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  • 1
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    Enhanced and delayed stress-induced alcohol drinking in mice lacking functional CRH1 receptors (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-05-04
    Description: There is a relation between stress and alcohol drinking. We show that the corticotropin-releasing hormone (CRH) system that mediates endocrine and behavioral responses to stress plays a role in the control of long-term alcohol drinking. In mice lacking a functional CRH1 receptor, stress leads to enhanced and progressively increasing alcohol intake. The effect of repeated stress on alcohol drinking behavior appeared with a delay and persisted throughout life. It was associated with an up-regulation of the N-methyl-d-aspartate receptor subunit NR2B. Alterations in the CRH1 receptor gene and adaptional changes in NR2B subunits may constitute a genetic risk factor for stress-induced alcohol drinking and alcoholism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sillaber, Inge -- Rammes, Gerhard -- Zimmermann, Stephan -- Mahal, Beatrice -- Zieglgansberger, Walter -- Wurst, Wolfgang -- Holsboer, Florian -- Spanagel, Rainer -- New York, N.Y. -- Science. 2002 May 3;296(5569):931-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute of Psychiatry, Kraepelinstrasse 2-10, 80804 Munich, Germany. sillaber@mpipsykl.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11988580" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; *Alcohol Drinking ; Alcoholism/*etiology/genetics ; Animals ; Brain/metabolism ; Corticotropin-Releasing Hormone/physiology ; Ethanol/blood ; Female ; Hippocampus/physiology ; In Vitro Techniques ; Male ; Mice ; Mice, Knockout ; Models, Animal ; Mutation ; Receptors, AMPA/metabolism ; Receptors, Corticotropin-Releasing Hormone/*genetics/*physiology ; Receptors, Kainic Acid/metabolism ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Signal Transduction ; Stress, Physiological/physiopathology ; Stress, Psychological/*physiopathology ; Up-Regulation
    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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  • 2
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    Precisely localized LTD in the neocortex revealed by infrared-guided laser stimulation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-03
    Description: In a direct approach to elucidate the origin of long-term depression (LTD), glutamate was applied onto dendrites of neurons in rat neocortical slices. An infrared-guided laser stimulation was used to release glutamate from caged glutamate in the focal spot of an ultraviolet laser. A burst of light flashes caused an LTD-like depression of glutamate receptor responses, which was highly confined to the region of "tetanic" stimulation (〈10 micrometers). A similar depression of glutamate receptor responses was observed during LTD of synaptic transmission. A spatially highly specific postsynaptic mechanism can account for the LTD induced by glutamate release.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dodt, H -- Eder, M -- Frick, A -- Zieglgansberger, W -- New York, N.Y. -- Science. 1999 Oct 1;286(5437):110-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institute of Psychiatry, Kraepelinstrasse 2, 80804 Munich, Germany. dodt@mpipsykl.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10506556" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dizocilpine Maleate/pharmacology ; Electric Stimulation ; Excitatory Amino Acid Antagonists/pharmacology ; Excitatory Postsynaptic Potentials ; Glutamates/pharmacology ; Glutamic Acid/metabolism ; In Vitro Techniques ; Infrared Rays ; Lasers ; Microscopy, Video ; Neocortex/cytology/*physiology ; *Neuronal Plasticity ; Patch-Clamp Techniques ; Photolysis ; Pyramidal Cells/*physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, Glutamate/*metabolism ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/metabolism ; 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
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    CB1 cannabinoid receptors and on-demand defense against excitotoxicity (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-04
    Description: Abnormally high spiking activity can damage neurons. Signaling systems to protect neurons from the consequences of abnormal discharge activity have been postulated. We generated conditional mutant mice that lack expression of the cannabinoid receptor type 1 in principal forebrain neurons but not in adjacent inhibitory interneurons. In mutant mice,the excitotoxin kainic acid (KA) induced excessive seizures in vivo. The threshold to KA-induced neuronal excitation in vitro was severely reduced in hippocampal pyramidal neurons of mutants. KA administration rapidly raised hippocampal levels of anandamide and induced protective mechanisms in wild-type principal hippocampal neurons. These protective mechanisms could not be triggered in mutant mice. The endogenous cannabinoid system thus provides on-demand protection against acute excitotoxicity in central nervous system neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marsicano, Giovanni -- Goodenough, Sharon -- Monory, Krisztina -- Hermann, Heike -- Eder, Matthias -- Cannich, Astrid -- Azad, Shahnaz C -- Cascio, Maria Grazia -- Gutierrez, Silvia Ortega -- van der Stelt, Mario -- Lopez-Rodriguez, Maria Luz -- Casanova, Emilio -- Schutz, Gunther -- Zieglgansberger, Walter -- Di Marzo, Vincenzo -- Behl, Christian -- Lutz, Beat -- New York, N.Y. -- Science. 2003 Oct 3;302(5642):84-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Genetics of Behaviour, Max-Planck-Institute of Psychiatry, Kraepelinstrabetae 2-10, 80804 Munich, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14526074" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arachidonic Acids/*metabolism/pharmacology ; Brain/drug effects/*metabolism ; Brain-Derived Neurotrophic Factor/genetics/metabolism ; Cannabinoids/*metabolism ; Endocannabinoids ; Epilepsy/*metabolism/physiopathology ; Excitatory Amino Acid Agonists/pharmacology ; Excitatory Postsynaptic Potentials ; Furans/pharmacology ; Gene Expression Regulation/drug effects ; Genes, Immediate-Early ; Glutamic Acid/metabolism ; Glycerides/metabolism ; Hippocampus/drug effects/metabolism ; In Vitro Techniques ; Kainic Acid/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Mitogen-Activated Protein Kinases/metabolism ; Mutation ; Neurons/drug effects/*metabolism/physiology ; Neuroprotective Agents/metabolism ; Piperidines/pharmacology ; Polyunsaturated Alkamides ; Prosencephalon/drug effects/metabolism ; Pyrazoles/pharmacology ; Receptors, Cannabinoid ; Receptors, Drug/antagonists & inhibitors/genetics/*metabolism ; Signal Transduction ; gamma-Aminobutyric Acid/metabolism
    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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    Opioid peptides may excite hippocampal pyramidal neurons by inhibiting adjacent inhibitory interneurons (1979)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1979-07-27
    Description: The atypical excitation by opiates and opioid peptides of hippocampal pyramidal cells can be antagonized by iontophoresis of naloxone, the gamma-aminobutyric acid antagonists bicuculline, or magnesium ion. The recurrent inhibition of these cells evoked by transcallosal stimulation of the contralateral hippocampus is blocked by enkephalin but only shortened by acetylcholine. The results suggest that the opioids excite pyramidal neurons indirectly by inhibition of neighboring inhibitory interneurons (probably containing gamma-aminobutyric acid). This mechanism may be pertinent to the electrographic signs of addictive drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zieglgansberger, W -- French, E D -- Siggins, G R -- Bloom, F E -- New York, N.Y. -- Science. 1979 Jul 27;205(4404):415-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/451610" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bicuculline/pharmacology ; Endorphins/*pharmacology ; Enkephalins/*pharmacology ; Hippocampus/drug effects/*physiology ; Magnesium/pharmacology ; Neurons/drug effects/*physiology ; Rats
    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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