The Experts below are selected from a list of 195 Experts worldwide ranked by ideXlab platform
Gert Lubec - One of the best experts on this subject based on the ideXlab platform.
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frontal cortex and hippocampus neurotransmitter Receptor complex level parallels spatial memory performance in the radial arm maze
Behavioural Brain Research, 2015Co-Authors: Bharanidharan Shanmugasundaram, Marion Groger, Fernando J Sialana, Harald Höger, Ajinkya Sase, Andras G Miklosi, Saraswathi Subramaniyan, Yogesh D Aher, Keiryn L Bennett, Gert LubecAbstract:Abstract Several neurotransmitter Receptors have been proposed to be involved in memory formation. However, information on Receptor complexes (RCs) in the radial arm maze (RAM) is missing. It was therefore the aim of this study to determine major neurotransmitter RCs levels that are modulated by RAM training because Receptors are known to work in homo-or heteromeric assemblies. Immediate early gene Arc expression was determined by immunohistochemistry to show if prefrontal cortices (PFC) and hippocampi were activated following RAM training as these regions are known to be mainly implicated in spatial memory. Twelve rats per group, trained and untrained in the twelve arm RAM were used, frontal cortices and hippocampi were taken, RCs in membrane protein were quantified by blue-native PAGE immunoblotting. RCs components were characterised by co-immunoprecipitation followed by mass spectrometrical analysis and by the use of the proximity ligation assay. Arc expression was significantly higher in PFC of trained as compared to untrained rats whereas it was comparable in hippocampi. Frontal cortical levels of RCs containing AMPA Receptors GluA1, GluA2, NMDA Receptors GluN1 and GluN2A, Dopamine Receptor D1, acetylcholine nicotinic Receptor alpha 7 (nAChR-α7) and hippocampal levels of RCs containing D1, GluN1, GluN2B and nAChR-α7 were increased in the trained group; phosphorylated Dopamine transporter levels were decreased in the trained group. D1 and GluN1 Receptors were shown to be in the same complex. Taken together, distinct RCs were paralleling performance in the RAM which is relevant for interpretation of previous and design of future work on RCs in memory studies.
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drebrin depletion alters neurotransmitter Receptor levels in protein complexes dendritic spine morphogenesis and memory related synaptic plasticity in the mouse hippocampus
Journal of Neurochemistry, 2015Co-Authors: Gangsoo Jung, Sunetra Sase, Marion Groger, Fernando J Sialana, Ana Cicvaric, Francisco J. Monje, Johannes Berger, Harald Höger, Gert LubecAbstract:Drebrin an actin-bundling key regulator of dendritic spine genesis and morphology, has been recently proposed as a regulator of hippocampal glutamatergic activity which is critical for memory formation and maintenance. Here, we examined the effects of genetic deletion of drebrin on dendritic spine and on the level of complexes containing major brain Receptors. To this end, homozygous and heterozygous drebrin knockout mice generated in our laboratory and related wild-type control animals were studied. Level of protein complexes containing Dopamine Receptor D1/Dopamine Receptor D2, 5-hydroxytryptamine Receptor 1A (5-HT1AR), and 5-hydroxytryptamine Receptor 7 (5-HT7R) were significantly reduced in hippocampus of drebrin knockout mice whereas no significant changes were detected for GluR1, 2, and 3 and NR1 as examined by native gel-based immunoblotting. Drebrin depletion also altered dendritic spine formation, morphology, and reduced levels of Dopamine Receptor D1 in dendritic spines as evaluated using immunohistochemistry/confocal microscopy. Electrophysiological studies further showed significant reduction in memory-related hippocampal synaptic plasticity upon drebrin depletion. These findings provide unprecedented experimental support for a role of drebrin in the regulation of memory-related synaptic plasticity and neurotransmitter Receptor signaling, offer relevant information regarding the interpretation of previous studies and help in the design of future studies on dendritic spines. We examined effect of genetic deletion of drebrin, which an actin-bundling key regulator of dendritic spine genesis and morphology, on dendritic spine density, maturity, level of complexes containing major brain Receptors and also, in synaptic plasticity. These findings support for a role of drebrin in the regulation of memory-related synaptic plasticity and neurotransmitter Receptors signaling in dendritic spines.
