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  • 1
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    Prior alcohol use enhances vulnerability to compulsive cocaine self-administration by promoting degradation of HDAC4 and HDAC5 (2017)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2017-11-02
    Description: Addiction to cocaine is commonly preceded by experiences with legal or decriminalized drugs, such as alcohol, nicotine, and marijuana. The biological mechanisms by which these gateway drugs contribute to cocaine addiction are only beginning to be understood. We report that in the rat, prior alcohol consumption results in enhanced addiction-like behavior to cocaine, including continued cocaine use despite aversive consequences. Conversely, prior cocaine use has no effect on alcohol preference. Long-term, but not short-term, alcohol consumption promotes proteasome-mediated degradation of the nuclear histone deacetylases HDAC4 and HDAC5 in the nucleus accumbens, a brain region critical for reward-based memory. Decreased nuclear HDAC activity results in global H3 acetylation, creating a permissive environment for cocaine-induced gene expression. We also find that selective degradation of HDAC4 and HDAC5, facilitated by the class II–specific HDAC inhibitor MC1568, enhances compulsive cocaine self-administration. These results parallel our previously reported findings that the gateway drug nicotine enhances the behavioral effects of cocaine via HDAC inhibition. Together, our findings suggest a shared mechanism of action for the gateway drugs alcohol and nicotine, and reveal a novel mechanism by which environmental factors may alter the epigenetic landscape of the reward system to increase vulnerability to cocaine addiction.
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Heading direction with respect to a reference point modulates place-cell activity (2019)
    Springer Nature
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    Publication Date: 2019
    Electronic ISSN: 2041-1723
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General , Physics
    Published by Springer Nature
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  • 3
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    Memory suppressor genes: inhibitory constraints on the storage of long-term memory (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-07
    Description: Synaptic plasticity, the ability of neurons to alter the strength of their synaptic connections with activity and experience, is thought to play a critical role in memory storage. Molecular studies of gene expression during long-lasting synaptic plasticity related to memory storage initially focused on the identification of positive regulators. More recent work has revealed that the establishment of long-lasting synaptic plasticity and long-term memory also requires the removal of inhibitory constraints. By analogy to tumor suppressor genes, which restrain cell proliferation, we propose that these inhibitory constraints of memory storage, which restrain synapse growth, be termed memory suppressor genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abel, T -- Martin, K C -- Bartsch, D -- Kandel, E R -- New York, N.Y. -- Science. 1998 Jan 16;279(5349):338-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Center for Neurobiology and Behavior, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9454331" target="_blank"〉PubMed〈/a〉
    Keywords: Activating Transcription Factor 2 ; Animals ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Adhesion Molecules/physiology ; Cyclic AMP Response Element-Binding Protein/physiology ; Cyclic AMP-Dependent Protein Kinases/metabolism ; *Genes ; Memory/*physiology ; *Nerve Tissue Proteins ; Neuronal Plasticity/*genetics ; *Repressor Proteins ; Synapses/*physiology ; Transcription Factors/physiology ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Neuroscience: breaking down scientific barriers to the study of brain and mind (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-02-24
    Description: In this month's essay, Eric R. Kandel and Larry R. Squire chronicle how brain research has migrated from the peripheries of biology and psychology to assume a central position within those disciplines. The multidiscipline of neuroscience that emerged from this process now ranges from genes to cognition, from molecules to minds.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kandel, E R -- Squire, L R -- New York, N.Y. -- Science. 2000 Nov 10;290(5494):1113-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Columbia University, New York, NY, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11185010" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/growth & development ; Cognition ; History, 17th Century ; History, 18th Century ; History, 19th Century ; History, 20th Century ; History, Ancient ; Humans ; Memory ; Mental Disorders/history ; Molecular Biology/history ; Nervous System Diseases/history ; *Nervous System Physiological Phenomena ; Neurosciences/*history ; Psychology/history ; 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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  • 5
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    The molecular biology of memory storage: a dialogue between genes and synapses (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-11-03
