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Christopher J. Frederickson - One of the best experts on this subject based on the ideXlab platform.

  • Release of synaptic zinc is substantially depressed by conventional Brain Slice preparations.
    Brain research, 2000
    Co-Authors: Sang Won Suh, Gorm Danscher, Morten Skovgaard Jensen, Massoud Motamedi, R Thompson, Christopher J. Frederickson
    Abstract:

    Research on synaptically-released zinc is frequently done in vitro with acute Brain Slice preparations. We show here the in vitro hippocampal Slice preparation has two major pitfalls for zinc research. First, up to 50% of the synaptic zinc is lost during Slice cutting and/or the first 10 min of Slice incubation, with the losses being most pronounced on the edges of the Slice. Second, the release of the remaining zinc from a Slice is substantially depressed (up to 50%) at the low temperatures (32 degrees C) typically used for Brain Slice studies. In concert, these effects reduce zinc release about 75% in vitro, compared to in vivo. Implications for research on synaptically-released zinc are discussed.

  • Release of synaptic zinc is substantially depressed by conventional Brain Slice preparations.
    Brain Research, 2000
    Co-Authors: Sang Won Suh, Gorm Danscher, Morten Skovgaard Jensen, Richard B. Thompson, Massoud Motamedi, Christopher J. Frederickson
    Abstract:

    Research on synaptically-released zinc is frequently done in vitro with acute Brain Slice preparations. We show here the in vitro hippocampal Slice preparation has two major pitfalls for zinc research. First, up to 50% of the synaptic zinc is lost during Slice cutting and/or the first 10 min of Slice incubation, with the losses being most pronounced on the edges of the Slice. Second, the release of the remaining zinc from a Slice is substantially depressed (up to 50%) at the low temperatures (32°C) typically used for Brain Slice studies. In concert, these effects reduce zinc release about 75% in vitro, compared to in vivo. Implications for research on synaptically-released zinc are discussed.

  • Research report Release of synaptic zinc is substantially depressed by conventional Brain Slice preparations
    2000
    Co-Authors: Sang Won Suh, Gorm Danscher, Morten Skovgaard Jensen, Richard B. Thompson, Massoud Motamedi, Christopher J. Frederickson
    Abstract:

    Research on synaptically-released zinc is frequently done in vitro with acute Brain Slice preparations. We show here the in vitro hippocampal Slice preparation has two major pitfalls for zinc research. First, up to 50% of the synaptic zinc is lost during Slice cutting and / or the first 10 min of Slice incubation, with the losses being most pronounced on the edges of the Slice. Second, the release of the remaining zinc from a Slice is substantially depressed (up to 50%) at the low temperatures (328C) typically used for Brain Slice studies. In concert, these effects reduce zinc release about 75% in vitro, compared to in vivo. Implications for research on synaptically-released zinc are discussed. © 2000 Elsevier Science B.V. All rights reserved. Theme: Excitable membranes and synaptic transmission Topic: Mechanisms of neurotransmitter release

Jens Zimmer - One of the best experts on this subject based on the ideXlab platform.

  • Biocompatibility of silicon-based arrays of electrodes coupled to organotypic hippocampal Brain Slice cultures
    Brain Research, 2001
    Co-Authors: Bjarne Winther Kristensen, P. Thiébaud, Jens Noraberg, Milena Koudelka-hep, Jens Zimmer
    Abstract:

    In this study we examined the passive biocompatibility of a three-dimensional microelectrode array (MEA), designed to be coupled to organotypic Brain Slice cultures for multisite recording of electrophysiological signals. Hippocampal (and corticostriatal) Brain Slices from 1-week-old (and newborn) rats were grown for 4-8 weeks on the perforated silicon chips with silicon nitride surfaces and 40 μm sized holes and compared with corresponding tissue Slices grown on conventional semiporous membranes. In terms of preservation of the basic cellular and connective organization, as visualized by Nissl staining, Timm sulphide silver-staining, microtubule-associated protein 2 (MAP2) and glial fibrillary acidic protein (GFAP) immunostaining, the Slice cultures grown on chips did not differ from conventionally grown Slice cultures. Neither were there any signs of astrogliosis or neurodegeneration around the upper recording part of the 47-μm-high platinum-tip electrodes. Slice cultures grown on a separate set of chips with platinum instead of silicon nitride surfaces also displayed normal MAP2 and GFAP immunostaining. The width of the GFAP-rich zone (glia limitans) at the bottom surface of the Slice cultures was the same (∼20 μm) in cultures grown on chips with silicon nitride and platinum surfaces and on conventional insert membranes. The Slice cultures grown on chips maintained a normal, subfield differentiated susceptibility to the glutamate receptor agonist N-methyl-D-aspartate (NMDA) and the neurotoxin trimethyltin (TMT), as demonstrated by the cellular uptake of propidium iodide (PI), which was used as a reproducible and quantifiable marker for neuronal degeneration. We conclude that organotypic Brain Slice cultures can grow on silicon-based three-dimensional microelectrode arrays and develop normally with display of normal subfield differentiated susceptibilities to known excito- and neurotoxins. From this it is anticipated that the set-up, designed for recording of electrophysiological parameters, can be used for long-term studies of defined neuronal networks and provide valuable information on both normal, neurotoxicological and neuropathological conditions. © 2001 Elsevier Science B.V.

  • Biocompatibility of silicon-based arrays of electrodes coupled to organotypic hippocampal Brain Slice cultures.
    Brain Research, 2001
    Co-Authors: Bjarne Winther Kristensen, P. Thiébaud, Jens Noraberg, Milena Koudelka-hep, Jens Zimmer
    Abstract:

    In this study we examined the passive biocompatibility of a three-dimensional microelectrode array (MEA), designed to be coupled to organotypic Brain Slice cultures for multisite recording of electrophysiological signals. Hippocampal (and corticostriatal) Brain Slices from 1-week-old (and newborn) rats were grown for 4-8 weeks on the perforated silicon chips with silicon nitride surfaces and 40 microm sized holes and compared with corresponding tissue Slices grown on conventional semiporous membranes. In terms of preservation of the basic cellular and connective organization, as visualized by Nissl staining, Timm sulphide silver-staining, microtubule-associated protein 2 (MAP2) and glial fibrillary acidic protein (GFAP) immunostaining, the Slice cultures grown on chips did not differ from conventionally grown Slice cultures. Neither were there any signs of astrogliosis or neurodegeneration around the upper recording part of the 47-microm-high platinum-tip electrodes. Slice cultures grown on a separate set of chips with platinum instead of silicon nitride surfaces also displayed normal MAP2 and GFAP immunostaining. The width of the GFAP-rich zone (glia limitans) at the bottom surface of the Slice cultures was the same ( approximately 20 microm) in cultures grown on chips with silicon nitride and platinum surfaces and on conventional insert membranes. The Slice cultures grown on chips maintained a normal, subfield differentiated susceptibility to the glutamate receptor agonist N-methyl-D-aspartate (NMDA) and the neurotoxin trimethyltin (TMT), as demonstrated by the cellular uptake of propidium iodide (PI), which was used as a reproducible and quantifiable marker for neuronal degeneration. We conclude that organotypic Brain Slice cultures can grow on silicon-based three-dimensional microelectrode arrays and develop normally with display of normal subfield differentiated susceptibilities to known excito- and neurotoxins. From this it is anticipated that the set-up, designed for recording of electrophysiological parameters, can be used for long-term studies of defined neuronal networks and provide valuable information on both normal, neurotoxicological and neuropathological conditions.

  • Coupling of organotypic Brain Slice cultures to silicon-based arrays of electrodes.
    Methods, 1999
    Co-Authors: Henrik Jahnsen, Bjarne Winther Kristensen, P. Thiébaud, Jens Noraberg, Birthe Jakobsen, Marco Bove, Sergio Martinoia, Milena Koudelka-hep, Massimo Grattarola, Jens Zimmer
    Abstract:

    Fetal or early postnatal Brain tissue can be cultured in viable and healthy condition for several weeks with development and preservation of the basic cellular and connective organization as so-called organotypic Brain Slice cultures. Here we demonstrate and describe how it is possible to establish such hippocampal rat Brain Slice cultures on biocompatible silicon-based chips with arrays of electrodes with a histological organization comparable to that of conventional Brain Slice cultures grown by the roller drum technique and on semiporous membranes. Intracellular and extracellular recordings from neurons in the Slice cultures show that the electroresponsive properties of the neurons and synaptic circuitry are in accordance with those described for cells in acutely prepared Slices of the adult rat hippocampus. Based on the recordings and the possibilities of stimulating the cultured cells through the electrode arrays it is anticipated that the setup eventually will allow long-term studies of defined neuronal networks and provide valuable information on both normal and neurotoxicological and neuropathological conditions.

Elizabeth Nance - One of the best experts on this subject based on the ideXlab platform.

  • superoxide dismutase reduces monosodium glutamate induced injury in an organotypic whole hemisphere Brain Slice model of excitotoxicity
    Journal of Biological Engineering, 2020
    Co-Authors: Rick Liao, Thomas R Wood, Elizabeth Nance
    Abstract:

    Knowledge of glutamate excitotoxicity has increased substantially over the past few decades, with multiple proposed pathways involved in inflicting damage. We sought to develop a monosodium glutamate (MSG) exposed ex vivo organotypic whole hemisphere (OWH) Brain Slice model of excitotoxicity to study excitotoxic processes and screen the efficacy of superoxide dismutase (SOD). The OWH model is a reproducible platform with high cell viability and retained cellular morphology. OWH Slices exposed to MSG induced significant cytotoxicity and downregulation of neuronal excitation-related gene expression. The OWH Brain Slice model has enabled us to isolate and study components of excitotoxicity, distinguishing the effects of glutamate excitation, hyperosmolar stress, and inflammation. We find that extracellularly administered SOD is significantly protective in inhibiting cell death and restoring healthy mitochondrial morphology. SOD efficacy suggests that superoxide scavenging is a promising therapeutic strategy in excitotoxic injury. Using OWH Brain Slice models, we can obtain a better understanding of the pathological mechanisms of excitotoxic injury, and more rapidly screen potential therapeutics.

  • Superoxide dismutase reduces monosodium glutamate-induced injury in an organotypic whole hemisphere Brain Slice model of excitotoxicity
    Journal of Biological Engineering, 2020
    Co-Authors: Rick Liao, Thomas R Wood, Elizabeth Nance
    Abstract:

    Background Knowledge of glutamate excitotoxicity has increased substantially over the past few decades, with multiple proposed pathways involved in inflicting damage. We sought to develop a monosodium glutamate (MSG) exposed ex vivo organotypic whole hemisphere (OWH) Brain Slice model of excitotoxicity to study excitotoxic processes and screen the efficacy of superoxide dismutase (SOD). Results The OWH model is a reproducible platform with high cell viability and retained cellular morphology. OWH Slices exposed to MSG induced significant cytotoxicity and downregulation of neuronal excitation-related gene expression. The OWH Brain Slice model has enabled us to isolate and study components of excitotoxicity, distinguishing the effects of glutamate excitation, hyperosmolar stress, and inflammation. We find that extracellularly administered SOD is significantly protective in inhibiting cell death and restoring healthy mitochondrial morphology. SOD efficacy suggests that superoxide scavenging is a promising therapeutic strategy in excitotoxic injury. Conclusions Using OWH Brain Slice models, we can obtain a better understanding of the pathological mechanisms of excitotoxic injury, and more rapidly screen potential therapeutics.

Sang Won Suh - One of the best experts on this subject based on the ideXlab platform.

  • Release of synaptic zinc is substantially depressed by conventional Brain Slice preparations.
    Brain research, 2000
    Co-Authors: Sang Won Suh, Gorm Danscher, Morten Skovgaard Jensen, Massoud Motamedi, R Thompson, Christopher J. Frederickson
    Abstract:

    Research on synaptically-released zinc is frequently done in vitro with acute Brain Slice preparations. We show here the in vitro hippocampal Slice preparation has two major pitfalls for zinc research. First, up to 50% of the synaptic zinc is lost during Slice cutting and/or the first 10 min of Slice incubation, with the losses being most pronounced on the edges of the Slice. Second, the release of the remaining zinc from a Slice is substantially depressed (up to 50%) at the low temperatures (32 degrees C) typically used for Brain Slice studies. In concert, these effects reduce zinc release about 75% in vitro, compared to in vivo. Implications for research on synaptically-released zinc are discussed.