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drebrin depletion alters neurotransmitter Receptor levels in protein complexes dendritic spine morphogenesis and memory related synaptic plasticity in the mouse hippocampus
Journal of Neurochemistry, 2015Co-Authors: Gangsoo Jung, Sunetra Sase, Marion Groger, Fernando J Sialana, Ana Cicvaric, Francisco J. Monje, Johannes Berger, Harald Höger, Eun Jung Kim, Gert LubecAbstract:Drebrin an actin-bundling key regulator of dendritic spine genesis and morphology, has been recently proposed as a regulator of hippocampal glutamatergic activity which is critical for memory formation and maintenance. Here, we examined the effects of genetic deletion of drebrin on dendritic spine and on the level of complexes containing major brain Receptors. To this end, homozygous and heterozygous drebrin knockout mice generated in our laboratory and related wild-type control animals were studied. Level of protein complexes containing Dopamine Receptor D1/Dopamine Receptor D2, 5-hydroxytryptamine Receptor 1A (5-HT1(A)R), and 5-hydroxytryptamine Receptor 7 (5-HT7R) were significantly reduced in hippocampus of drebrin knockout mice whereas no significant changes were detected for GluR1, 2, and 3 and NR1 as examined by native gel-based immunoblotting. Drebrin depletion also altered dendritic spine formation, morphology, and reduced levels of Dopamine Receptor D1 in dendritic spines as evaluated using immunohistochemistry/confocal microscopy. Electrophysiological studies further showed significant reduction in memory-related hippocampal synaptic plasticity upon drebrin depletion. These findings provide unprecedented experimental support for a role of drebrin in the regulation of memory-related synaptic plasticity and neurotransmitter Receptor signaling, offer relevant information regarding the interpretation of previous studies and help in the design of future studies on dendritic spines.
Gangsoo Jung - One of the best experts on this subject based on the ideXlab platform.
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drebrin depletion alters neurotransmitter Receptor levels in protein complexes dendritic spine morphogenesis and memory related synaptic plasticity in the mouse hippocampus
Journal of Neurochemistry, 2015Co-Authors: Gangsoo Jung, Sunetra Sase, Marion Groger, Fernando J Sialana, Ana Cicvaric, Francisco J. Monje, Johannes Berger, Harald Höger, Gert LubecAbstract:Drebrin an actin-bundling key regulator of dendritic spine genesis and morphology, has been recently proposed as a regulator of hippocampal glutamatergic activity which is critical for memory formation and maintenance. Here, we examined the effects of genetic deletion of drebrin on dendritic spine and on the level of complexes containing major brain Receptors. To this end, homozygous and heterozygous drebrin knockout mice generated in our laboratory and related wild-type control animals were studied. Level of protein complexes containing Dopamine Receptor D1/Dopamine Receptor D2, 5-hydroxytryptamine Receptor 1A (5-HT1AR), and 5-hydroxytryptamine Receptor 7 (5-HT7R) were significantly reduced in hippocampus of drebrin knockout mice whereas no significant changes were detected for GluR1, 2, and 3 and NR1 as examined by native gel-based immunoblotting. Drebrin depletion also altered dendritic spine formation, morphology, and reduced levels of Dopamine Receptor D1 in dendritic spines as evaluated using immunohistochemistry/confocal microscopy. Electrophysiological studies further showed significant reduction in memory-related hippocampal synaptic plasticity upon drebrin depletion. These findings provide unprecedented experimental support for a role of drebrin in the regulation of memory-related synaptic plasticity and neurotransmitter Receptor signaling, offer relevant information regarding the interpretation of previous studies and help in the design of future studies on dendritic spines. We examined effect of genetic deletion of drebrin, which an actin-bundling key regulator of dendritic spine genesis and morphology, on dendritic spine density, maturity, level of complexes containing major brain Receptors and also, in synaptic plasticity. These findings support for a role of drebrin in the regulation of memory-related synaptic plasticity and neurotransmitter Receptors signaling in dendritic spines.
