Nitric oxide-mediated activation of extracellular signal-regulated kinase (erk) and c-jun n-terminal kinase (jnk) during hypoxia in cerebral cortical nuclei of newborn piglets
Previous studies have shown that mitogen-activated protein kinases, such as extracellular signal-related kinase (ERK) and c-Jun N-terminal kinase (JNK), mediate signal transduction from cell surface receptors to the nucleus and phosphorylate anti-apoptotic proteins thereby regulating programmed cell...
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| description | Previous studies have shown that mitogen-activated protein kinases, such as extracellular signal-related kinase (ERK) and c-Jun N-terminal kinase (JNK), mediate signal transduction from cell surface receptors to the nucleus and phosphorylate anti-apoptotic proteins thereby regulating programmed cell death. The present study tests the hypotheses that hypoxia activates ERK and JNK in neuronal nuclei of newborn piglets and the hypoxia-induced activation of ERK and JNK is mediated by nitric oxide (NO). Activated ERK and JNK were assessed by determining phosphorylated ERK and JNK using immunoblotting in six normoxic (Nx) and 10 hypoxic (Hx) and five
N-nitro-
l-arginine (a NOS inhibitor, 40 mg/kg,) -pretreated hypoxic (
N-nitro-
l-arginine [NN
lA]-Hx) 3–5 day old piglets. Hypoxia was induced by decreasing inspired oxygen from 21% to 7% for 60 min. Cerebral tissue hypoxia was documented biochemically by determining the tissue levels of ATP and phosphocreatine (PCr). Cortical neuronal nuclei were isolated and the nuclear protein was analyzed for activated ERK and JNK using anti-phosphorylated ERK and JNK antibodies. Protein bands were detected using enhanced chemiluminescence method and analyzed by imaging densitometry. Protein density was expressed as absorbance OD×mm
2. ATP levels were 4.57±0.45 μmoles/g brain in the Nx group, 1.29±0.23 μmoles/g brain in the Hx group (
P |
| doi_str_mv | 10.1016/j.neuroscience.2003.08.008 |
| format | Article |
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N-nitro-
l-arginine (a NOS inhibitor, 40 mg/kg,) -pretreated hypoxic (
N-nitro-
l-arginine [NN
lA]-Hx) 3–5 day old piglets. Hypoxia was induced by decreasing inspired oxygen from 21% to 7% for 60 min. Cerebral tissue hypoxia was documented biochemically by determining the tissue levels of ATP and phosphocreatine (PCr). Cortical neuronal nuclei were isolated and the nuclear protein was analyzed for activated ERK and JNK using anti-phosphorylated ERK and JNK antibodies. Protein bands were detected using enhanced chemiluminescence method and analyzed by imaging densitometry. Protein density was expressed as absorbance OD×mm
2. ATP levels were 4.57±0.45 μmoles/g brain in the Nx group, 1.29±0.23 μmoles/g brain in the Hx group (
P<0.05 vs Nx) and 1.50±0.14 μmoles/g brain in the NN
lA-Hx group (
P<0.05 vs Nx). PCr levels were 3.77±0.36 μmoles/g brain in the Nx group, 0.77±0.13 μmoles/g brain in the hypoxic group (
P<0.05) and 1.02±0.24 in the NN
lA-Hx group (
P<0.05 vs Nx). Density of phosphorylated ERK protein was 170.5±53.7 OD×mm
2 in the Nx group as compared with 419.6±63.9 OD×mm
2 in the hypoxic group (
P<0.001 vs Nx) and 270.0±28.7 in the NN
lA-Hx group (
P<0.002 vs Hx). Density of phosphorylated JNK protein was 172.8±42.8 OD×mm
2 in the normoxic group as compared with 364.6±60.1 OD×mm
2 in the Hx group (
P<0.002) and 254.8±24.8 in the NN
lA-Hx group (
P<0.002 vs Hx). The data demonstrate increased phosphorylation of ERK and JNK during hypoxia indicating that hypoxia results in activation of ERK and JNK in neuronal nuclei of newborn piglets. The administration of NN
