |
| title | Dopamine attenuates ethanol-induced neuroapoptosis in the developing rat retina via the cAMP/PKA pathway |
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