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  • 1
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    Mediation of hippocampal mossy fiber long-term potentiation by presynaptic Ih channels (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-01-05
    Description: Hippocampal mossy fiber long-term potentiation (LTP) is expressed presynaptically, but the exact mechanisms remain unknown. Here, we demonstrate the involvement of the hyperpolarization-activated cation channel (Ih) in the expression of mossy fiber LTP. Established LTP was blocked and reversed by Ih channel antagonists. Whole-cell recording from granule cells revealed that repetitive stimulation causes a calcium- and Ih-dependent long-lasting depolarization mediated by protein kinase A. Depolarization at the terminals would be expected to enhance transmitter release, whereas somatic depolarization would enhance the responsiveness of granule cells to afferent input. Thus, Ih channels play an important role in the long-lasting control of transmitter release and neuronal excitability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mellor, Jack -- Nicoll, Roger A -- Schmitz, Dietmar -- New York, N.Y. -- Science. 2002 Jan 4;295(5552):143-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Pharmacology, University of California, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11778053" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/metabolism ; Animals ; Benzazepines/pharmacology ; Calcium/metabolism ; Cesium/pharmacology ; Chlorides/pharmacology ; Colforsin/pharmacology ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors/metabolism ; Cyclic Nucleotide-Gated Cation Channels ; Dentate Gyrus/cytology/drug effects/physiology ; Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels ; In Vitro Techniques ; Ion Channels/antagonists & inhibitors/*physiology ; Isoquinolines/pharmacology ; Long-Term Potentiation/drug effects/*physiology ; Membrane Potentials ; *Membrane Proteins ; Models, Neurological ; Mossy Fibers, Hippocampal/drug effects/*physiology ; *Nerve Tissue Proteins ; Patch-Clamp Techniques ; Potassium/pharmacology ; Potassium Channels ; Presynaptic Terminals/*physiology ; Pyramidal Cells/drug effects/physiology ; Pyrimidines/pharmacology ; Rats ; Rats, Sprague-Dawley ; *Sulfonamides ; Synaptic Transmission
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Postsynaptic membrane fusion and long-term potentiation (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-07
    Description: The possibility that membrane fusion events in the postsynaptic cell may be required for the change in synaptic strength resulting from long-term potentiation (LTP) was examined. Introducing substances into the postsynaptic cell that block membrane fusion at a number of different steps reduced LTP. Introducing SNAP, a protein that promotes membrane fusion, into cells enhanced synaptic transmission, and this enhancement was significantly less when generated in synapses that expressed LTP. Thus, postsynaptic fusion events, which could be involved either in retrograde signaling or in regulating postsynaptic receptor function or both, contribute to LTP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lledo, P M -- Zhang, X -- Sudhof, T C -- Malenka, R C -- Nicoll, R A -- New York, N.Y. -- Science. 1998 Jan 16;279(5349):399-403.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Pharmacology, University of California, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9430593" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Botulinum Toxins/pharmacology ; Carrier Proteins/metabolism/pharmacology ; Ethylmaleimide/pharmacology ; Excitatory Postsynaptic Potentials ; Exocytosis ; Guinea Pigs ; Hippocampus/drug effects/*physiology ; In Vitro Techniques ; *Long-Term Potentiation/drug effects ; *Membrane Fusion ; Membrane Proteins/metabolism/pharmacology ; Molecular Sequence Data ; N-Ethylmaleimide-Sensitive Proteins ; Patch-Clamp Techniques ; Peptides/pharmacology ; Pyramidal Cells/physiology ; Receptors, N-Methyl-D-Aspartate/physiology ; Recombinant Proteins/pharmacology ; Soluble N-Ethylmaleimide-Sensitive Factor Attachment Proteins ; Synaptic Membranes/*physiology ; Synaptic Transmission ; *Vesicular Transport Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Presynaptic kainate receptor mediation of frequency facilitation at hippocampal mossy fiber synapses (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-03-10
