Metabotropic glutamate receptor subtypes differentially influence neuronal recovery from in vitro hypoxia/hypoglycemia in rat hippocampal slices
Hippocampal slices were transiently exposed to an oxygen- and glucose-free environment which causes a pronounced drop of both ATP and creatine phosphate, an anoxic depolarization, and an incomplete recovery of synaptically evoked population spike in the CA1 region after 1 h (48.5 ± 3.6% of baseline...
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creator | Opitz, T. Richter, P. Carter, A.J. Kozikowski, A.P. Shinozaki, H. Reymann, K.G. |
description | Hippocampal slices were transiently exposed to an oxygen- and glucose-free environment which causes a pronounced drop of both ATP and creatine phosphate, an anoxic depolarization, and an incomplete recovery of synaptically evoked population spike in the CA1 region after 1 h (48.5 ± 3.6% of baseline values). This recovery could be markedly enhanced by the application of
N-methyl-
d-aspartate receptor antagonists.
To examine the influence of metabotropic glutamate receptors on neuronal recovery from hypoxia/ hypoglycemia, we applied various antagonists and agonists of the metabotropic glutamate receptors to the bath during the interval from 20 min before to 10 min after hypoxia/hypoglycemia. The metabotropic glutamate receptor antagonists (+)-α-methyl-4-carboxyphenylglycine and
l-2-amino-3-phosphonopropionic acid were both able to enhance the population spike recovery significantly. However, the mixed metabotropic glutamate receptor agonist 1
S,3
R-1-aminocyclopentane-1,3-dicarboxylic acid also exhibited a protective effect on population spike recovery, leaving the anoxic depolarization and
N-methyl-
d-aspartate responses during the hypoxia/hypoglycemia untouched.
With the help of more subtype-specific agonists, we found that an activation of phospholipase C coupled (class 1) metabotropic glutamate receptors prior to hypoxia/hypoglycemia may be responsible for the protective effect seen with 1
S,3
R-1-aminocyclopentane-1,3-dicarboxylic acid, because the specific class 1 metabotropic glutamate receptor agonist
trans-azetidine-2,4-dicarboxylic acid appeared to be highly protective, but only if it was applied 20 min before the hypoxia/hypoglycemia. An activation of class 2 metabotropic glutamate receptors by (2
S1′
R,2′
R,3′
R)-2-(2,3-dicarboxycycloprophyl)glycine, which inhibits adenylyl cyclase activity, led to a marked deterioration of the population spike recovery and even to a total prevention of the protective effect of the
N-methyl-
d-aspartate agonist
d-2-amino-5-phosphonopentanoic acid.
Our data suggest that prior activation of class 1 metabotropic glutamate receptors is beneficial, while their activation during hypoxia/hypoglycemia is detrimental. Furthermore, the activation of class 2 metabotropic glutamate receptors decreases the recovery from hypoxia/hypoglycemia. |
doi_str_mv | 10.1016/0306-4522(95)00195-O |
format | Article |
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N-methyl-
d-aspartate receptor antagonists.
To examine the influence of metabotropic glutamate receptors on neuronal recovery from hypoxia/ hypoglycemia, we applied various antagonists and agonists of the metabotropic glutamate receptors to the bath during the interval from 20 min before to 10 min after hypoxia/hypoglycemia. The metabotropic glutamate receptor antagonists (+)-α-methyl-4-carboxyphenylglycine and
l-2-amino-3-phosphonopropionic acid were both able to enhance the population spike recovery significantly. However, the mixed metabotropic glutamate receptor agonist 1
S,3
R-1-aminocyclopentane-1,3-dicarboxylic acid also exhibited a protective effect on population spike recovery, leaving the anoxic depolarization and
N-methyl-
d-aspartate responses during the hypoxia/hypoglycemia untouched.
With the help of more subtype-specific agonists, we found that an activation of phospholipase C coupled (class 1) metabotropic glutamate receptors prior to hypoxia/hypoglycemia may be responsible for the protective effect seen with 1
S,3
R-1-aminocyclopentane-1,3-dicarboxylic acid, because the specific class 1 metabotropic glutamate receptor agonist
trans-azetidine-2,4-dicarboxylic acid appeared to be highly protective, but only if it was applied 20 min before the hypoxia/hypoglycemia. An activation of class 2 metabotropic glutamate receptors by (2
S1′
R,2′
R,3′
R)-2-(2,3-dicarboxycycloprophyl)glycine, which inhibits adenylyl cyclase activity, led to a marked deterioration of the population spike recovery and even to a total prevention of the protective effect of the
N-methyl-
d-aspartate agonist
d-2-amino-5-phosphonopentanoic acid.
