Trans-synaptic increase of hypoxic tolerance in hippocampus upon physical challenge with two-photon microscopy

Neuronal hypoxic tolerance is modulated by preceding challenges. We investigated hypoxic tolerance in CA1 pyramidal cells of murine hippocampal slices upon preceding physical challenge with two‐photon illumination in close spatial proximity to the recorded area, at distant presynaptic neurons, or pr...

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Veröffentlicht in:Hippocampus 2002, Vol.12 (6), p.765-773
Hauptverfasser: Büchner, Maren, Huber, Roman, Riepe, Matthias W.
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Huber, Roman
Riepe, Matthias W.
description Neuronal hypoxic tolerance is modulated by preceding challenges. We investigated hypoxic tolerance in CA1 pyramidal cells of murine hippocampal slices upon preceding physical challenge with two‐photon illumination in close spatial proximity to the recorded area, at distant presynaptic neurons, or preceding chemical treatment with acetylsalicylic acid while zinc fluorescence was assessed with fluorescence measurement upon staining with N‐(6‐methoxy‐8‐quinolyl)‐para‐toluenesulfonamide (TSQ). Posthypoxic recovery (15 min hypoxia, 45 min recovery) of CA1 population spike amplitude (PSAP) upon stimulation of Schaffer collaterals in hippocampal region CA3 was 20 ± 38% (mean ±SD; n = 15) in control slices. At the end of hypoxia, zinc fluorescence increased to 120 ± 16% (P < 0.05 to control) in slices that later recovered and 141 ± 20% in slices that did not recover (P < 0.01 to control; P < 0.05 compared with returns). Multi‐photon illumination alone was an appropriate physical challenge to improve hypoxic tolerance, even trans‐synaptically. Depending on the number of illuminations posthypoxic PSAP increased up to 84 ± 25% (P < 0.01 to control) upon illumination of hippocampal region CA1 and 85 ± 28% (P < 0.01 to control) upon illumination of CA3. With the latter treatment, zinc fluorescence in CA1 increased to 126 ± 20% before hypoxia (P < 0.05 to control), and no further zinc increase was observed upon subsequent hypoxia. Similar results were obtained upon chemical preconditioning with acetylsalicylate. We conclude that observation of live specimen with multi‐photon imaging alters the physiology of neuronal cell ensembles, including hypoxic tolerance, even trans‐synaptically at long distances from the imaged area. This is mediated in part through endogenous modulation by zinc. Mild zinc increase improves hypoxic tolerance while pronounced increase predicts neuronal cell death. Hippocampus 2002;12:765–773. © 2002 Wiley‐Liss, Inc.
doi_str_mv 10.1002/hipo.10028
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We investigated hypoxic tolerance in CA1 pyramidal cells of murine hippocampal slices upon preceding physical challenge with two‐photon illumination in close spatial proximity to the recorded area, at distant presynaptic neurons, or preceding chemical treatment with acetylsalicylic acid while zinc fluorescence was assessed with fluorescence measurement upon staining with N‐(6‐methoxy‐8‐quinolyl)‐para‐toluenesulfonamide (TSQ). Posthypoxic recovery (15 min hypoxia, 45 min recovery) of CA1 population spike amplitude (PSAP) upon stimulation of Schaffer collaterals in hippocampal region CA3 was 20 ± 38% (mean ±SD; n = 15) in control slices. At the end of hypoxia, zinc fluorescence increased to 120 ± 16% (P < 0.05 to control) in slices that later recovered and 141 ± 20% in slices that did not recover (P < 0.01 to control; P < 0.05 compared with returns). Multi‐photon illumination alone was an appropriate physical challenge to improve hypoxic tolerance, even trans‐synaptically. Depending on the number of illuminations posthypoxic PSAP increased up to 84 ± 25% (P < 0.01 to control) upon illumination of hippocampal region CA1 and 85 ± 28% (P < 0.01 to control) upon illumination of CA3. With the latter treatment, zinc fluorescence in CA1 increased to 126 ± 20% before hypoxia (P < 0.05 to control), and no further zinc increase was observed upon subsequent hypoxia. Similar results were obtained upon chemical preconditioning with acetylsalicylate. We conclude that observation of live specimen with multi‐photon imaging alters the physiology of neuronal cell ensembles, including hypoxic tolerance, even trans‐synaptically at long distances from the imaged area. This is mediated in part through endogenous modulation by zinc. Mild zinc increase improves hypoxic tolerance while pronounced increase predicts neuronal cell death. 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We investigated hypoxic tolerance in CA1 pyramidal cells of murine hippocampal slices upon preceding physical challenge with two‐photon illumination in close spatial proximity to the recorded area, at distant presynaptic neurons, or preceding chemical treatment with acetylsalicylic acid while zinc fluorescence was assessed with fluorescence measurement upon staining with N‐(6‐methoxy‐8‐quinolyl)‐para‐toluenesulfonamide (TSQ). Posthypoxic recovery (15 min hypoxia, 45 min recovery) of CA1 population spike amplitude (PSAP) upon stimulation of Schaffer collaterals in hippocampal region CA3 was 20 ± 38% (mean ±SD; n = 15) in control slices. At the end of hypoxia, zinc fluorescence increased to 120 ± 16% (P < 0.05 to control) in slices that later recovered and 141 ± 20% in slices that did not recover (P < 0.01 to control; P < 0.05 compared with returns). Multi‐photon illumination alone was an appropriate physical challenge to improve hypoxic tolerance, even trans‐synaptically. Depending on the number of illuminations posthypoxic PSAP increased up to 84 ± 25% (P < 0.01 to control) upon illumination of hippocampal region CA1 and 85 ± 28% (P < 0.01 to control) upon illumination of CA3. With the latter treatment, zinc fluorescence in CA1 increased to 126 ± 20% before hypoxia (P < 0.05 to control), and no further zinc increase was observed upon subsequent hypoxia. Similar results were obtained upon chemical preconditioning with acetylsalicylate. We conclude that observation of live specimen with multi‐photon imaging alters the physiology of neuronal cell ensembles, including hypoxic tolerance, even trans‐synaptically at long distances from the imaged area. This is mediated in part through endogenous modulation by zinc. Mild zinc increase improves hypoxic tolerance while pronounced increase predicts neuronal cell death. 