The Experts below are selected from a list of 60693 Experts worldwide ranked by ideXlab platform
Hilmar Bading - One of the best experts on this subject based on the ideXlab platform.
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requirement for nuclear Calcium Signaling in drosophila long term memory
Science Signaling, 2013Co-Authors: Janmarek Weislogel, Peter C Bengtson, Michaela Muller, Jan N Hortzsch, Martina Bujard, Christoph M Schuster, Hilmar BadingAbstract:Calcium is used throughout evolution as an intracellular signal transducer. In the mammalian central nervous system, Calcium mediates the dialogue between the synapse and the nucleus that is required for transcription-dependent persistent neuronal adaptations. A role for nuclear Calcium Signaling in similar processes in the invertebrate brain has yet to be investigated. Here, we show by in vivo Calcium imaging of adult brain neurons of the fruit fly Drosophila melanogaster , that electrical foot shocks used in olfactory avoidance conditioning evoked transient increases in cytosolic and nuclear Calcium concentrations in neurons. These Calcium signals were detected in Kenyon cells of the flies’ mushroom bodies, which are sites of learning and memory related to smell. Acute blockade of nuclear Calcium Signaling during conditioning selectively and reversibly abolished the formation of long-term olfactory avoidance memory, whereas short-term, middle-term, or anesthesia-resistant olfactory memory remained unaffected. Thus, nuclear Calcium Signaling is required in flies for the progression of memories from labile to transcription-dependent long-lasting forms. These results identify nuclear Calcium as an evolutionarily conserved signal needed in both invertebrate and vertebrate brains for transcription-dependent memory consolidation.
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nuclear Calcium Signaling controls expression of a large gene pool identification of a gene program for acquired neuroprotection induced by synaptic activity
PLOS Genetics, 2009Co-Authors: Shengjia Zhang, Li Lu, Desiree A W Ditzel, Celine Delucingevivier, Patrick Descombes, Hilmar BadingAbstract:Synaptic activity can boost neuroprotection through a mechanism that requires synapse-to-nucleus communication and Calcium signals in the cell nucleus. Here we show that in hippocampal neurons nuclear Calcium is one of the most potent signals in neuronal gene expression. The induction or repression of 185 neuronal activity-regulated genes is dependent upon nuclear Calcium Signaling. The nuclear Calcium-regulated gene pool contains a genomic program that mediates synaptic activity-induced, acquired neuroprotection. The core set of neuroprotective genes consists of 9 principal components, termed Activity-regulated Inhibitor of Death (AID) genes, and includes Atf3, Btg2, GADD45β, GADD45γ, Inhibin β-A, Interferon activated gene 202B, Npas4, Nr4a1, and Serpinb2, which strongly promote survival of cultured hippocampal neurons. Several AID genes provide neuroprotection through a common process that renders mitochondria more resistant to cellular stress and toxic insults. Stereotaxic delivery of AID gene-expressing recombinant adeno-associated viruses to the hippocampus confers protection in vivo against seizure-induced brain damage. Thus, treatments that enhance nuclear Calcium Signaling or supplement AID genes represent novel therapies to combat neurodegenerative conditions and neuronal cell loss caused by synaptic dysfunction, which may be accompanied by a deregulation of Calcium signal initiation and/or propagation to the cell nucleus.
Ilya Bezprozvanny - One of the best experts on this subject based on the ideXlab platform.
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Calcium Signaling and molecular mechanisms underlying neurodegenerative diseases
Cell Calcium, 2017Co-Authors: Ekaterina Pchitskaya, Elena Popugaeva, Ilya BezprozvannyAbstract:Calcium (Ca2+) is a ubiquitous second messenger that regulates various activities in eukaryotic cells. Especially important role Calcium plays in excitable cells. Neurons require extremely precise spatial-temporal control of Calcium-dependent processes because they regulate such vital functions as synaptic plasticity. Recent evidence indicates that neuronal Calcium Signaling is abnormal in many of neurodegenerative disorders such as Alzheimer’s disease (AD), Huntington’s disease (HD) and Parkinson’s disease (PD). These diseases represent a major medical, social, financial and scientific problem, but despite enormous research efforts, they are still incurable and only symptomatic relief drugs are available. Thus, new approaches and targets are needed. This review highlight neuronal Calcium-Signaling abnormalities in these diseases, with particular emphasis on the role of neuronal store-operated Ca2+ entry (SOCE) pathway and its potential relevance as a therapeutic target for treatment of neurodegeneration.