lA, a NOS inhibitor, prevented the hypoxia-induced phosphorylation of ERK and JNK indicating that the hypoxia-induced activation of ERK and JNK in the cerebral cortical nuclei of newborn piglets is NO-mediated]]></description><identifier>ISSN: 0306-4522</identifier><identifier>EISSN: 1873-7544</identifier><identifier>DOI: 10.1016/j.neuroscience.2003.08.008</identifier><identifier>PMID: 14667452</identifier><identifier>CODEN: NRSCDN</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Animals ; Animals, Newborn ; Biological and medical sciences ; Cerebral Cortex - enzymology ; Cerebral Cortex - metabolism ; Enzyme Activation - drug effects ; Enzyme Activation - physiology ; Enzyme Inhibitors - pharmacology ; ERK ; Fundamental and applied biological sciences. Psychology ; hypoxia ; Hypoxia, Brain - enzymology ; Hypoxia, Brain - metabolism ; JNK ; JNK Mitogen-Activated Protein Kinases ; Mitogen-Activated Protein Kinases - antagonists & inhibitors ; Mitogen-Activated Protein Kinases - metabolism ; newborn brain ; Nitric Oxide - antagonists & inhibitors ; Nitric Oxide - metabolism ; phosphorylation ; Swine ; Vertebrates: nervous system and sense organs</subject><ispartof>Neuroscience, 2004, Vol.123 (1), p.179-186</ispartof><rights>2003 IBRO</rights><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c352t-64f77daabb29641fa3d9b94568e7edaa8d9e6946333c95b2b34a377a77b906563</citedby><cites>FETCH-LOGICAL-c352t-64f77daabb29641fa3d9b94568e7edaa8d9e6946333c95b2b34a377a77b906563</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.neuroscience.2003.08.008$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3537,4010,27904,27905,27906,45976</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15367639$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14667452$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mishra, O.P</creatorcontrib><creatorcontrib>Zubrow, A.B</creatorcontrib><creatorcontrib>Ashraf, Q.M</creatorcontrib><title>Nitric oxide-mediated activation of extracellular signal-regulated kinase (erk) and c-jun n-terminal kinase (jnk) during hypoxia in cerebral cortical nuclei of newborn piglets</title><title>Neuroscience</title><addtitle>Neuroscience</addtitle><description><![CDATA[Previous studies have shown that mitogen-activated protein kinases, such as extracellular signal-related kinase (ERK) and c-Jun N-terminal kinase (JNK), mediate signal transduction from cell surface receptors to the nucleus and phosphorylate anti-apoptotic proteins thereby regulating programmed cell death. The present study tests the hypotheses that hypoxia activates ERK and JNK in neuronal nuclei of newborn piglets and the hypoxia-induced activation of ERK and JNK is mediated by nitric oxide (NO). Activated ERK and JNK were assessed by determining phosphorylated ERK and JNK using immunoblotting in six normoxic (Nx) and 10 hypoxic (Hx) and five
N-nitro-
l-arginine (a NOS inhibitor, 40 mg/kg,) -pretreated hypoxic (
N-nitro-
l-arginine [NN
lA]-Hx) 3–5 day old piglets. Hypoxia was induced by decreasing inspired oxygen from 21% to 7% for 60 min. Cerebral tissue hypoxia was documented biochemically by determining the tissue levels of ATP and phosphocreatine (PCr). Cortical neuronal nuclei were isolated and the nuclear protein was analyzed for activated ERK and JNK using anti-phosphorylated ERK and JNK antibodies. Protein bands were detected using enhanced chemiluminescence method and analyzed by imaging densitometry. Protein density was expressed as absorbance OD×mm
2. ATP levels were 4.57±0.45 μmoles/g brain in the Nx group, 1.29±0.23 μmoles/g brain in the Hx group (
P<0.05 vs Nx) and 1.50±0.14 μmoles/g brain in the NN
lA-Hx group (
P<0.05 vs Nx). PCr levels were 3.77±0.36 μmoles/g brain in the Nx group, 0.77±0.13 μmoles/g brain in the hypoxic group (
P<0.05) and 1.02±0.24 in the NN
lA-Hx group (
P<0.05 vs Nx). Density of phosphorylated ERK protein was 170.5±53.7 OD×mm
2 in the Nx group as compared with 419.6±63.9 OD×mm
2 in the hypoxic group (
P<0.001 vs Nx) and 270.0±28.7 in the NN
lA-Hx group (
P<0.002 vs Hx). Density of phosphorylated JNK protein was 172.8±42.8 OD×mm
2 in the normoxic group as compared with 364.6±60.1 OD×mm
2 in the Hx group (