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drebrin depletion alters neurotransmitter Receptor levels in protein complexes dendritic spine morphogenesis and memory related synaptic plasticity in the mouse hippocampus
Journal of Neurochemistry, 2015Co-Authors: Gangsoo Jung, Sunetra Sase, Marion Groger, Fernando J Sialana, Ana Cicvaric, Francisco J. Monje, Johannes Berger, Harald Höger, Eun Jung Kim, Gert LubecAbstract:Drebrin an actin-bundling key regulator of dendritic spine genesis and morphology, has been recently proposed as a regulator of hippocampal glutamatergic activity which is critical for memory formation and maintenance. Here, we examined the effects of genetic deletion of drebrin on dendritic spine and on the level of complexes containing major brain Receptors. To this end, homozygous and heterozygous drebrin knockout mice generated in our laboratory and related wild-type control animals were studied. Level of protein complexes containing Dopamine Receptor D1/Dopamine Receptor D2, 5-hydroxytryptamine Receptor 1A (5-HT1(A)R), and 5-hydroxytryptamine Receptor 7 (5-HT7R) were significantly reduced in hippocampus of drebrin knockout mice whereas no significant changes were detected for GluR1, 2, and 3 and NR1 as examined by native gel-based immunoblotting. Drebrin depletion also altered dendritic spine formation, morphology, and reduced levels of Dopamine Receptor D1 in dendritic spines as evaluated using immunohistochemistry/confocal microscopy. Electrophysiological studies further showed significant reduction in memory-related hippocampal synaptic plasticity upon drebrin depletion. These findings provide unprecedented experimental support for a role of drebrin in the regulation of memory-related synaptic plasticity and neurotransmitter Receptor signaling, offer relevant information regarding the interpretation of previous studies and help in the design of future studies on dendritic spines.
Harald Höger - One of the best experts on this subject based on the ideXlab platform.
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frontal cortex and hippocampus neurotransmitter Receptor complex level parallels spatial memory performance in the radial arm maze
Behavioural Brain Research, 2015Co-Authors: Bharanidharan Shanmugasundaram, Marion Groger, Fernando J Sialana, Harald Höger, Ajinkya Sase, Andras G Miklosi, Saraswathi Subramaniyan, Yogesh D Aher, Keiryn L Bennett, Gert LubecAbstract:Abstract Several neurotransmitter Receptors have been proposed to be involved in memory formation. However, information on Receptor complexes (RCs) in the radial arm maze (RAM) is missing. It was therefore the aim of this study to determine major neurotransmitter RCs levels that are modulated by RAM training because Receptors are known to work in homo-or heteromeric assemblies. Immediate early gene Arc expression was determined by immunohistochemistry to show if prefrontal cortices (PFC) and hippocampi were activated following RAM training as these regions are known to be mainly implicated in spatial memory. Twelve rats per group, trained and untrained in the twelve arm RAM were used, frontal cortices and hippocampi were taken, RCs in membrane protein were quantified by blue-native PAGE immunoblotting. RCs components were characterised by co-immunoprecipitation followed by mass spectrometrical analysis and by the use of the proximity ligation assay. Arc expression was significantly higher in PFC of trained as compared to untrained rats whereas it was comparable in hippocampi. Frontal cortical levels of RCs containing AMPA Receptors GluA1, GluA2, NMDA Receptors GluN1 and GluN2A, Dopamine Receptor D1, acetylcholine nicotinic Receptor alpha 7 (nAChR-α7) and hippocampal levels of RCs containing D1, GluN1, GluN2B and nAChR-α7 were increased in the trained group; phosphorylated Dopamine transporter levels were decreased in the trained group. D1 and GluN1 Receptors were shown to be in the same complex. Taken together, distinct RCs were paralleling performance in the RAM which is relevant for interpretation of previous and design of future work on RCs in memory studies.