    Description: Inhibition of transmitter release by presynaptic receptors is widespread in the central nervous system and is typically mediated via metabotropic receptors. In contrast, very little is known about facilitatory receptors, and synaptic activation of a facilitatory autoreceptor has not been established. Here we show that activation of presynaptic kainate receptors can facilitate transmitter release from hippocampal mossy fiber synapses. Synaptic activation of these presumed ionotropic kainate receptors is very fast (〈10 ms) and lasts for seconds. Thus, these presynaptic kainate receptors contribute to the short-term plasticity characteristics of mossy fiber synapses, which were previously thought to be an intrinsic property of the synapse.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schmitz, D -- Mellor, J -- Nicoll, R A -- New York, N.Y. -- Science. 2001 Mar 9;291(5510):1972-6. Epub 2001 Feb 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Cellular and Molecular Pharmacology and Physiology, University of California, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11239159" target="_blank"〉PubMed〈/a〉
    Keywords: 6-Cyano-7-nitroquinoxaline-2,3-dione/pharmacology ; Animals ; Excitatory Amino Acid Antagonists/pharmacology ; Excitatory Postsynaptic Potentials ; Glutamic Acid/*metabolism ; In Vitro Techniques ; Kainic Acid/pharmacology ; Mossy Fibers, Hippocampal/*physiology ; Neuronal Plasticity ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/drug effects/physiology ; Receptors, Kainic Acid/*physiology ; Receptors, N-Methyl-D-Aspartate/drug effects/physiology ; Synapses/*physiology ; *Synaptic Transmission/drug effects
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Long-term potentiation--a decade of progress? (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-18
    Description: Long-term potentiation of synaptic transmission in the hippocampus is the leading experimental model for the synaptic changes that may underlie learning and memory. This review presents a current understanding of the molecular mechanisms of this long-lasting increase in synaptic strength and describes a simple model that unifies much of the data that previously were viewed as contradictory.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malenka, R C -- Nicoll, R A -- New York, N.Y. -- Science. 1999 Sep 17;285(5435):1870-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nancy Friend Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, CA 94304, USA. malenka@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10489359" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium Signaling ; Hippocampus/*physiology ; Humans ; Long-Term Potentiation/*physiology ; Models, Neurological ; Protein Kinases/metabolism ; Pyramidal Cells/physiology ; Receptors, AMPA/metabolism ; Receptors, N-Methyl-D-Aspartate/physiology ; Synapses/*physiology ; Synaptic Transmission/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Comparison of two forms of long-term potentiation in single hippocampal neurons (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-29
    Description: In invertebrate nervous systems, some long-lasting increases in synaptic efficacy result from changes in the presynaptic cell. In the vertebrate nervous system, the best understood long-lasting change in synaptic strength is long-term potentiation (LTP) in the CA1 region of the hippocampus. Here the process is initiated postsynaptically, but the site of the persistent change is unresolved. Single CA3 hippocampal pyramidal cells receive excitatory inputs from associational-commissural fibers and from the mossy fibers of dentate granule cells and both pathways exhibit LTP. Although the induction of associational-commissural LTP requires in the postsynaptic cell N-methyl-D-aspartate (NMDA) receptor activation, membrane depolarization, and a rise in calcium, mossy fiber LTP does not. Paired-pulse facilitation, which is an index of increased transmitter release, is unaltered during associational-commissural LTP but is reduced during mossy fiber LTP. Thus, both the induction and the persistent change may be presynaptic in mossy fiber LTP but not in associational-commissural LTP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zalutsky, R A -- Nicoll, R A -- MH0437/MH/NIMH NIH HHS/ -- MH38256/MH/NIMH NIH HHS/ -- NS24205/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 29;248(4963):1619-24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Physiology, University of California, San Francisco, CA 94114-0450.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2114039" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Egtazic Acid/pharmacology ; Electric Stimulation ; Evoked Potentials ; Fluorides/pharmacology ; Guinea Pigs ; Hippocampus/*physiology ; In Vitro Techniques ; Membrane Potentials/drug effects ; Microelectrodes ; Neurons/drug effects/*physiology ; Synapses/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Dynamic interaction of stargazin-like TARPs with cycling AMPA receptors at synapses (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-03-06
