Calcium and increase excitability promote tolerance against anoxia in hippocampal slices
We have previously demonstrated that anoxic preconditioning (APC) protects against a subsequent otherwise `lethal' anoxic insult in hippocampal slices. Tested here are two hypotheses: (a) APC requires calcium to improve electrical recovery in hippocampal slices; and (b) mild excitation promotes...
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| Veröffentlicht in: | Brain research 1999-06, Vol.833 (1), p.20-26 |
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| description | We have previously demonstrated that anoxic preconditioning (APC) protects against a subsequent otherwise `lethal' anoxic insult in hippocampal slices. Tested here are two hypotheses: (a) APC requires calcium to improve electrical recovery in hippocampal slices; and (b) mild excitation promotes preconditioning neuroprotection. Control hippocampal slices were given a single `test' anoxic insult followed by reoxygenation. Experimental slices were preconditioned by three short anoxic insults of 1 min separated by 10 min of reoxygenation. At 30 min after the third `conditioning' insult, slices underwent a `test' anoxic insult [1 min of anoxic depolarization (AD)], and then slices were reoxygenated. Evoked potentials (EPs) were recorded throughout the experiment. In other slices, APC was emulated by inducing spreading depression (as determined by a negative DC shift) with KCL or by inducing increased neuronal excitability with the excitatory agent 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) (an adenosine A1 receptor blocker). `Test' anoxic insults lasted 2 min of AD in these groups. To determine the role of calcium during APC, extracellular CaCl
2 was decreased to 0.5 mM but only during the APC episodes (`test' anoxia, 1 min of AD). EP amplitudes recovered significantly better after anoxia in preconditioned slices, and in KCl- and DPCPX-treated slices (147.2±33.3,
n=8, **
p |
| doi_str_mv | 10.1016/S0006-8993(99)01462-6 |
| format | Article |
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2 was decreased to 0.5 mM but only during the APC episodes (`test' anoxia, 1 min of AD). EP amplitudes recovered significantly better after anoxia in preconditioned slices, and in KCl- and DPCPX-treated slices (147.2±33.3,
n=8, **
p<0.01, 71.7±13.5,
n=7, **
p<0.01, and 117.8±37.3,
n=5, ***
p<0.001, respectively) compared to controls. Decreases in extracellular CaCl
2 during APC blocked the recovery of EPs after `test' anoxia (80.6±23.0,
n=8). These data confirm that increases in excitability can emulate APC. These data also demonstrate that calcium influx during preconditioning is required for the induction of tolerance during APC.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/S0006-8993(99)01462-6</identifier><identifier>PMID: 10375673</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>London: Elsevier B.V</publisher><subject>Adaptation, Physiological - physiology ; Adenosine ; Animals ; Anoxia ; Biological and medical sciences ; Calcium - physiology ; Central nervous system ; Conditioning (Psychology) - physiology ; Cortical Spreading Depression - physiology ; Electrophysiology ; Evoked Potentials - drug effects ; Evoked Potentials - physiology ; Fundamental and applied biological sciences. Psychology ; Hippocampus ; Hippocampus - drug effects ; Hippocampus - physiopathology ; Hypoxia - physiopathology ; In Vitro Techniques ; Ischemia ; Male ; Potassium Chloride - pharmacology ; Rats ; Rats, Wistar ; Tolerance ; Vertebrates: nervous system and sense organs ; Xanthines - pharmacology</subject><ispartof>Brain research, 1999-06, Vol.833 (1), p.20-26</ispartof><rights>1999 Elsevier Science B.V.</rights><rights>1999 INIST-CNRS</rights><rights>Copyright 1999 Elsevier Science B.V.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c468t-e407bfef6c0007288ea462bbff0c68d709f42b4753c855355580a1ca96ecede93</citedby><cites>FETCH-LOGICAL-c468t-e407bfef6c0007288ea462bbff0c68d709f42b4753c855355580a1ca96ecede93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0006-8993(99)01462-6$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1876031$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10375673$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pérez-Pinzón, Miguel A.