Our data suggest that prior activation of class 1 metabotropic glutamate receptors is beneficial, while their activation during hypoxia/hypoglycemia is detrimental. Furthermore, the activation of class 2 metabotropic glutamate receptors decreases the recovery from hypoxia/hypoglycemia.</description><identifier>ISSN: 0306-4522</identifier><identifier>EISSN: 1873-7544</identifier><identifier>DOI: 10.1016/0306-4522(95)00195-O</identifier><identifier>PMID: 8545005</identifier><identifier>CODEN: NRSCDN</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Adenosine Triphosphate - metabolism ; Animals ; Biological and medical sciences ; Central nervous system ; Central neurotransmission. Neuromudulation. Pathways and receptors ; Cycloleucine - analogs & derivatives ; Cycloleucine - pharmacology ; Electrophysiology ; Energy Metabolism - drug effects ; Excitatory Amino Acid Agonists - pharmacology ; Excitatory Amino Acid Antagonists - pharmacology ; Fundamental and applied biological sciences. Psychology ; Hippocampus - cytology ; Hippocampus - drug effects ; Hippocampus - metabolism ; Hypoglycemia - pathology ; Hypoxia, Brain - pathology ; In Vitro Techniques ; Male ; N-Methylaspartate - antagonists & inhibitors ; Neurons - physiology ; Phosphocreatine - metabolism ; Pyramidal Cells - drug effects ; Pyramidal Cells - metabolism ; Rats ; Rats, Wistar ; Receptors, Metabotropic Glutamate - agonists ; Receptors, Metabotropic Glutamate - antagonists & inhibitors ; Vertebrates: nervous system and sense organs</subject><ispartof>Neuroscience, 1995, Vol.68 (4), p.989-1001</ispartof><rights>1995</rights><rights>1995 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c512t-dc83a1fb3ca6942cc4f9e0cced691c9f3ae721f09191454596de1ce67fa22f233</citedby><cites>FETCH-LOGICAL-c512t-dc83a1fb3ca6942cc4f9e0cced691c9f3ae721f09191454596de1ce67fa22f233</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0306-4522(95)00195-O$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,4024,27923,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3654581$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8545005$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Opitz, T.</creatorcontrib><creatorcontrib>Richter, P.</creatorcontrib><creatorcontrib>Carter, A.J.</creatorcontrib><creatorcontrib>Kozikowski, A.P.</creatorcontrib><creatorcontrib>Shinozaki, H.</creatorcontrib><creatorcontrib>Reymann, K.G.</creatorcontrib><title>Metabotropic glutamate receptor subtypes differentially influence neuronal recovery from in vitro hypoxia/hypoglycemia in rat hippocampal slices</title><title>Neuroscience</title><addtitle>Neuroscience</addtitle><description>Hippocampal slices were transiently exposed to an oxygen- and glucose-free environment which causes a pronounced drop of both ATP and creatine phosphate, an anoxic depolarization, and an incomplete recovery of synaptically evoked population spike in the CA1 region after 1 h (48.5 ± 3.6% of baseline values). This recovery could be markedly enhanced by the application of
N-methyl-
d-aspartate receptor antagonists.
To examine the influence of metabotropic glutamate receptors on neuronal recovery from hypoxia/ hypoglycemia, we applied various antagonists and agonists of the metabotropic glutamate receptors to the bath during the interval from 20 min before to 10 min after hypoxia/hypoglycemia. The metabotropic glutamate receptor antagonists (+)-α-methyl-4-carboxyphenylglycine and
l-2-amino-3-phosphonopropionic acid were both able to enhance the population spike recovery significantly. However, the mixed metabotropic glutamate receptor agonist 1
S,3
R-1-aminocyclopentane-1,3-dicarboxylic acid also exhibited a protective effect on population spike recovery, leaving the anoxic depolarization and
N-methyl-
d-aspartate responses during the hypoxia/hypoglycemia untouched.
With the help of more subtype-specific agonists, we found that an activation of phospholipase C coupled (class 1) metabotropic glutamate receptors prior to hypoxia/hypoglycemia may be responsible for the protective effect seen with 1
S,3
R-1-aminocyclopentane-1,3-dicarboxylic acid, because the specific class 1 metabotropic glutamate receptor agonist
trans-azetidine-2,4-dicarboxylic acid appeared to be highly protective, but only if it was applied 20 min before the hypoxia/hypoglycemia. An activation of class 2 metabotropic glutamate receptors by (2
S1′
R,2′
R,3′
R)-2-(2,3-dicarboxycycloprophyl)glycine, which inhibits adenylyl cyclase activity, led to a marked deterioration of the population spike recovery and even to a total prevention of the protective effect of the
N-methyl-
d-aspartate agonist
d-2-amino-5-phosphonopentanoic acid.