    Description: Activity-dependent plasticity in the brain arises in part from changes in the number of synaptic AMPA receptors. Synaptic trafficking of AMPA receptors is controlled by stargazin and homologous transmembrane AMPA receptor regulatory proteins (TARPs). We found that TARPs were stable at the plasma membrane, whereas AMPA receptors were internalized in a glutamate-regulated manner. Interaction with AMPA receptors involved both extra- and intracellular determinants of TARPs. Upon binding to glutamate, AMPA receptors detached from TARPs. This did not require ion flux or intracellular second messengers. This allosteric mechanism for AMPA receptor dissociation from TARPs may participate in glutamate-mediated internalization of receptors in synaptic plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tomita, Susumu -- Fukata, Masaki -- Nicoll, Roger A -- Bredt, David S -- New York, N.Y. -- Science. 2004 Mar 5;303(5663):1508-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of California, San Francisco, San Francisco, CA 94143-2140, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15001777" target="_blank"〉PubMed〈/a〉
    Keywords: 6-Cyano-7-nitroquinoxaline-2,3-dione/pharmacology ; Animals ; Calcium Channels/analysis/*metabolism ; Cell Line ; Cells, Cultured ; Cerebral Cortex/chemistry/cytology ; Endocytosis ; Glutamic Acid/metabolism/pharmacology ; Humans ; Neuronal Plasticity ; Protein Binding ; Protein Structure, Tertiary ; Rats ; Receptors, AMPA/agonists/antagonists & inhibitors/*metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Recombinant Fusion Proteins/metabolism ; Synapses/*metabolism ; Xenopus laevis ; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 7
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    Endocannabinoid signaling in the brain (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-04-27
    Description: The primary psychoactive ingredient in cannabis, Delta9-tetrahydrocannabinol (Delta9-THC), affects the brain mainly by activating a specific receptor (CB1). CB1 is expressed at high levels in many brain regions, and several endogenous brain lipids have been identified as CB1 ligands. In contrast to classical neurotransmitters, endogenous cannabinoids can function as retrograde synaptic messengers: They are released from postsynaptic neurons and travel backward across synapses, activating CB1 on presynaptic axons and suppressing neurotransmitter release. Cannabinoids may affect memory, cognition, and pain perception by means of this cellular mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, Rachel I -- Nicoll, Roger A -- New York, N.Y. -- Science. 2002 Apr 26;296(5568):678-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, 139-74, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11976437" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/metabolism ; Brain/*metabolism ; Cannabinoid Receptor Modulators ; Cannabinoids/*metabolism ; Endocannabinoids ; Humans ; Mental Processes ; Mice ; Neurons/*metabolism ; Neurotransmitter Agents/metabolism ; Pain ; Receptors, Cannabinoid ; Receptors, Drug/*metabolism ; *Signal Transduction ; Synapses/*metabolism ; Synaptic Transmission
    Print ISSN: 0036-8075
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  • 8
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    Epilepsy-related ligand/receptor complex LGI1 and ADAM22 regulate synaptic transmission (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-23
    Description: Abnormally synchronized synaptic transmission in the brain causes epilepsy. Most inherited forms of epilepsy result from mutations in ion channels. However, one form of epilepsy, autosomal dominant partial epilepsy with auditory features (ADPEAF), is characterized by mutations in a secreted neuronal protein, LGI1. We show that ADAM22, a transmembrane protein that when mutated itself causes seizure, serves as a receptor for LGI1. LGI1 enhances AMPA receptor-mediated synaptic transmission in hippocampal slices. The mutated form of LGI1 fails to bind to ADAM22. ADAM22 is anchored to the postsynaptic density by cytoskeletal scaffolds containing stargazin. These studies in rat brain indicate possible avenues for understanding human epilepsy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fukata, Yuko -- Adesnik, Hillel -- Iwanaga, Tsuyoshi -- Bredt, David S -- Nicoll, Roger A -- Fukata, Masaki -- New York, N.Y. -- Science. 2006 Sep 22;313(5794):1792-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genomics and Proteomics, National Institute for Longevity Sciences, National Center for Geriatrics and Gerontology, Obu, Aichi 474-8522, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16990550" target="_blank"〉PubMed〈/a〉