Grazia Paola Nicchia - One of the best experts on this subject based on the ideXlab platform.
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the speed of swelling kinetics modulates cell volume regulation and Calcium Signaling in astrocytes a different point of view on the role of aquaporins
Glia, 2016Co-Authors: Maria Grazia Mola, Angelo Sparaneo, Concetta Domenica Gargano, David C Spray, Maria Svelto, Antonio Frigeri, Eliana Scemes, Grazia Paola NicchiaAbstract:Regulatory volume decrease (RVD) is a process by which cells restore their original volume in response to swelling. In this study, we have focused on the role played by two different Aquaporins (AQPs), Aquaporin-4 (AQP4), and Aquaporin-1 (AQP1), in triggering RVD and in mediating Calcium Signaling in astrocytes under hypotonic stimulus. Using biophysical techniques to measure water flux through the plasma membrane of wild-type (WT) and AQP4 knockout (KO) astrocytes and of an astrocyte cell line (DI TNC1) transfected with AQP4 or AQP1, we here show that AQP-mediated fast swelling kinetics play a key role in triggering and accelerating RVD. Using Calcium imaging, we show that AQP-mediated fast swelling kinetics also significantly increases the amplitude of Calcium transients inhibited by Gadolinium and Ruthenium Red, two inhibitors of the transient receptor potential vanilloid 4 (TRPV4) channels, and prevented by removing extracellular Calcium. Finally, inhibition of TRPV4 or removal of extracellular Calcium does not affect RVD. All together our study provides evidence that (1) AQP influenced swelling kinetics is the main trigger for RVD and in mediating Calcium Signaling after hypotonic stimulus together with TRPV4, and (2) Calcium influx from the extracellular space and/or TRPV4 are not essential for RVD to occur in astrocytes.
Janmarek Weislogel - One of the best experts on this subject based on the ideXlab platform.
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requirement for nuclear Calcium Signaling in drosophila long term memory
Science Signaling, 2013Co-Authors: Janmarek Weislogel, Peter C Bengtson, Michaela Muller, Jan N Hortzsch, Martina Bujard, Christoph M Schuster, Hilmar BadingAbstract:Calcium is used throughout evolution as an intracellular signal transducer. In the mammalian central nervous system, Calcium mediates the dialogue between the synapse and the nucleus that is required for transcription-dependent persistent neuronal adaptations. A role for nuclear Calcium Signaling in similar processes in the invertebrate brain has yet to be investigated. Here, we show by in vivo Calcium imaging of adult brain neurons of the fruit fly Drosophila melanogaster , that electrical foot shocks used in olfactory avoidance conditioning evoked transient increases in cytosolic and nuclear Calcium concentrations in neurons. These Calcium signals were detected in Kenyon cells of the flies’ mushroom bodies, which are sites of learning and memory related to smell. Acute blockade of nuclear Calcium Signaling during conditioning selectively and reversibly abolished the formation of long-term olfactory avoidance memory, whereas short-term, middle-term, or anesthesia-resistant olfactory memory remained unaffected. Thus, nuclear Calcium Signaling is required in flies for the progression of memories from labile to transcription-dependent long-lasting forms. These results identify nuclear Calcium as an evolutionarily conserved signal needed in both invertebrate and vertebrate brains for transcription-dependent memory consolidation.
David Attwell - One of the best experts on this subject based on the ideXlab platform.
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astrocyte Calcium Signaling the third wave
Nature Neuroscience, 2016Co-Authors: Nooshin Bazargani, David AttwellAbstract:The discovery that transient elevations of Calcium concentration occur in astrocytes, and release 'gliotransmitters' which act on neurons and vascular smooth muscle, led to the idea that astrocytes are powerful regulators of neuronal spiking, synaptic plasticity and brain blood flow. These findings were challenged by a second wave of reports that astrocyte Calcium transients did not mediate functions attributed to gliotransmitters and were too slow to generate blood flow increases. Remarkably, the tide has now turned again: the most important Calcium transients occur in fine astrocyte processes not resolved in earlier studies, and new mechanisms have been discovered by which astrocyte [Ca(2+)]i is raised and exerts its effects. Here we review how this third wave of discoveries has changed our understanding of astrocyte Calcium Signaling and its consequences for neuronal function.