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drebrin depletion alters neurotransmitter Receptor levels in protein complexes dendritic spine morphogenesis and memory related synaptic plasticity in the mouse hippocampus
Journal of Neurochemistry, 2015Co-Authors: Gangsoo Jung, Sunetra Sase, Marion Groger, Fernando J Sialana, Ana Cicvaric, Francisco J. Monje, Johannes Berger, Harald Höger, Gert LubecAbstract:Drebrin an actin-bundling key regulator of dendritic spine genesis and morphology, has been recently proposed as a regulator of hippocampal glutamatergic activity which is critical for memory formation and maintenance. Here, we examined the effects of genetic deletion of drebrin on dendritic spine and on the level of complexes containing major brain Receptors. To this end, homozygous and heterozygous drebrin knockout mice generated in our laboratory and related wild-type control animals were studied. Level of protein complexes containing Dopamine Receptor D1/Dopamine Receptor D2, 5-hydroxytryptamine Receptor 1A (5-HT1AR), and 5-hydroxytryptamine Receptor 7 (5-HT7R) were significantly reduced in hippocampus of drebrin knockout mice whereas no significant changes were detected for GluR1, 2, and 3 and NR1 as examined by native gel-based immunoblotting. Drebrin depletion also altered dendritic spine formation, morphology, and reduced levels of Dopamine Receptor D1 in dendritic spines as evaluated using immunohistochemistry/confocal microscopy. Electrophysiological studies further showed significant reduction in memory-related hippocampal synaptic plasticity upon drebrin depletion. These findings provide unprecedented experimental support for a role of drebrin in the regulation of memory-related synaptic plasticity and neurotransmitter Receptor signaling, offer relevant information regarding the interpretation of previous studies and help in the design of future studies on dendritic spines. We examined effect of genetic deletion of drebrin, which an actin-bundling key regulator of dendritic spine genesis and morphology, on dendritic spine density, maturity, level of complexes containing major brain Receptors and also, in synaptic plasticity. These findings support for a role of drebrin in the regulation of memory-related synaptic plasticity and neurotransmitter Receptors signaling in dendritic spines.
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drebrin depletion alters neurotransmitter Receptor levels in protein complexes dendritic spine morphogenesis and memory related synaptic plasticity in the mouse hippocampus
Journal of Neurochemistry, 2015Co-Authors: Gangsoo Jung, Sunetra Sase, Marion Groger, Fernando J Sialana, Ana Cicvaric, Francisco J. Monje, Johannes Berger, Harald Höger, Eun Jung Kim, Gert LubecAbstract:Drebrin an actin-bundling key regulator of dendritic spine genesis and morphology, has been recently proposed as a regulator of hippocampal glutamatergic activity which is critical for memory formation and maintenance. Here, we examined the effects of genetic deletion of drebrin on dendritic spine and on the level of complexes containing major brain Receptors. To this end, homozygous and heterozygous drebrin knockout mice generated in our laboratory and related wild-type control animals were studied. Level of protein complexes containing Dopamine Receptor D1/Dopamine Receptor D2, 5-hydroxytryptamine Receptor 1A (5-HT1(A)R), and 5-hydroxytryptamine Receptor 7 (5-HT7R) were significantly reduced in hippocampus of drebrin knockout mice whereas no significant changes were detected for GluR1, 2, and 3 and NR1 as examined by native gel-based immunoblotting. Drebrin depletion also altered dendritic spine formation, morphology, and reduced levels of Dopamine Receptor D1 in dendritic spines as evaluated using immunohistochemistry/confocal microscopy. Electrophysiological studies further showed significant reduction in memory-related hippocampal synaptic plasticity upon drebrin depletion. These findings provide unprecedented experimental support for a role of drebrin in the regulation of memory-related synaptic plasticity and neurotransmitter Receptor signaling, offer relevant information regarding the interpretation of previous studies and help in the design of future studies on dendritic spines.