    Keywords: ADAM Proteins/chemistry/genetics/*metabolism ; Animals ; Calcium Channels/metabolism ; Cell Line ; Cerebellar Cortex/metabolism ; Cerebral Cortex/metabolism ; Epilepsies, Partial/physiopathology ; Hippocampus/metabolism/*physiology ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Ligands ; Membrane Proteins/metabolism ; Mice ; N-Methylaspartate/metabolism ; Nerve Tissue Proteins/genetics/metabolism ; Protein Binding ; Protein Structure, Tertiary ; Proteins/*metabolism ; Rats ; Receptors, AMPA/*metabolism ; Recombinant Fusion Proteins/metabolism ; Synapses/metabolism ; *Synaptic Transmission ; Transfection ; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid/metabolism
    Print ISSN: 0036-8075
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  • 9
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    Bidirectional control of quantal size by synaptic activity in the hippocampus (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-01
    Description: Analysis of strontium-induced asynchronous release of quanta from stimulated synapses revealed that long-term potentiation and long-term depression in the CA1 region of the mammalian hippocampus are associated with an increase and a decrease, respectively, in quantal size. At a single set of synapses, the increase in quantal size seen with long-term potentiation was completely reversed by depotentiating stimuli. Long-term potentiation and depression are also associated with an increase and decrease, respectively, in the frequency of quantal events, consistent with an all-or-none regulation (up or down) of clusters of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, a change in the release of transmitter, or both.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oliet, S H -- Malenka, R C -- Nicoll, R A -- New York, N.Y. -- Science. 1996 Mar 1;271(5253):1294-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Pharmacology, University of California, San Francisco 94143-0450, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638114" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/pharmacology ; Electric Stimulation ; Evoked Potentials ; Guinea Pigs ; Hippocampus/cytology/*physiology ; In Vitro Techniques ; Long-Term Potentiation/*physiology ; Neuronal Plasticity/*physiology ; Neurons/*physiology ; Patch-Clamp Techniques ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/physiology ; Strontium/pharmacology ; Synapses/*physiology ; *Synaptic Transmission
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Mediation of hippocampal mossy fiber long-term potentiation by cyclic AMP (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-23
    Description: Repetitive activation of hippocampal mossy fibers evokes a long-term potentiation (LTP) of synaptic responses in pyramidal cells in the CA3 region that is independent of N-methyl-D-aspartate receptor activation. Previous results suggest that the site for both the induction and expression of this form of LTP is presynaptic. Experimental elevation of cyclic adenosine 3',5'-monophosphate (cAMP) both mimics and interferes with tetanus-induced mossy fiber LTP, and blockers of the cAMP cascade block mossy fiber LTP. It is proposed that calcium entry into the presynaptic terminal may activate Ca(2+)-calmodulin-sensitive adenylyl cyclase I which, through protein kinase A, causes a persistent enhancement of evoked glutamate release.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weisskopf, M G -- Castillo, P E -- Zalutsky, R A -- Nicoll, R A -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1878-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience Graduate Program, University of California, San Francisco 94143-0450.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7916482" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; *Carbazoles ; Colforsin/pharmacology ; Cyclic AMP/*metabolism ; Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors/metabolism ; Glutamates/metabolism/pharmacology ; Glutamic Acid ; Guinea Pigs ; Hippocampus/*physiology ; In Vitro Techniques ; Indoles/pharmacology ; Isoquinolines/pharmacology ; *Long-Term Potentiation/drug effects ; Models, Biological ; Nerve Fibers/*physiology ; Presynaptic Terminals/metabolism ; Pyramidal Cells/physiology ; Pyrroles/pharmacology ; *Sulfonamides ; Synaptic Transmission/drug effects
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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