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  • 1
    Publikationsdatum: 2010-11-12
    Beschreibung: The central amygdala (CEA), a nucleus predominantly composed of GABAergic inhibitory neurons, is essential for fear conditioning. How the acquisition and expression of conditioned fear are encoded within CEA inhibitory circuits is not understood. Using in vivo electrophysiological, optogenetic and pharmacological approaches in mice, we show that neuronal activity in the lateral subdivision of the central amygdala (CEl) is required for fear acquisition, whereas conditioned fear responses are driven by output neurons in the medial subdivision (CEm). Functional circuit analysis revealed that inhibitory CEA microcircuits are highly organized and that cell-type-specific plasticity of phasic and tonic activity in the CEl to CEm pathway may gate fear expression and regulate fear generalization. Our results define the functional architecture of CEA microcircuits and their role in the acquisition and regulation of conditioned fear behaviour.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ciocchi, Stephane -- Herry, Cyril -- Grenier, Francois -- Wolff, Steffen B E -- Letzkus, Johannes J -- Vlachos, Ioannis -- Ehrlich, Ingrid -- Sprengel, Rolf -- Deisseroth, Karl -- Stadler, Michael B -- Muller, Christian -- Luthi, Andreas -- England -- Nature. 2010 Nov 11;468(7321):277-82. doi: 10.1038/nature09559.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Friedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, 4058 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21068837" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Action Potentials ; Amygdala/anatomy & histology/cytology/*physiology ; Animals ; Conditioning, Classical/*physiology ; Fear/*physiology ; Freezing Reaction, Cataleptic ; Male ; Mice ; Mice, Inbred C57BL ; Neural Inhibition/*physiology ; Neural Pathways/cytology/*physiology ; Neuronal Plasticity/physiology ; Neurons/physiology ; gamma-Aminobutyric Acid/metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
    Publikationsdatum: 2008-07-11
    Beschreibung: Switching between exploratory and defensive behaviour is fundamental to survival of many animals, but how this transition is achieved by specific neuronal circuits is not known. Here, using the converse behavioural states of fear extinction and its context-dependent renewal as a model in mice, we show that bi-directional transitions between states of high and low fear are triggered by a rapid switch in the balance of activity between two distinct populations of basal amygdala neurons. These two populations are integrated into discrete neuronal circuits differentially connected with the hippocampus and the medial prefrontal cortex. Targeted and reversible neuronal inactivation of the basal amygdala prevents behavioural changes without affecting memory or expression of behaviour. Our findings indicate that switching between distinct behavioural states can be triggered by selective activation of specific neuronal circuits integrating sensory and contextual information. These observations provide a new framework for understanding context-dependent changes of fear behaviour.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Herry, Cyril -- Ciocchi, Stephane -- Senn, Verena -- Demmou, Lynda -- Muller, Christian -- Luthi, Andreas -- England -- Nature. 2008 Jul 31;454(7204):600-6. doi: 10.1038/nature07166. Epub 2008 Jul 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Friedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, CH-4058 Basel, Switzerland. cyril.herry@fmi.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18615015" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amygdala/cytology/physiology ; Animals ; Conditioning (Psychology) ; Extinction, Psychological ; Fear/*physiology ; Freezing Reaction, Cataleptic/drug effects/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Models, Animal ; Muscimol/pharmacology ; Neural Pathways ; Neurons/classification/*physiology
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 3
    Publikationsdatum: 2010-11-12
    Beschreibung: The role of different amygdala nuclei (neuroanatomical subdivisions) in processing Pavlovian conditioned fear has been studied extensively, but the function of the heterogeneous neuronal subtypes within these nuclei remains poorly understood. Here we use molecular genetic approaches to map the functional connectivity of a subpopulation of GABA-containing neurons, located in the lateral subdivision of the central amygdala (CEl), which express protein kinase C-delta (PKC-delta). Channelrhodopsin-2-assisted circuit mapping in amygdala slices and cell-specific viral tracing indicate that PKC-delta(+) neurons inhibit output neurons in the medial central amygdala (CEm), and also make reciprocal inhibitory synapses with PKC-delta(-) neurons in CEl. Electrical silencing of PKC-delta(+) neurons in vivo suggests that they correspond to physiologically identified units that are inhibited by the conditioned stimulus, called CEl(off) units. This correspondence, together with behavioural data, defines an inhibitory microcircuit in CEl that gates CEm output to control the level of conditioned freezing.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3597095/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3597095/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haubensak, Wulf -- Kunwar, Prabhat S -- Cai, Haijiang -- Ciocchi, Stephane -- Wall, Nicholas R -- Ponnusamy, Ravikumar -- Biag, Jonathan -- Dong, Hong-Wei -- Deisseroth, Karl -- Callaway, Edward M -- Fanselow, Michael S -- Luthi, Andreas -- Anderson, David J -- 1 R01 MH085082-01A1/MH/NIMH NIH HHS/ -- R01 MH063912/MH/NIMH NIH HHS/ -- R01 MH063912-09/MH/NIMH NIH HHS/ -- R01 MH063912-09S1/MH/NIMH NIH HHS/ -- R01 MH063912-10/MH/NIMH NIH HHS/ -- R01 MH085082/MH/NIMH NIH HHS/ -- R01 MH085082-01A1/MH/NIMH NIH HHS/ -- RC2 NS069464/NS/NINDS NIH HHS/ -- RC2 NS069464-01/NS/NINDS NIH HHS/ -- RC2 NS069464-02/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Nov 11;468(7321):270-6. doi: 10.1038/nature09553.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology 216-76, California Institute of Technology, Pasadena, California 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21068836" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amygdala/anatomy & histology/cytology/enzymology/*physiology ; Animals ; Axonal Transport ; Cells, Cultured ; Conditioning, Classical/*physiology ; Fear/*physiology ; Female ; Freezing Reaction, Cataleptic ; Genetic Techniques ; Humans ; Male ; Mice ; Mice, Transgenic ; Neural Inhibition/*physiology ; Neural Pathways/cytology/enzymology/*physiology ; Neurons/enzymology/metabolism ; Protein Kinase C-delta/deficiency/genetics/metabolism ; Synapses/metabolism ; gamma-Aminobutyric Acid/metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
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