Our data suggest that prior activation of class 1 metabotropic glutamate receptors is beneficial, while their activation during hypoxia/hypoglycemia is detrimental. Furthermore, the activation of class 2 metabotropic glutamate receptors decreases the recovery from hypoxia/hypoglycemia.</description><subject>Adenosine Triphosphate - metabolism</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Central nervous system</subject><subject>Central neurotransmission. Neuromudulation. Pathways and receptors</subject><subject>Cycloleucine - analogs & derivatives</subject><subject>Cycloleucine - pharmacology</subject><subject>Electrophysiology</subject><subject>Energy Metabolism - drug effects</subject><subject>Excitatory Amino Acid Agonists - pharmacology</subject><subject>Excitatory Amino Acid Antagonists - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hippocampus - cytology</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - metabolism</subject><subject>Hypoglycemia - pathology</subject><subject>Hypoxia, Brain - pathology</subject><subject>In Vitro Techniques</subject><subject>Male</subject><subject>N-Methylaspartate - antagonists & inhibitors</subject><subject>Neurons - physiology</subject><subject>Phosphocreatine - metabolism</subject><subject>Pyramidal Cells - drug effects</subject><subject>Pyramidal Cells - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptors, Metabotropic Glutamate - agonists</subject><subject>Receptors, Metabotropic Glutamate - antagonists & inhibitors</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0306-4522</issn><issn>1873-7544</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcFu1DAQhi0EKtvCG4DkA0JwCLWT2FlfkFBFAaloL3C2vJNxa-TEwXZW5C14ZBx2tUfwZSzN94_G_gh5wdk7zri8Zg2TVSvq-o0SbxnjSlS7R2TDt11TdaJtH5PNGXlKLlP6wcoRbXNBLraiFeW-Ib-_Yjb7kGOYHNB7P2czmIw0IuCUQ6Rp3udlwkR7Zy1GHLMz3i_UjdbPOALSEecYRuPXTDhgXKiNYSgAPbgylz4sU_jlzPVa7_0CODizdqPJ9MFNUwAzTCWevANMz8gTa3zC56d6Rb7ffvx287m62336cvPhrgLB61z1sG0Mt_sGjFRtDdBahQwAe6k4KNsY7GpumeKKt-WxSvbIAWVnTV3bummuyOvj3CmGnzOmrAeXAL03I4Y56a7ratbJ_4NcKimUkAVsjyDEkFJEq6foBhMXzZlejelVh151aCX0X2N6V2IvT_Pn_YD9OXRSVPqvTn2TwHgbzQgunbFGFm7LC_b-iGH5tIPDqBO41U_vipes--D-vccfEda26w</recordid><startdate>1995</startdate><enddate>1995</enddate><creator>Opitz, T.</creator><creator>Richter, P.</creator><creator>Carter, A.J.</creator><creator>Kozikowski, A.P.</creator><creator>Shinozaki, H.</creator><creator>Reymann, K.G.</creator><general>Elsevier Ltd</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>1995</creationdate><title>Metabotropic glutamate receptor subtypes differentially influence neuronal recovery from in vitro hypoxia/hypoglycemia in rat hippocampal slices</title><author>Opitz, T. ; Richter, P. ; Carter, A.J. ; Kozikowski, A.P. ; Shinozaki, H. ; Reymann, K.G.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c512t-dc83a1fb3ca6942cc4f9e0cced691c9f3ae721f09191454596de1ce67fa22f233</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Adenosine Triphosphate - metabolism</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Central nervous system</topic><topic>Central neurotransmission. Neuromudulation. Pathways and receptors</topic><topic>Cycloleucine - analogs & derivatives</topic><topic>Cycloleucine - pharmacology</topic><topic>Electrophysiology</topic><topic>Energy Metabolism - drug effects</topic><topic>Excitatory Amino Acid Agonists - pharmacology</topic><topic>Excitatory Amino Acid Antagonists - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hippocampus - cytology</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - metabolism</topic><topic>Hypoglycemia - pathology</topic><topic>Hypoxia, Brain - pathology</topic><topic>In Vitro Techniques</topic><topic>Male</topic><topic>N-Methylaspartate - antagonists & inhibitors</topic><topic>Neurons - physiology</topic><topic>Phosphocreatine - metabolism</topic><topic>Pyramidal Cells - drug effects</topic><topic>Pyramidal Cells - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptors, Metabotropic Glutamate - agonists</topic><topic>Receptors, Metabotropic Glutamate - antagonists & inhibitors</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Opitz, T.</creatorcontrib><creatorcontrib>Richter, P.</creatorcontrib><creatorcontrib>Carter, A.J.</creatorcontrib><creatorcontrib>Kozikowski, A.P.</creatorcontrib><creatorcontrib>Shinozaki, H.</creatorcontrib><creatorcontrib>Reymann, K.G.