Fernando J Sialana - One of the best experts on this subject based on the ideXlab platform.
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frontal cortex and hippocampus neurotransmitter Receptor complex level parallels spatial memory performance in the radial arm maze
Behavioural Brain Research, 2015Co-Authors: Bharanidharan Shanmugasundaram, Marion Groger, Fernando J Sialana, Harald Höger, Ajinkya Sase, Andras G Miklosi, Saraswathi Subramaniyan, Yogesh D Aher, Keiryn L Bennett, Gert LubecAbstract:Abstract Several neurotransmitter Receptors have been proposed to be involved in memory formation. However, information on Receptor complexes (RCs) in the radial arm maze (RAM) is missing. It was therefore the aim of this study to determine major neurotransmitter RCs levels that are modulated by RAM training because Receptors are known to work in homo-or heteromeric assemblies. Immediate early gene Arc expression was determined by immunohistochemistry to show if prefrontal cortices (PFC) and hippocampi were activated following RAM training as these regions are known to be mainly implicated in spatial memory. Twelve rats per group, trained and untrained in the twelve arm RAM were used, frontal cortices and hippocampi were taken, RCs in membrane protein were quantified by blue-native PAGE immunoblotting. RCs components were characterised by co-immunoprecipitation followed by mass spectrometrical analysis and by the use of the proximity ligation assay. Arc expression was significantly higher in PFC of trained as compared to untrained rats whereas it was comparable in hippocampi. Frontal cortical levels of RCs containing AMPA Receptors GluA1, GluA2, NMDA Receptors GluN1 and GluN2A, Dopamine Receptor D1, acetylcholine nicotinic Receptor alpha 7 (nAChR-α7) and hippocampal levels of RCs containing D1, GluN1, GluN2B and nAChR-α7 were increased in the trained group; phosphorylated Dopamine transporter levels were decreased in the trained group. D1 and GluN1 Receptors were shown to be in the same complex. Taken together, distinct RCs were paralleling performance in the RAM which is relevant for interpretation of previous and design of future work on RCs in memory studies.
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drebrin depletion alters neurotransmitter Receptor levels in protein complexes dendritic spine morphogenesis and memory related synaptic plasticity in the mouse hippocampus
Journal of Neurochemistry, 2015Co-Authors: Gangsoo Jung, Sunetra Sase, Marion Groger, Fernando J Sialana, Ana Cicvaric, Francisco J. Monje, Johannes Berger, Harald Höger, Gert LubecAbstract:Drebrin an actin-bundling key regulator of dendritic spine genesis and morphology, has been recently proposed as a regulator of hippocampal glutamatergic activity which is critical for memory formation and maintenance. Here, we examined the effects of genetic deletion of drebrin on dendritic spine and on the level of complexes containing major brain Receptors. To this end, homozygous and heterozygous drebrin knockout mice generated in our laboratory and related wild-type control animals were studied. Level of protein complexes containing Dopamine Receptor D1/Dopamine Receptor D2, 5-hydroxytryptamine Receptor 1A (5-HT1AR), and 5-hydroxytryptamine Receptor 7 (5-HT7R) were significantly reduced in hippocampus of drebrin knockout mice whereas no significant changes were detected for GluR1, 2, and 3 and NR1 as examined by native gel-based immunoblotting. Drebrin depletion also altered dendritic spine formation, morphology, and reduced levels of Dopamine Receptor D1 in dendritic spines as evaluated using immunohistochemistry/confocal microscopy. Electrophysiological studies further showed significant reduction in memory-related hippocampal synaptic plasticity upon drebrin depletion. These findings provide unprecedented experimental support for a role of drebrin in the regulation of memory-related synaptic plasticity and neurotransmitter Receptor signaling, offer relevant information regarding the interpretation of previous studies and help in the design of future studies on dendritic spines. We examined effect of genetic deletion of drebrin, which an actin-bundling key regulator of dendritic spine genesis and morphology, on dendritic spine density, maturity, level of complexes containing major brain Receptors and also, in synaptic plasticity. These findings support for a role of drebrin in the regulation of memory-related synaptic plasticity and neurotransmitter Receptors signaling in dendritic spines.