  • Release of synaptic zinc is substantially depressed by conventional Brain Slice preparations.
    Brain Research, 2000
    Co-Authors: Sang Won Suh, Gorm Danscher, Morten Skovgaard Jensen, Richard B. Thompson, Massoud Motamedi, Christopher J. Frederickson
    Abstract:

    Research on synaptically-released zinc is frequently done in vitro with acute Brain Slice preparations. We show here the in vitro hippocampal Slice preparation has two major pitfalls for zinc research. First, up to 50% of the synaptic zinc is lost during Slice cutting and/or the first 10 min of Slice incubation, with the losses being most pronounced on the edges of the Slice. Second, the release of the remaining zinc from a Slice is substantially depressed (up to 50%) at the low temperatures (32°C) typically used for Brain Slice studies. In concert, these effects reduce zinc release about 75% in vitro, compared to in vivo. Implications for research on synaptically-released zinc are discussed.

  • Research report Release of synaptic zinc is substantially depressed by conventional Brain Slice preparations
    2000
    Co-Authors: Sang Won Suh, Gorm Danscher, Morten Skovgaard Jensen, Richard B. Thompson, Massoud Motamedi, Christopher J. Frederickson
    Abstract:

    Research on synaptically-released zinc is frequently done in vitro with acute Brain Slice preparations. We show here the in vitro hippocampal Slice preparation has two major pitfalls for zinc research. First, up to 50% of the synaptic zinc is lost during Slice cutting and / or the first 10 min of Slice incubation, with the losses being most pronounced on the edges of the Slice. Second, the release of the remaining zinc from a Slice is substantially depressed (up to 50%) at the low temperatures (328C) typically used for Brain Slice studies. In concert, these effects reduce zinc release about 75% in vitro, compared to in vivo. Implications for research on synaptically-released zinc are discussed. © 2000 Elsevier Science B.V. All rights reserved. Theme: Excitable membranes and synaptic transmission Topic: Mechanisms of neurotransmitter release

Bjarne Winther Kristensen - One of the best experts on this subject based on the ideXlab platform.

  • Biocompatibility of silicon-based arrays of electrodes coupled to organotypic hippocampal Brain Slice cultures
    Brain Research, 2001
    Co-Authors: Bjarne Winther Kristensen, P. Thiébaud, Jens Noraberg, Milena Koudelka-hep, Jens Zimmer
    Abstract:

    In this study we examined the passive biocompatibility of a three-dimensional microelectrode array (MEA), designed to be coupled to organotypic Brain Slice cultures for multisite recording of electrophysiological signals. Hippocampal (and corticostriatal) Brain Slices from 1-week-old (and newborn) rats were grown for 4-8 weeks on the perforated silicon chips with silicon nitride surfaces and 40 μm sized holes and compared with corresponding tissue Slices grown on conventional semiporous membranes. In terms of preservation of the basic cellular and connective organization, as visualized by Nissl staining, Timm sulphide silver-staining, microtubule-associated protein 2 (MAP2) and glial fibrillary acidic protein (GFAP) immunostaining, the Slice cultures grown on chips did not differ from conventionally grown Slice cultures. Neither were there any signs of astrogliosis or neurodegeneration around the upper recording part of the 47-μm-high platinum-tip electrodes. Slice cultures grown on a separate set of chips with platinum instead of silicon nitride surfaces also displayed normal MAP2 and GFAP immunostaining. The width of the GFAP-rich zone (glia limitans) at the bottom surface of the Slice cultures was the same (∼20 μm) in cultures grown on chips with silicon nitride and platinum surfaces and on conventional insert membranes. The Slice cultures grown on chips maintained a normal, subfield differentiated susceptibility to the glutamate receptor agonist N-methyl-D-aspartate (NMDA) and the neurotoxin trimethyltin (TMT), as demonstrated by the cellular uptake of propidium iodide (PI), which was used as a reproducible and quantifiable marker for neuronal degeneration. We conclude that organotypic Brain Slice cultures can grow on silicon-based three-dimensional microelectrode arrays and develop normally with display of normal subfield differentiated susceptibilities to known excito- and neurotoxins. From this it is anticipated that the set-up, designed for recording of electrophysiological parameters, can be used for long-term studies of defined neuronal networks and provide valuable information on both normal, neurotoxicological and neuropathological conditions. © 2001 Elsevier Science B.V.