P<0.002) and 254.8±24.8 in the NN
lA-Hx group (
P<0.002 vs Hx). The data demonstrate increased phosphorylation of ERK and JNK during hypoxia indicating that hypoxia results in activation of ERK and JNK in neuronal nuclei of newborn piglets. The administration of NN
lA, a NOS inhibitor, prevented the hypoxia-induced phosphorylation of ERK and JNK indicating that the hypoxia-induced activation of ERK and JNK in the cerebral cortical nuclei of newborn piglets is NO-mediated]]></description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Biological and medical sciences</subject><subject>Cerebral Cortex - enzymology</subject><subject>Cerebral Cortex - metabolism</subject><subject>Enzyme Activation - drug effects</subject><subject>Enzyme Activation - physiology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>ERK</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>hypoxia</subject><subject>Hypoxia, Brain - enzymology</subject><subject>Hypoxia, Brain - metabolism</subject><subject>JNK</subject><subject>JNK Mitogen-Activated Protein Kinases</subject><subject>Mitogen-Activated Protein Kinases - antagonists & inhibitors</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>newborn brain</subject><subject>Nitric Oxide - antagonists & inhibitors</subject><subject>Nitric Oxide - metabolism</subject><subject>phosphorylation</subject><subject>Swine</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0306-4522</issn><issn>1873-7544</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkctu1DAUhi0EokPhFZCFBCqLDHZ8S9ihlptUwQbWlmOfDE4zzmA7pX0qXhGHiSg78MaX853zW_-P0DNKtpRQ-WrYBpjjlKyHYGFbE8K2pNkS0txDG9ooVinB-X20IYzIiou6PkGPUhpIWYKzh-iEcilVKWzQz08-R2_xdOMdVHtw3mRw2Njsr032U8BTj-EmR2NhHOfRRJz8LpixirAr1wW-8sEkwGcQr15iExy21TAHHKoMcV9q4x9iCIVwc_Rhh7_dHoqowT5gCxG6WDg7xextOYTZjuAX7QA_uikGfPC7EXJ6jB70ZkzwZN1P0dd3b7-cf6guP7__eP7msrJM1LmSvFfKGdN1dSs57Q1zbddyIRtQUN4b14JsuWSM2VZ0dce4YUoZpbqWSCHZKXpxnHuI0_cZUtZ7nxYLTIBpTlpRIakQ5J8gbWuiBGkK-PoI2hJditDrQ_R7E281JXrJVQ_671z1kqsmjSa_m5-uKnNXQrprXYMswPMVMKkY2EcTrE93nGBSSdYW7uLIQTHv2kPUq5zzEWzWbvL_859fJnLLkw</recordid><startdate>2004</startdate><enddate>2004</enddate><creator>Mishra, O.P</creator><creator>Zubrow, A.B</creator><creator>Ashraf, Q.M</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>2004</creationdate><title>Nitric oxide-mediated activation of extracellular signal-regulated kinase (erk) and c-jun n-terminal kinase (jnk) during hypoxia in cerebral cortical nuclei of newborn piglets</title><author>Mishra, O.P ; Zubrow, A.B ; Ashraf, Q.M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c352t-64f77daabb29641fa3d9b94568e7edaa8d9e6946333c95b2b34a377a77b906563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Biological and medical sciences</topic><topic>Cerebral Cortex - enzymology</topic><topic>Cerebral Cortex - metabolism</topic><topic>Enzyme Activation - drug effects</topic><topic>Enzyme Activation - physiology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>ERK</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>hypoxia</topic><topic>Hypoxia, Brain - enzymology</topic><topic>Hypoxia, Brain - metabolism</topic><topic>JNK</topic><topic>JNK Mitogen-Activated Protein Kinases</topic><topic>Mitogen-Activated Protein Kinases - antagonists & inhibitors</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>newborn brain</topic><topic>Nitric Oxide - antagonists & inhibitors</topic><topic>Nitric Oxide - metabolism</topic><topic>phosphorylation</topic><topic>Swine</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mishra, O.P</creatorcontrib><creatorcontrib>Zubrow, A.B</creatorcontrib><creatorcontrib>Ashraf, Q.