Neuroprotection by nicotine against hypoxia-induced apoptosis in cortical cultures involves activation of multiple nicotinic acetylcholine receptor subtypes
Activation of neuronal nicotinic acetylcholine receptors (nAChR) by nicotine has been suggested to protect neurons against a hypoxic insult. The objective of this study was to examine the nature of cell death induced by acute hypoxia in rat primary cortical cultures and the neuroprotective potential...
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| Veröffentlicht in: | Molecular and cellular neuroscience 2003-11, Vol.24 (3), p.779-786 |
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| creator | Hejmadi, M V Dajas-Bailador, F Barns, S M Jones, B Wonnacott, S |
| description | Activation of neuronal nicotinic acetylcholine receptors (nAChR) by nicotine has been suggested to protect neurons against a hypoxic insult. The objective of this study was to examine the nature of cell death induced by acute hypoxia in rat primary cortical cultures and the neuroprotective potential of nicotine in ameliorating these processes. Neuronal cell death induced by a 4-h exposure to hypoxia (0.1% O(2)) was apoptotic, as shown by TUNEL staining and assays monitoring DNA strand breaks and caspase-3/7 activity. The presence of nicotine (10 microM) during the hypoxic insult protected a subpopulation of susceptible neurones against DNA damage and apoptosis induced by oxygen deprivation. This protective effect of nicotine was prevented by a 30-min pre-incubation with either 100 nM alpha-bungarotoxin or 1 microM dihydro-beta-erythroidine, but not 1 microM atropine, suggesting that activation of at least two subtypes of nAChR, alpha7 and beta2* nAChR, is involved in mediating nicotine neuroprotection. |
| doi_str_mv | 10.1016/s1044-7431(03)00244-6 |
| format | Article |
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The objective of this study was to examine the nature of cell death induced by acute hypoxia in rat primary cortical cultures and the neuroprotective potential of nicotine in ameliorating these processes. Neuronal cell death induced by a 4-h exposure to hypoxia (0.1% O(2)) was apoptotic, as shown by TUNEL staining and assays monitoring DNA strand breaks and caspase-3/7 activity. The presence of nicotine (10 microM) during the hypoxic insult protected a subpopulation of susceptible neurones against DNA damage and apoptosis induced by oxygen deprivation. This protective effect of nicotine was prevented by a 30-min pre-incubation with either 100 nM alpha-bungarotoxin or 1 microM dihydro-beta-erythroidine, but not 1 microM atropine, suggesting that activation of at least two subtypes of nAChR, alpha7 and beta2* nAChR, is involved in mediating nicotine neuroprotection.</description><subject>alpha7 Nicotinic Acetylcholine Receptor</subject><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - physiology</subject><subject>Bungarotoxins - pharmacology</subject><subject>Cell Hypoxia - drug effects</subject><subject>Cell Hypoxia - physiology</subject><subject>Cells, Cultured</subject><subject>Cerebral Cortex - drug effects</subject><subject>Cerebral Cortex - metabolism</subject><subject>Cerebral Cortex - physiopathology</subject><subject>Dihydro-beta-Erythroidine - pharmacology</subject><subject>DNA Damage - drug effects</subject><subject>DNA Damage - physiology</subject><subject>Hypoxia-Ischemia, Brain - drug therapy</subject><subject>Hypoxia-Ischemia, Brain - metabolism</subject><subject>Neurons - cytology</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Nicotine - pharmacology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptors, Nicotinic - drug effects</subject><subject>Receptors, Nicotinic - metabolism</subject><issn>1044-7431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1OHiEUhlnYqFUvQcOqqYupwMD8LBvTHxOjC3VNgDkoDd8wBeZL5168WBn9apddAYf3PCc5D0KnlHyhhDYXiRLOq5bX9DOpzwlh5dXsocP38gH6mNIvQohgfb2PDihvGt4xcYieb2COYYohg8kujFgveHQmZDcCVo_KjSnjp2UKf5yq3DjMBgaspjDlkFzCbsQmxOyM8tjMPs8R1uI2-G25qILcqldssHhT_t3k4S_fmRKAvHjzFPw6LoKBwo04zTovE6Rj9MEqn-Bkdx6hh-_f7i9_Vte3P64uv15XhgueK6XbnmnW085SO_DG9FZY4JQQ3bFBC8U6Rbm13SBMq0U72J50oBoOum0HQuoj9OmNW_bwe4aU5cYlA96rEcKcZEu5oLUQ_w3SnomuY7QExVvQxJBSBCun6DYqLpISuTqTd6scucqRpJavzmRT-s52A2a9geFf105Y_QI0mJqa</recordid><startdate>20031101</startdate><enddate>20031101</enddate><creator>Hejmadi, M V</creator><creator>Dajas-Bailador, F</creator><creator>Barns, S