</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>Neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Opitz, T.</au><au>Richter, P.</au><au>Carter, A.J.</au><au>Kozikowski, A.P.</au><au>Shinozaki, H.</au><au>Reymann, K.G.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Metabotropic glutamate receptor subtypes differentially influence neuronal recovery from in vitro hypoxia/hypoglycemia in rat hippocampal slices</atitle><jtitle>Neuroscience</jtitle><addtitle>Neuroscience</addtitle><date>1995</date><risdate>1995</risdate><volume>68</volume><issue>4</issue><spage>989</spage><epage>1001</epage><pages>989-1001</pages><issn>0306-4522</issn><eissn>1873-7544</eissn><coden>NRSCDN</coden><abstract>Hippocampal slices were transiently exposed to an oxygen- and glucose-free environment which causes a pronounced drop of both ATP and creatine phosphate, an anoxic depolarization, and an incomplete recovery of synaptically evoked population spike in the CA1 region after 1 h (48.5 ± 3.6% of baseline values). This recovery could be markedly enhanced by the application of
N-methyl-
d-aspartate receptor antagonists.
To examine the influence of metabotropic glutamate receptors on neuronal recovery from hypoxia/ hypoglycemia, we applied various antagonists and agonists of the metabotropic glutamate receptors to the bath during the interval from 20 min before to 10 min after hypoxia/hypoglycemia. The metabotropic glutamate receptor antagonists (+)-α-methyl-4-carboxyphenylglycine and
l-2-amino-3-phosphonopropionic acid were both able to enhance the population spike recovery significantly. However, the mixed metabotropic glutamate receptor agonist 1
S,3
R-1-aminocyclopentane-1,3-dicarboxylic acid also exhibited a protective effect on population spike recovery, leaving the anoxic depolarization and
N-methyl-
d-aspartate responses during the hypoxia/hypoglycemia untouched.
With the help of more subtype-specific agonists, we found that an activation of phospholipase C coupled (class 1) metabotropic glutamate receptors prior to hypoxia/hypoglycemia may be responsible for the protective effect seen with 1
S,3
R-1-aminocyclopentane-1,3-dicarboxylic acid, because the specific class 1 metabotropic glutamate receptor agonist
trans-azetidine-2,4-dicarboxylic acid appeared to be highly protective, but only if it was applied 20 min before the hypoxia/hypoglycemia. An activation of class 2 metabotropic glutamate receptors by (2
S1′
R,2′
R,3′
R)-2-(2,3-dicarboxycycloprophyl)glycine, which inhibits adenylyl cyclase activity, led to a marked deterioration of the population spike recovery and even to a total prevention of the protective effect of the
N-methyl-
d-aspartate agonist
d-2-amino-5-phosphonopentanoic acid.
Our data suggest that prior activation of class 1 metabotropic glutamate receptors is beneficial, while their activation during hypoxia/hypoglycemia is detrimental. Furthermore, the activation of class 2 metabotropic glutamate receptors decreases the recovery from hypoxia/hypoglycemia.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>8545005</pmid><doi>10.1016/0306-4522(95)00195-O</doi><tpages>13</tpages></addata></record> |
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subjects | Adenosine Triphosphate - metabolism Animals Biological and medical sciences Central nervous system Central neurotransmission. Neuromudulation. Pathways and receptors Cycloleucine - analogs & derivatives Cycloleucine - pharmacology Electrophysiology Energy Metabolism - drug effects Excitatory Amino Acid Agonists - pharmacology Excitatory Amino Acid Antagonists - pharmacology Fundamental and applied biological sciences. Psychology Hippocampus - cytology Hippocampus - drug effects Hippocampus - metabolism Hypoglycemia - pathology Hypoxia, Brain - pathology In Vitro Techniques Male N-Methylaspartate - antagonists & inhibitors Neurons - physiology Phosphocreatine - metabolism Pyramidal Cells - drug effects Pyramidal Cells - metabolism Rats Rats, Wistar Receptors, Metabotropic Glutamate - agonists Receptors, Metabotropic Glutamate - antagonists & inhibitors Vertebrates: nervous system and sense organs |
title | Metabotropic glutamate receptor subtypes differentially influence neuronal recovery from in vitro hypoxia/hypoglycemia in rat hippocampal slices |
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