</creatorcontrib><creatorcontrib>Born, James G.</creatorcontrib><creatorcontrib>Centeno, José M.</creatorcontrib><title>Calcium and increase excitability promote tolerance against anoxia in hippocampal slices</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>We have previously demonstrated that anoxic preconditioning (APC) protects against a subsequent otherwise `lethal' anoxic insult in hippocampal slices. Tested here are two hypotheses: (a) APC requires calcium to improve electrical recovery in hippocampal slices; and (b) mild excitation promotes preconditioning neuroprotection. Control hippocampal slices were given a single `test' anoxic insult followed by reoxygenation. Experimental slices were preconditioned by three short anoxic insults of 1 min separated by 10 min of reoxygenation. At 30 min after the third `conditioning' insult, slices underwent a `test' anoxic insult [1 min of anoxic depolarization (AD)], and then slices were reoxygenated. Evoked potentials (EPs) were recorded throughout the experiment. In other slices, APC was emulated by inducing spreading depression (as determined by a negative DC shift) with KCL or by inducing increased neuronal excitability with the excitatory agent 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) (an adenosine A1 receptor blocker). `Test' anoxic insults lasted 2 min of AD in these groups. To determine the role of calcium during APC, extracellular CaCl
2 was decreased to 0.5 mM but only during the APC episodes (`test' anoxia, 1 min of AD). EP amplitudes recovered significantly better after anoxia in preconditioned slices, and in KCl- and DPCPX-treated slices (147.2±33.3,
n=8, **
p<0.01, 71.7±13.5,
n=7, **
p<0.01, and 117.8±37.3,
n=5, ***
p<0.001, respectively) compared to controls. Decreases in extracellular CaCl
2 during APC blocked the recovery of EPs after `test' anoxia (80.6±23.0,
n=8). These data confirm that increases in excitability can emulate APC. These data also demonstrate that calcium influx during preconditioning is required for the induction of tolerance during APC.</description><subject>Adaptation, Physiological - physiology</subject><subject>Adenosine</subject><subject>Animals</subject><subject>Anoxia</subject><subject>Biological and medical sciences</subject><subject>Calcium - physiology</subject><subject>Central nervous system</subject><subject>Conditioning (Psychology) - physiology</subject><subject>Cortical Spreading Depression - physiology</subject><subject>Electrophysiology</subject><subject>Evoked Potentials - drug effects</subject><subject>Evoked Potentials - physiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hippocampus</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - physiopathology</subject><subject>Hypoxia - physiopathology</subject><subject>In Vitro Techniques</subject><subject>Ischemia</subject><subject>Male</subject><subject>Potassium Chloride - pharmacology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Tolerance</subject><subject>Vertebrates: nervous system and sense organs</subject><subject>Xanthines - pharmacology</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1rFTEUhkNR2mv1J7TMQkQXoyc3k6-VyMVWoeBCBXfhTOZMTcl8NJkr7b83t_di3XWVBJ73nDcPY2cc3nPg6sN3AFC1sVa8tfYd8Eata3XEVtzoclk38Iyt_iEn7EXON-UphIVjdsJBaKm0WLFfG4w-bIcKx64Ko0-EmSq682HBNsSw3FdzmoZpoWqZIiUcPVV4jWHMS8lMdwFLrPod5nnyOMwYqxyDp_ySPe8xZnp1OE_Zz4vPPzZf6qtvl183n65q3yiz1NSAbnvqlS_t9NoYwvKTtu178Mp0GmzfrNtGS-GNlEJKaQC5R6vIU0dWnLI3-7ml5u2W8uKGkD3FiCNN2-yUNcJaDU-CXAvgQu5AuQd9mnJO1Ls5hQHTvePgdu7dg3u3E-usdQ_unSq588OCbTtQ919qL7sArw8AZo-x38kM-ZEzWoHgBfu4x6ho-xMouewDFe9dSOQX103hiSZ_AfMkoT8</recordid><startdate>19990626</startdate><enddate>19990626</enddate><creator>Pérez-Pinzón, Miguel A.</creator><creator>Born, James G.</creator><creator>Centeno, José M.