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Huber, Roman ; Riepe, Matthias W.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3638-d40851f05eecbc46e9292bf32b9a41af691a9fbb20d1c6e312882b4564c0e2143</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Action Potentials - drug effects</topic><topic>Action Potentials - physiology</topic><topic>Aminoquinolines</topic><topic>Animals</topic><topic>Aspirin - pharmacology</topic><topic>cell death</topic><topic>Chelating Agents - pharmacology</topic><topic>Fluorescent Dyes</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - metabolism</topic><topic>Hippocampus - physiopathology</topic><topic>Hypoxia-Ischemia, Brain - metabolism</topic><topic>Hypoxia-Ischemia, Brain - physiopathology</topic><topic>Ischemic Preconditioning - methods</topic><topic>Lasers</topic><topic>Light</topic><topic>Male</topic><topic>Mice</topic><topic>mouse</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>neuroprotection</topic><topic>Photic Stimulation</topic><topic>preconditioning</topic><topic>slice</topic><topic>Synapses - drug effects</topic><topic>Synapses - metabolism</topic><topic>Synaptic Transmission - drug effects</topic><topic>Synaptic Transmission - physiology</topic><topic>Tosyl Compounds</topic><topic>Zinc - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Büchner, Maren</creatorcontrib><creatorcontrib>Huber, Roman</creatorcontrib><creatorcontrib>Riepe, Matthias W.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Hippocampus</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Büchner, Maren</au><au>Huber, Roman</au><au>Riepe, Matthias W.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Trans-synaptic increase of hypoxic tolerance in hippocampus upon physical challenge with two-photon microscopy</atitle><jtitle>Hippocampus</jtitle><addtitle>Hippocampus</addtitle><date>2002</date><risdate>2002</risdate><volume>12</volume><issue>6</issue><spage>765</spage><epage>773</epage><pages>765-773</pages><issn>1050-9631</issn><eissn>1098-1063</eissn><abstract><![CDATA[Neuronal hypoxic tolerance is modulated by preceding challenges. We investigated hypoxic tolerance in CA1 pyramidal cells of murine hippocampal slices upon preceding physical challenge with two‐photon illumination in close spatial proximity to the recorded area, at distant presynaptic neurons, or preceding chemical treatment with acetylsalicylic acid while zinc fluorescence was assessed with fluorescence measurement upon staining with N‐(6‐methoxy‐8‐quinolyl)‐para‐toluenesulfonamide (TSQ). Posthypoxic recovery (15 min hypoxia, 45 min recovery) of CA1 population spike amplitude (PSAP) upon stimulation of Schaffer collaterals in hippocampal region CA3 was 20 ± 38% (mean ±SD; n = 15) in control slices. At the end of hypoxia, zinc fluorescence increased to 120 ± 16% (P < 0.05 to control) in slices that later recovered and 141 ± 20% in slices that did not recover (P < 0.01 to control; P < 0.05 compared with returns). Multi‐photon illumination alone was an appropriate physical challenge to improve hypoxic tolerance, even trans‐synaptically. Depending on the number of illuminations posthypoxic PSAP increased up to 84 ± 25% (P < 0.01 to control) upon illumination of hippocampal region CA1 and 85 ± 28% (P < 0.01 to control) upon illumination of CA3. With the latter treatment, zinc fluorescence in CA1 increased to 126 ± 20% before hypoxia (P < 0.05 to control), and no further zinc increase was observed upon subsequent hypoxia. Similar results were obtained upon chemical preconditioning with acetylsalicylate. We conclude that observation of live specimen with multi‐photon imaging alters the physiology of neuronal cell ensembles, including hypoxic tolerance, even trans‐synaptically at long distances from the imaged area. This is mediated in part through endogenous modulation by zinc. Mild zinc increase improves hypoxic tolerance while pronounced increase predicts neuronal cell death. Hippocampus 2002;12:765–773. © 2002 Wiley‐Liss, Inc.]]></abstract><cop>New York</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>12542228</pmid><doi>10.1002/hipo.10028</doi><tpages>9</tpages></addata></record>
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subjects Action Potentials - drug effects
Action Potentials - physiology
Aminoquinolines
Animals
Aspirin - pharmacology
cell death
Chelating Agents - pharmacology
Fluorescent Dyes
Hippocampus - drug effects
Hippocampus - metabolism
Hippocampus - physiopathology
Hypoxia-Ischemia, Brain - metabolism
Hypoxia-Ischemia, Brain - physiopathology
Ischemic Preconditioning - methods
Lasers
Light
Male
Mice
mouse
Neurons - drug effects
Neurons - metabolism
neuroprotection
Photic Stimulation
preconditioning
slice
Synapses - drug effects
Synapses - metabolism
Synaptic Transmission - drug effects
Synaptic Transmission - physiology
Tosyl Compounds
Zinc - metabolism
title Trans-synaptic increase of hypoxic tolerance in hippocampus upon physical challenge with two-photon microscopy
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