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drebrin depletion alters neurotransmitter Receptor levels in protein complexes dendritic spine morphogenesis and memory related synaptic plasticity in the mouse hippocampus
Journal of Neurochemistry, 2015Co-Authors: Gangsoo Jung, Sunetra Sase, Marion Groger, Fernando J Sialana, Ana Cicvaric, Francisco J. Monje, Johannes Berger, Harald Höger, Eun Jung Kim, Gert LubecAbstract:Drebrin an actin-bundling key regulator of dendritic spine genesis and morphology, has been recently proposed as a regulator of hippocampal glutamatergic activity which is critical for memory formation and maintenance. Here, we examined the effects of genetic deletion of drebrin on dendritic spine and on the level of complexes containing major brain Receptors. To this end, homozygous and heterozygous drebrin knockout mice generated in our laboratory and related wild-type control animals were studied. Level of protein complexes containing Dopamine Receptor D1/Dopamine Receptor D2, 5-hydroxytryptamine Receptor 1A (5-HT1(A)R), and 5-hydroxytryptamine Receptor 7 (5-HT7R) were significantly reduced in hippocampus of drebrin knockout mice whereas no significant changes were detected for GluR1, 2, and 3 and NR1 as examined by native gel-based immunoblotting. Drebrin depletion also altered dendritic spine formation, morphology, and reduced levels of Dopamine Receptor D1 in dendritic spines as evaluated using immunohistochemistry/confocal microscopy. Electrophysiological studies further showed significant reduction in memory-related hippocampal synaptic plasticity upon drebrin depletion. These findings provide unprecedented experimental support for a role of drebrin in the regulation of memory-related synaptic plasticity and neurotransmitter Receptor signaling, offer relevant information regarding the interpretation of previous studies and help in the design of future studies on dendritic spines.
Marion Groger - One of the best experts on this subject based on the ideXlab platform.
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frontal cortex and hippocampus neurotransmitter Receptor complex level parallels spatial memory performance in the radial arm maze
Behavioural Brain Research, 2015Co-Authors: Bharanidharan Shanmugasundaram, Marion Groger, Fernando J Sialana, Harald Höger, Ajinkya Sase, Andras G Miklosi, Saraswathi Subramaniyan, Yogesh D Aher, Keiryn L Bennett, Gert LubecAbstract:Abstract Several neurotransmitter Receptors have been proposed to be involved in memory formation. However, information on Receptor complexes (RCs) in the radial arm maze (RAM) is missing. It was therefore the aim of this study to determine major neurotransmitter RCs levels that are modulated by RAM training because Receptors are known to work in homo-or heteromeric assemblies. Immediate early gene Arc expression was determined by immunohistochemistry to show if prefrontal cortices (PFC) and hippocampi were activated following RAM training as these regions are known to be mainly implicated in spatial memory. Twelve rats per group, trained and untrained in the twelve arm RAM were used, frontal cortices and hippocampi were taken, RCs in membrane protein were quantified by blue-native PAGE immunoblotting. RCs components were characterised by co-immunoprecipitation followed by mass spectrometrical analysis and by the use of the proximity ligation assay. Arc expression was significantly higher in PFC of trained as compared to untrained rats whereas it was comparable in hippocampi. Frontal cortical levels of RCs containing AMPA Receptors GluA1, GluA2, NMDA Receptors GluN1 and GluN2A, Dopamine Receptor D1, acetylcholine nicotinic Receptor alpha 7 (nAChR-α7) and hippocampal levels of RCs containing D1, GluN1, GluN2B and nAChR-α7 were increased in the trained group; phosphorylated Dopamine transporter levels were decreased in the trained group. D1 and GluN1 Receptors were shown to be in the same complex. Taken together, distinct RCs were paralleling performance in the RAM which is relevant for interpretation of previous and design of future work on RCs in memory studies.