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>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mishra, O.P</au><au>Zubrow, A.B</au><au>Ashraf, Q.M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nitric oxide-mediated activation of extracellular signal-regulated kinase (erk) and c-jun n-terminal kinase (jnk) during hypoxia in cerebral cortical nuclei of newborn piglets</atitle><jtitle>Neuroscience</jtitle><addtitle>Neuroscience</addtitle><date>2004</date><risdate>2004</risdate><volume>123</volume><issue>1</issue><spage>179</spage><epage>186</epage><pages>179-186</pages><issn>0306-4522</issn><eissn>1873-7544</eissn><coden>NRSCDN</coden><abstract><![CDATA[Previous studies have shown that mitogen-activated protein kinases, such as extracellular signal-related kinase (ERK) and c-Jun N-terminal kinase (JNK), mediate signal transduction from cell surface receptors to the nucleus and phosphorylate anti-apoptotic proteins thereby regulating programmed cell death. The present study tests the hypotheses that hypoxia activates ERK and JNK in neuronal nuclei of newborn piglets and the hypoxia-induced activation of ERK and JNK is mediated by nitric oxide (NO). Activated ERK and JNK were assessed by determining phosphorylated ERK and JNK using immunoblotting in six normoxic (Nx) and 10 hypoxic (Hx) and five
N-nitro-
l-arginine (a NOS inhibitor, 40 mg/kg,) -pretreated hypoxic (
N-nitro-
l-arginine [NN
lA]-Hx) 3–5 day old piglets. Hypoxia was induced by decreasing inspired oxygen from 21% to 7% for 60 min. Cerebral tissue hypoxia was documented biochemically by determining the tissue levels of ATP and phosphocreatine (PCr). Cortical neuronal nuclei were isolated and the nuclear protein was analyzed for activated ERK and JNK using anti-phosphorylated ERK and JNK antibodies. Protein bands were detected using enhanced chemiluminescence method and analyzed by imaging densitometry. Protein density was expressed as absorbance OD×mm
2. ATP levels were 4.57±0.45 μmoles/g brain in the Nx group, 1.29±0.23 μmoles/g brain in the Hx group (
P<0.05 vs Nx) and 1.50±0.14 μmoles/g brain in the NN
lA-Hx group (
P<0.05 vs Nx). PCr levels were 3.77±0.36 μmoles/g brain in the Nx group, 0.77±0.13 μmoles/g brain in the hypoxic group (
P<0.05) and 1.02±0.24 in the NN
lA-Hx group (
P<0.05 vs Nx). Density of phosphorylated ERK protein was 170.5±53.7 OD×mm
2 in the Nx group as compared with 419.6±63.9 OD×mm
2 in the hypoxic group (
P<0.001 vs Nx) and 270.0±28.7 in the NN
lA-Hx group (
P<0.002 vs Hx). Density of phosphorylated JNK protein was 172.8±42.8 OD×mm
2 in the normoxic group as compared with 364.6±60.1 OD×mm
2 in the Hx group (
P<0.002) and 254.8±24.8 in the NN
lA-Hx group (
P<0.002 vs Hx). The data demonstrate increased phosphorylation of ERK and JNK during hypoxia indicating that hypoxia results in activation of ERK and JNK in neuronal nuclei of newborn piglets. The administration of NN
lA, a NOS inhibitor, prevented the hypoxia-induced phosphorylation of ERK and JNK indicating that the hypoxia-induced activation of ERK and JNK in the cerebral cortical nuclei of newborn piglets is NO-mediated]]></abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>14667452</pmid><doi>10.1016/j.neuroscience.2003.08.008</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Neuroscience, 2004, Vol.123 (1), p.179-186 |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Animals Animals, Newborn Biological and medical sciences Cerebral Cortex - enzymology Cerebral Cortex - metabolism Enzyme Activation - drug effects Enzyme Activation - physiology Enzyme Inhibitors - pharmacology ERK Fundamental and applied biological sciences. Psychology hypoxia Hypoxia, Brain - enzymology Hypoxia, Brain - metabolism JNK JNK Mitogen-Activated Protein Kinases Mitogen-Activated Protein Kinases - antagonists & inhibitors Mitogen-Activated Protein Kinases - metabolism newborn brain Nitric Oxide - antagonists & inhibitors Nitric Oxide - metabolism phosphorylation Swine Vertebrates: nervous system and sense organs |
| title | Nitric oxide-mediated activation of extracellular signal-regulated kinase (erk) and c-jun n-terminal kinase (jnk) during hypoxia in cerebral cortical nuclei of newborn piglets |
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