  • Biocompatibility of silicon-based arrays of electrodes coupled to organotypic hippocampal Brain Slice cultures.
    Brain Research, 2001
    Co-Authors: Bjarne Winther Kristensen, P. Thiébaud, Jens Noraberg, Milena Koudelka-hep, Jens Zimmer
    Abstract:

    In this study we examined the passive biocompatibility of a three-dimensional microelectrode array (MEA), designed to be coupled to organotypic Brain Slice cultures for multisite recording of electrophysiological signals. Hippocampal (and corticostriatal) Brain Slices from 1-week-old (and newborn) rats were grown for 4-8 weeks on the perforated silicon chips with silicon nitride surfaces and 40 microm sized holes and compared with corresponding tissue Slices grown on conventional semiporous membranes. In terms of preservation of the basic cellular and connective organization, as visualized by Nissl staining, Timm sulphide silver-staining, microtubule-associated protein 2 (MAP2) and glial fibrillary acidic protein (GFAP) immunostaining, the Slice cultures grown on chips did not differ from conventionally grown Slice cultures. Neither were there any signs of astrogliosis or neurodegeneration around the upper recording part of the 47-microm-high platinum-tip electrodes. Slice cultures grown on a separate set of chips with platinum instead of silicon nitride surfaces also displayed normal MAP2 and GFAP immunostaining. The width of the GFAP-rich zone (glia limitans) at the bottom surface of the Slice cultures was the same ( approximately 20 microm) in cultures grown on chips with silicon nitride and platinum surfaces and on conventional insert membranes. The Slice cultures grown on chips maintained a normal, subfield differentiated susceptibility to the glutamate receptor agonist N-methyl-D-aspartate (NMDA) and the neurotoxin trimethyltin (TMT), as demonstrated by the cellular uptake of propidium iodide (PI), which was used as a reproducible and quantifiable marker for neuronal degeneration. We conclude that organotypic Brain Slice cultures can grow on silicon-based three-dimensional microelectrode arrays and develop normally with display of normal subfield differentiated susceptibilities to known excito- and neurotoxins. From this it is anticipated that the set-up, designed for recording of electrophysiological parameters, can be used for long-term studies of defined neuronal networks and provide valuable information on both normal, neurotoxicological and neuropathological conditions.

  • Coupling of organotypic Brain Slice cultures to silicon-based arrays of electrodes.
    Methods, 1999
    Co-Authors: Henrik Jahnsen, Bjarne Winther Kristensen, P. Thiébaud, Jens Noraberg, Birthe Jakobsen, Marco Bove, Sergio Martinoia, Milena Koudelka-hep, Massimo Grattarola, Jens Zimmer
    Abstract:

    Fetal or early postnatal Brain tissue can be cultured in viable and healthy condition for several weeks with development and preservation of the basic cellular and connective organization as so-called organotypic Brain Slice cultures. Here we demonstrate and describe how it is possible to establish such hippocampal rat Brain Slice cultures on biocompatible silicon-based chips with arrays of electrodes with a histological organization comparable to that of conventional Brain Slice cultures grown by the roller drum technique and on semiporous membranes. Intracellular and extracellular recordings from neurons in the Slice cultures show that the electroresponsive properties of the neurons and synaptic circuitry are in accordance with those described for cells in acutely prepared Slices of the adult rat hippocampus. Based on the recordings and the possibilities of stimulating the cultured cells through the electrode arrays it is anticipated that the setup eventually will allow long-term studies of defined neuronal networks and provide valuable information on both normal and neurotoxicological and neuropathological conditions.