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drebrin depletion alters neurotransmitter Receptor levels in protein complexes dendritic spine morphogenesis and memory related synaptic plasticity in the mouse hippocampus
Journal of Neurochemistry, 2015Co-Authors: Gangsoo Jung, Sunetra Sase, Marion Groger, Fernando J Sialana, Ana Cicvaric, Francisco J. Monje, Johannes Berger, Harald Höger, Gert LubecAbstract:Drebrin an actin-bundling key regulator of dendritic spine genesis and morphology, has been recently proposed as a regulator of hippocampal glutamatergic activity which is critical for memory formation and maintenance. Here, we examined the effects of genetic deletion of drebrin on dendritic spine and on the level of complexes containing major brain Receptors. To this end, homozygous and heterozygous drebrin knockout mice generated in our laboratory and related wild-type control animals were studied. Level of protein complexes containing Dopamine Receptor D1/Dopamine Receptor D2, 5-hydroxytryptamine Receptor 1A (5-HT1AR), and 5-hydroxytryptamine Receptor 7 (5-HT7R) were significantly reduced in hippocampus of drebrin knockout mice whereas no significant changes were detected for GluR1, 2, and 3 and NR1 as examined by native gel-based immunoblotting. Drebrin depletion also altered dendritic spine formation, morphology, and reduced levels of Dopamine Receptor D1 in dendritic spines as evaluated using immunohistochemistry/confocal microscopy. Electrophysiological studies further showed significant reduction in memory-related hippocampal synaptic plasticity upon drebrin depletion. These findings provide unprecedented experimental support for a role of drebrin in the regulation of memory-related synaptic plasticity and neurotransmitter Receptor signaling, offer relevant information regarding the interpretation of previous studies and help in the design of future studies on dendritic spines. We examined effect of genetic deletion of drebrin, which an actin-bundling key regulator of dendritic spine genesis and morphology, on dendritic spine density, maturity, level of complexes containing major brain Receptors and also, in synaptic plasticity. These findings support for a role of drebrin in the regulation of memory-related synaptic plasticity and neurotransmitter Receptors signaling in dendritic spines.
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drebrin depletion alters neurotransmitter Receptor levels in protein complexes dendritic spine morphogenesis and memory related synaptic plasticity in the mouse hippocampus
Journal of Neurochemistry, 2015Co-Authors: Gangsoo Jung, Sunetra Sase, Marion Groger, Fernando J Sialana, Ana Cicvaric, Francisco J. Monje, Johannes Berger, Harald Höger, Eun Jung Kim, Gert LubecAbstract:Drebrin an actin-bundling key regulator of dendritic spine genesis and morphology, has been recently proposed as a regulator of hippocampal glutamatergic activity which is critical for memory formation and maintenance. Here, we examined the effects of genetic deletion of drebrin on dendritic spine and on the level of complexes containing major brain Receptors. To this end, homozygous and heterozygous drebrin knockout mice generated in our laboratory and related wild-type control animals were studied. Level of protein complexes containing Dopamine Receptor D1/Dopamine Receptor D2, 5-hydroxytryptamine Receptor 1A (5-HT1(A)R), and 5-hydroxytryptamine Receptor 7 (5-HT7R) were significantly reduced in hippocampus of drebrin knockout mice whereas no significant changes were detected for GluR1, 2, and 3 and NR1 as examined by native gel-based immunoblotting. Drebrin depletion also altered dendritic spine formation, morphology, and reduced levels of Dopamine Receptor D1 in dendritic spines as evaluated using immunohistochemistry/confocal microscopy. Electrophysiological studies further showed significant reduction in memory-related hippocampal synaptic plasticity upon drebrin depletion. These findings provide unprecedented experimental support for a role of drebrin in the regulation of memory-related synaptic plasticity and neurotransmitter Receptor signaling, offer relevant information regarding the interpretation of previous studies and help in the design of future studies on dendritic spines.