M</creator><creator>Jones, B</creator><creator>Wonnacott, S</creator><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>20031101</creationdate><title>Neuroprotection by nicotine against hypoxia-induced apoptosis in cortical cultures involves activation of multiple nicotinic acetylcholine receptor subtypes</title><author>Hejmadi, M V ; Dajas-Bailador, F ; Barns, S M ; Jones, B ; Wonnacott, S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c454t-ab792b2918f1fd46c9f5fe4100b82db5a28a14ff8d5c7b57df908ea64eb77d003</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>alpha7 Nicotinic Acetylcholine Receptor</topic><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - physiology</topic><topic>Bungarotoxins - pharmacology</topic><topic>Cell Hypoxia - drug effects</topic><topic>Cell Hypoxia - physiology</topic><topic>Cells, Cultured</topic><topic>Cerebral Cortex - drug effects</topic><topic>Cerebral Cortex - metabolism</topic><topic>Cerebral Cortex - physiopathology</topic><topic>Dihydro-beta-Erythroidine - pharmacology</topic><topic>DNA Damage - drug effects</topic><topic>DNA Damage - physiology</topic><topic>Hypoxia-Ischemia, Brain - drug therapy</topic><topic>Hypoxia-Ischemia, Brain - metabolism</topic><topic>Neurons - cytology</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Nicotine - pharmacology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptors, Nicotinic - drug effects</topic><topic>Receptors, Nicotinic - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hejmadi, M V</creatorcontrib><creatorcontrib>Dajas-Bailador, F</creatorcontrib><creatorcontrib>Barns, S M</creatorcontrib><creatorcontrib>Jones, B</creatorcontrib><creatorcontrib>Wonnacott, S</creatorcontrib><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>Molecular and cellular neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hejmadi, M V</au><au>Dajas-Bailador, F</au><au>Barns, S M</au><au>Jones, B</au><au>Wonnacott, S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuroprotection by nicotine against hypoxia-induced apoptosis in cortical cultures involves activation of multiple nicotinic acetylcholine receptor subtypes</atitle><jtitle>Molecular and cellular neuroscience</jtitle><addtitle>Mol Cell Neurosci</addtitle><date>2003-11-01</date><risdate>2003</risdate><volume>24</volume><issue>3</issue><spage>779</spage><epage>786</epage><pages>779-786</pages><issn>1044-7431</issn><abstract>Activation of neuronal nicotinic acetylcholine receptors (nAChR) by nicotine has been suggested to protect neurons against a hypoxic insult. The objective of this study was to examine the nature of cell death induced by acute hypoxia in rat primary cortical cultures and the neuroprotective potential of nicotine in ameliorating these processes. Neuronal cell death induced by a 4-h exposure to hypoxia (0.1% O(2)) was apoptotic, as shown by TUNEL staining and assays monitoring DNA strand breaks and caspase-3/7 activity. The presence of nicotine (10 microM) during the hypoxic insult protected a subpopulation of susceptible neurones against DNA damage and apoptosis induced by oxygen deprivation. This protective effect of nicotine was prevented by a 30-min pre-incubation with either 100 nM alpha-bungarotoxin or 1 microM dihydro-beta-erythroidine, but not 1 microM atropine, suggesting that activation of at least two subtypes of nAChR, alpha7 and beta2* nAChR, is involved in mediating nicotine neuroprotection.</abstract><cop>United States</cop><pmid>14664825</pmid><doi>10.1016/s1044-7431(03)00244-6</doi><tpages>8</tpages></addata></record> |
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| subjects | alpha7 Nicotinic Acetylcholine Receptor Animals Apoptosis - drug effects Apoptosis - physiology Bungarotoxins - pharmacology Cell Hypoxia - drug effects Cell Hypoxia - physiology Cells, Cultured Cerebral Cortex - drug effects Cerebral Cortex - metabolism Cerebral Cortex - physiopathology Dihydro-beta-Erythroidine - pharmacology DNA Damage - drug effects DNA Damage - physiology Hypoxia-Ischemia, Brain - drug therapy Hypoxia-Ischemia, Brain - metabolism Neurons - cytology Neurons - drug effects Neurons - metabolism Neuroprotective Agents - pharmacology Nicotine - pharmacology Rats Rats, Wistar Receptors, Nicotinic - drug effects Receptors, Nicotinic - metabolism |
| title | Neuroprotection by nicotine against hypoxia-induced apoptosis in cortical cultures involves activation of multiple nicotinic acetylcholine receptor subtypes |
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