</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>7QP</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>19990626</creationdate><title>Calcium and increase excitability promote tolerance against anoxia in hippocampal slices</title><author>Pérez-Pinzón, Miguel A. ; Born, James G. ; Centeno, José M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c468t-e407bfef6c0007288ea462bbff0c68d709f42b4753c855355580a1ca96ecede93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Adaptation, Physiological - physiology</topic><topic>Adenosine</topic><topic>Animals</topic><topic>Anoxia</topic><topic>Biological and medical sciences</topic><topic>Calcium - physiology</topic><topic>Central nervous system</topic><topic>Conditioning (Psychology) - physiology</topic><topic>Cortical Spreading Depression - physiology</topic><topic>Electrophysiology</topic><topic>Evoked Potentials - drug effects</topic><topic>Evoked Potentials - physiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hippocampus</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - physiopathology</topic><topic>Hypoxia - physiopathology</topic><topic>In Vitro Techniques</topic><topic>Ischemia</topic><topic>Male</topic><topic>Potassium Chloride - pharmacology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Tolerance</topic><topic>Vertebrates: nervous system and sense organs</topic><topic>Xanthines - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pérez-Pinzón, Miguel A.</creatorcontrib><creatorcontrib>Born, James G.</creatorcontrib><creatorcontrib>Centeno, José M.</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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pérez-Pinzón, Miguel A.</au><au>Born, James G.</au><au>Centeno, José M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Calcium and increase excitability promote tolerance against anoxia in hippocampal slices</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>1999-06-26</date><risdate>1999</risdate><volume>833</volume><issue>1</issue><spage>20</spage><epage>26</epage><pages>20-26</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract>We have previously demonstrated that anoxic preconditioning (APC) protects against a subsequent otherwise `lethal' anoxic insult in hippocampal slices. Tested here are two hypotheses: (a) APC requires calcium to improve electrical recovery in hippocampal slices; and (b) mild excitation promotes preconditioning neuroprotection. Control hippocampal slices were given a single `test' anoxic insult followed by reoxygenation. Experimental slices were preconditioned by three short anoxic insults of 1 min separated by 10 min of reoxygenation. At 30 min after the third `conditioning' insult, slices underwent a `test' anoxic insult [1 min of anoxic depolarization (AD)], and then slices were reoxygenated. Evoked potentials (EPs) were recorded throughout the experiment. In other slices, APC was emulated by inducing spreading depression (as determined by a negative DC shift) with KCL or by inducing increased neuronal excitability with the excitatory agent 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) (an adenosine A1 receptor blocker). `Test' anoxic insults lasted 2 min of AD in these groups. To determine the role of calcium during APC, extracellular CaCl
2 was decreased to 0.5 mM but only during the APC episodes (`test' anoxia, 1 min of AD). EP amplitudes recovered significantly better after anoxia in preconditioned slices, and in KCl- and DPCPX-treated slices (147.2±33.3,
n=8, **
p<0.01, 71.7±13.5,
n=7, **
p<0.01, and 117.8±37.3,
n=5, ***
p<0.001, respectively) compared to controls. Decreases in extracellular CaCl
2 during APC blocked the recovery of EPs after `test' anoxia (80.6±23.0,
n=8). These data confirm that increases in excitability can emulate APC. These data also demonstrate that calcium influx during preconditioning is required for the induction of tolerance during APC.</abstract><cop>London</cop><cop>Amsterdam</cop><cop>New York, NY</cop><pub>Elsevier B.V</pub><pmid>10375673</pmid><doi>10.1016/S0006-8993(99)01462-6</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adaptation, Physiological - physiology Adenosine Animals Anoxia Biological and medical sciences Calcium - physiology Central nervous system Conditioning (Psychology) - physiology Cortical Spreading Depression - physiology Electrophysiology Evoked Potentials - drug effects Evoked Potentials - physiology Fundamental and applied biological sciences. Psychology Hippocampus Hippocampus - drug effects Hippocampus - physiopathology Hypoxia - physiopathology In Vitro Techniques Ischemia Male Potassium Chloride - pharmacology Rats Rats, Wistar Tolerance Vertebrates: nervous system and sense organs Xanthines - pharmacology |
| title | Calcium and increase excitability promote tolerance against anoxia in hippocampal slices |
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