    Description: One of the most remarkable aspects of an animal's behavior is the ability to modify that behavior by learning, an ability that reaches its highest form in human beings. For me, learning and memory have proven to be endlessly fascinating mental processes because they address one of the fundamental features of human activity: our ability to acquire new ideas from experience and to retain these ideas over time in memory. Moreover, unlike other mental processes such as thought, language, and consciousness, learning seemed from the outset to be readily accessible to cellular and molecular analysis. I, therefore, have been curious to know: What changes in the brain when we learn? And, once something is learned, how is that information retained in the brain? I have tried to address these questions through a reductionist approach that would allow me to investigate elementary forms of learning and memory at a cellular molecular level-as specific molecular activities within identified nerve cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kandel, E R -- New York, N.Y. -- Science. 2001 Nov 2;294(5544):1030-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Center for Neurobiology and Behavior, College of Physicians and Surgeons of Columbia University, New York State Psychiatric Institute, 1051 Riverside Drive, New York, NY 10032, USA. erk5@columbia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11691980" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aplysia/physiology ; *Gene Expression Regulation ; Hippocampus/*physiology ; Learning/physiology ; Long-Term Potentiation ; Memory/*physiology ; Neural Pathways/physiology ; Neurons/*physiology ; Neurons, Afferent/physiology ; Neurotransmitter Agents/metabolism ; Second Messenger Systems/physiology ; Signal Transduction ; Synapses/*physiology ; Synaptic Transmission ; Transcription, Genetic
    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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    Rapid increase in clusters of presynaptic proteins at onset of long-lasting potentiation (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-10-20
    Description: A change in the efficiency of synaptic communication between neurons is thought to underlie learning. Consistent with recent studies of such changes, we find that long-lasting potentiation of synaptic transmission between cultured hippocampal neurons is accompanied by an increase in the number of clusters of postsynaptic glutamate receptors containing the subunit GluR1. In addition, potentiation is accompanied by a rapid and long-lasting increase in the number of clusters of the presynaptic protein synaptophysin and the number of sites at which synaptophysin and GluR1 are colocalized. These results suggest that potentiation involves rapid coordinate changes in the distribution of proteins in the presynaptic neuron as well as the postsynaptic neuron.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Antonova, I -- Arancio, O -- Trillat, A C -- Wang, H G -- Zablow, L -- Udo, H -- Kandel, E R -- Hawkins, R D -- MH26212/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2001 Nov 16;294(5546):1547-50. Epub 2001 Oct 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurobiology and Behavior, College of Physicians and Surgeons, Columbia University, Howard Hughes Medical Institute, New York State Psychiatric Institute, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11641465" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/physiology ; Animals ; Anisomycin/pharmacology ; Cells, Cultured ; Cytochalasin D/pharmacology ; Excitatory Postsynaptic Potentials ; Glutamic Acid/metabolism/pharmacology ; Hippocampus/*cytology/physiology ; Immunohistochemistry ; *Long-Term Potentiation ; Nerve Tissue Proteins/metabolism ; Neurons/metabolism/*physiology ; Protein Synthesis Inhibitors/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/*metabolism ; Recombinant Fusion Proteins/metabolism ; Synapses/*metabolism ; *Synaptic Transmission ; Synaptophysin/genetics/*metabolism ; Transfection
    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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  • 7
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    cAMP evokes long-term facilitation in Aplysia sensory neurons that requires new protein synthesis (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-06-17
    Description: Behavioral sensitization leads to both short- and long-term enhancement of synaptic transmission between the sensory and motor neurons of the gill-withdrawal reflex in Aplysia. Serotonin (5-HT), a transmitter important for short-term sensitization, can evoke long-term enhancement of synaptic strength detected 1 day later. Because 5-HT mediates short-term facilitation through adenosine 3',5'-monophosphate (cAMP)-dependent protein phosphorylation, the role of cAMP in the long-term modulation of this identified synapse was examined. Like 5-HT, cAMP can also evoke long-term facilitation lasting 24 hours. Unlike the short-term change, the long-lasting change is blocked by anisomycin, a reversible inhibitor of protein synthesis, and therefore must involve the synthesis of gene products not required for the short-term change.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schacher, S -- Castellucci, V F -- Kandel, E R -- GM 32099/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 17;240(4859):1667-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurobiology and Behavior, Howard Hughes Medical Institute, College of Physicians and Surgeons of Columbia University, New York State Psychiatric Institute, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2454509" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-3-isobutylxanthine/pharmacology ; Animals ; Anisomycin/pharmacology ; Aplysia/*physiology ; Cells, Cultured ; Cyclic AMP/analogs & derivatives/*pharmacology ; Evoked Potentials/drug effects ; Motor Neurons/physiology ; Neurons, Afferent/drug effects/*physiology ; *Protein Biosynthesis ; Serotonin/pharmacology ; Synapses/drug effects/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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  • 8
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    Involvement of pre- and postsynaptic mechanisms in posttetanic potentiation at Aplysia synapses (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-02-14
