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  • 1
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    Cortical 5-HT2A receptor signaling modulates anxiety-like behaviors in mice (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-29
    Description: Serotonin [5-hydroxytryptamine (5-HT)] neurotransmission in the central nervous system modulates depression and anxiety-related behaviors in humans and rodents, but the responsible downstream receptors remain poorly understood. We demonstrate that global disruption of 5-HT2A receptor (5HT2AR) signaling in mice reduces inhibition in conflict anxiety paradigms without affecting fear-conditioned and depression-related behaviors. Selective restoration of 5HT2AR signaling to the cortex normalized conflict anxiety behaviors. These findings indicate a specific role for cortical 5HT2AR function in the modulation of conflict anxiety, consistent with models of cortical, "top-down" influences on risk assessment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weisstaub, Noelia V -- Zhou, Mingming -- Lira, Alena -- Lambe, Evelyn -- Gonzalez-Maeso, Javier -- Hornung, Jean-Pierre -- Sibille, Etienne -- Underwood, Mark -- Itohara, Shigeyoshi -- Dauer, William T -- Ansorge, Mark S -- Morelli, Emanuela -- Mann, J John -- Toth, Miklos -- Aghajanian, George -- Sealfon, Stuart C -- Hen, Rene -- Gingrich, Jay A -- KO8 MH01711/MH/NIMH NIH HHS/ -- P01 DA12923/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2006 Jul 28;313(5786):536-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Columbia University and the 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/16873667" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anxiety/*physiopathology ; Cerebral Cortex/*metabolism ; Conditioning (Psychology) ; Conflict (Psychology) ; Depression/physiopathology ; Exploratory Behavior ; Fear ; Limbic System/metabolism ; Mice ; Mice, Knockout ; Patch-Clamp Techniques ; Periaqueductal Gray/metabolism ; Prosencephalon/metabolism ; Receptor, Serotonin, 5-HT2A/genetics/*metabolism ; Receptor, Serotonin, 5-HT2C/metabolism ; Receptors, Neurotransmitter/metabolism ; Risk-Taking ; Serotonin/physiology ; *Signal Transduction ; 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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  • 2
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    Cells of a common developmental origin regulate REM/non-REM sleep and wakefulness in mice (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-10-24
    Description: Mammalian sleep comprises rapid eye movement (REM) sleep and non-REM (NREM) sleep. To functionally isolate from the complex mixture of neurons populating the brainstem pons those involved in switching between REM and NREM sleep, we chemogenetically manipulated neurons of a specific embryonic cell lineage in mice. We identified excitatory glutamatergic neurons that inhibit REM sleep and promote NREM sleep. These neurons shared a common developmental origin with neurons promoting wakefulness; both derived from a pool of proneural hindbrain cells expressing Atoh1 at embryonic day 10.5. We also identified inhibitory gamma-aminobutyric acid-releasing neurons that act downstream to inhibit REM sleep. Artificial reduction or prolongation of REM sleep in turn affected slow-wave activity during subsequent NREM sleep, implicating REM sleep in the regulation of NREM sleep.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hayashi, Yu -- Kashiwagi, Mitsuaki -- Yasuda, Kosuke -- Ando, Reiko -- Kanuka, Mika -- Sakai, Kazuya -- Itohara, Shigeyoshi -- New York, N.Y. -- Science. 2015 Nov 20;350(6263):957-61. doi: 10.1126/science.aad1023. Epub 2015 Oct 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba, 1-1-1 Tennodai Tsukuba, Ibaraki 305-8575, Japan. Japan Science and Technology Agency (JST), PRESTO, 4-1-8 Honcho Kawaguchi, Saitama 332-0012, Japan. hayashi.yu.fp@u.tsukuba.ac.jp sitohara@brain.riken.jp. ; International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba, 1-1-1 Tennodai Tsukuba, Ibaraki 305-8575, Japan. ; Laboratory for Behavioral Genetics, Brain Science Institute, RIKEN, 2-1 Hirosawa, Wako-city, Saitama 351-0198, Japan. ; Integrative Physiology of the Brain Arousal System, Lyon Neuroscience Research Center, INSERM U1028-CNRS UMR5292, School of Medicine, Claude Bernard University Lyon 1, F-69373 Lyon, France. ; Laboratory for Behavioral Genetics, Brain Science Institute, RIKEN, 2-1 Hirosawa, Wako-city, Saitama 351-0198, Japan. hayashi.yu.fp@u.tsukuba.ac.jp sitohara@brain.riken.jp.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26494173" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism ; Brain Stem/cytology/physiology ; Cell Lineage ; Cell Separation ; Female ; Glutamates/metabolism ; Male ; Mice ; Mice, Transgenic ; Neurons/metabolism/*physiology ; Pons/cytology/physiology ; Rhombencephalon/*cytology/*embryology ; Sleep, REM/*physiology ; Wakefulness/*physiology ; gamma-Aminobutyric Acid
    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)
    Location Call Number Expected Availability
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