    Description: Posttetanic potentiation (PTP) is a common form of short-term synaptic plasticity that is generally thought to be entirely presynaptic. Consistent with that idea, PTP of evoked excitatory postsynaptic potentials at Aplysia sensory-motor neuron synapses in cell culture was reduced by presynaptic injection of a slow calcium chelator and was accompanied by an increase in the frequency but not the amplitude of spontaneous excitatory postsynaptic potentials. However, PTP was also reduced by postsynaptic injection of a rapid calcium chelator or postsynaptic hyperpolarization. Thus, PTP at these synapses is likely to involve a postsynaptic induction mechanism in addition to the known presynaptic mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bao, J X -- Kandel, E R -- Hawkins, R D -- MH 26212/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1997 Feb 14;275(5302):969-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurobiology and Behavior, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9020078" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Octanol ; Action Potentials ; Animals ; Aplysia ; Calcium/physiology ; Cells, Cultured ; Chelating Agents/pharmacology ; Egtazic Acid/analogs & derivatives/pharmacology ; Long-Term Potentiation ; Motor Neurons/*physiology ; *Neuronal Plasticity ; Neurons, Afferent/*physiology ; Octanols/pharmacology ; Serotonin/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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  • 9
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    Contributions of two types of calcium channels to synaptic transmission and plasticity (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-23
    Description: In Aplysia sensory and motor neurons in culture, the contributions of the major classes of calcium current can be selectively examined while transmitter release and its modulation are examined. A slowly inactivating, dihydropyridine-sensitive calcium current does not contribute either to normal synaptic transmission or to any of three different forms of plasticity: presynaptic inhibition, homosynaptic depression, and presynaptic facilitation. This current does contribute, however, to a fourth form of plasticity--modulation of transmitter release by tonic depolarization of the sensory neuron. By contrast, a second calcium current, which is rapidly inactivating and dihydropyridine-insensitive, contributes to release elicited by the transient depolarization of an action potential and to the other three forms of plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Edmonds, B -- Klein, M -- Dale, N -- Kandel, E R -- New York, N.Y. -- Science. 1990 Nov 23;250(4984):1142-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University College of London, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2174573" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Aplysia/*physiology ; Cadmium/pharmacology ; Calcium Channels/drug effects/*physiology ; Cells, Cultured ; Dihydropyridines/antagonists & inhibitors/pharmacology ; Electric Conductivity ; FMRFamide ; Motor Neurons/physiology ; Neuronal Plasticity/*physiology ; Neurons, Afferent/physiology ; Neuropeptides/pharmacology ; Nifedipine/pharmacology ; Serotonin/pharmacology ; 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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  • 10
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    Impaired long-term potentiation, spatial learning, and hippocampal development in fyn mutant mice (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-12-18
    Description: Mice with mutations in four nonreceptor tyrosine kinase genes, fyn, src, yes, and abl, were used to study the role of these kinases in long-term potentiation (LTP) and in the relation of LTP to spatial learning and memory. All four kinases were expressed in the hippocampus. Mutations in src, yes, and abl did not interfere with either the induction or the maintenance of LTP. However, in fyn mutants, LTP was blunted even though synaptic transmission and two short-term forms of synaptic plasticity, paired-pulse facilitation and post-tetanic potentiation, were normal. In parallel with the blunting of LTP, fyn mutants showed impaired spatial learning, consistent with a functional link between LTP and learning. Although fyn is expressed at mature synapses, its lack of expression during development resulted in an increased number of granule cells in the dentate gyrus and of pyramidal cells in the CA3 region. Thus, a common tyrosine kinase pathway may regulate the growth of neurons in the developing hippocampus and the strength of synaptic plasticity in the mature hippocampus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grant, S G -- O'Dell, T J -- Karl, K A -- Stein, P L -- Soriano, P -- Kandel, E R -- AG08702/AG/NIA NIH HHS/ -- HD24875/HD/NICHD NIH HHS/ -- MH45923/MH/NIMH NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 Dec 18;258(5090):1903-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurobiology and Behavior, Howard Hughes Medical Institute, College of Physicians and Surgeons, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1361685" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; Acetylcholinesterase/analysis ; Animals ; Brain/cytology/*physiology ; Cerebral Cortex/cytology/physiology ; Electric Stimulation ; Genes, abl ; Genes, src ; Hippocampus/drug effects/growth & development/*physiology ; In Vitro Techniques ; *Learning ; Mice ; Mice, Neurologic Mutants ; Neurons/drug effects/*physiology ; Protein-Tyrosine Kinases/*genetics/metabolism ; Proto-Oncogene Proteins/*genetics/metabolism ; Proto-Oncogene Proteins c-fyn ; Proto-Oncogene Proteins c-yes ; Pyramidal Tracts/physiology ; Receptors, N-Methyl-D-Aspartate/physiology ; Space Perception ; Synapses/physiology ; *src-Family Kinases
    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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