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  1. Article ; Online: Observational fear behavior in rodents as a model for empathy.

    Kim, Arie / Keum, Sehoon / Shin, Hee-Sup

    Genes, brain, and behavior

    2018  Volume 18, Issue 1, Page(s) e12521

    Abstract: Empathy enables social mammals to recognize and share emotion with others and is well-documented in non-human primates. During the past few years, systematic observations have showed that a primal form of empathy also exists in rodents, indicating that ... ...

    Abstract Empathy enables social mammals to recognize and share emotion with others and is well-documented in non-human primates. During the past few years, systematic observations have showed that a primal form of empathy also exists in rodents, indicating that empathy has an evolutionary continuity. Now, using rodents exhibiting emotional empathy, the molecular and cellular study of empathy in animals has begun in earnest. In this article, we will review recent reports that indicate that rodents can share states of fear with others, and will try to highlight new understandings of the neural circuitry, biochemistry and genetics of empathic fear. We hope that the use of rodent models will enhance understanding of the mechanisms of human empathy and provide insights into how to treat social deficits in neuropsychiatric disorders characterized by empathy impairment.
    MeSH term(s) Animals ; Brain/metabolism ; Brain/physiology ; Empathy ; Fear ; Gene-Environment Interaction ; Rodentia ; Social Environment
    Language English
    Publishing date 2018-10-12
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2075819-4
    ISSN 1601-183X ; 1601-1848
    ISSN (online) 1601-183X
    ISSN 1601-1848
    DOI 10.1111/gbb.12521
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: A Missense Variant at the Nrxn3 Locus Enhances Empathy Fear in the Mouse.

    Keum, Sehoon / Kim, Arie / Shin, Jae Jin / Kim, Jong-Hyun / Park, Joomin / Shin, Hee-Sup

    Neuron

    2018  Volume 98, Issue 3, Page(s) 588–601.e5

    Abstract: Empathy is crucial for our emotional experience and social interactions, and its abnormalities manifest in various psychiatric disorders. Observational fear is a useful behavioral paradigm for assessing affective empathy in rodents. However, specific ... ...

    Abstract Empathy is crucial for our emotional experience and social interactions, and its abnormalities manifest in various psychiatric disorders. Observational fear is a useful behavioral paradigm for assessing affective empathy in rodents. However, specific genes that regulate observational fear remain unknown. Here we showed that 129S1/SvImJ mice carrying a unique missense variant in neurexin 3 (Nrxn3) exhibited a profound and selective enhancement in observational fear. Using the CRISPR/Cas9 system, the arginine-to-tryptophan (R498W) change in Nrxn3 was confirmed to be the causative variant. Selective deletion of Nrxn3 in somatostatin-expressing (SST+) interneurons in the anterior cingulate cortex (ACC) markedly increased observational fear and impaired inhibitory synaptic transmission from SST+ neurons. Concordantly, optogenetic manipulation revealed that SST+ neurons in the ACC bidirectionally controlled the degree of socially transmitted fear. Together, these results provide insights into the genetic basis of behavioral variability and the neurophysiological mechanism controlling empathy in mammalian brains.
    MeSH term(s) Animals ; Empathy/physiology ; Fear/physiology ; Fear/psychology ; Genetic Loci/physiology ; Genetic Variation/physiology ; Male ; Mice ; Mice, 129 Strain ; Mice, Inbred ICR ; Mutation, Missense/physiology ; Nerve Tissue Proteins/genetics ; Species Specificity
    Chemical Substances Nerve Tissue Proteins ; neurexin 3, mouse
    Language English
    Publishing date 2018-04-19
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 808167-0
    ISSN 1097-4199 ; 0896-6273
    ISSN (online) 1097-4199
    ISSN 0896-6273
    DOI 10.1016/j.neuron.2018.03.041
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Opto-vTrap, an optogenetic trap for reversible inhibition of vesicular release, synaptic transmission, and behavior.

    Won, Joungha / Pankratov, Yuriy / Jang, Minwoo Wendy / Kim, Sunpil / Ju, Yeon Ha / Lee, Sangkyu / Lee, Seung Eun / Kim, Arie / Park, Soowon / Lee, C Justin / Heo, Won Do

    Neuron

    2021  Volume 110, Issue 3, Page(s) 423–435.e4

    Abstract: Spatiotemporal control of brain activity by optogenetics has emerged as an essential tool to study brain function. For silencing brain activity, optogenetic probes, such as halorhodopsin and archaerhodopsin, inhibit transmitter release indirectly by ... ...

    Abstract Spatiotemporal control of brain activity by optogenetics has emerged as an essential tool to study brain function. For silencing brain activity, optogenetic probes, such as halorhodopsin and archaerhodopsin, inhibit transmitter release indirectly by hyperpolarizing membrane potentials. However, these probes cause an undesirable ionic imbalance and rebound spikes. Moreover, they are not applicable to use in non-excitable glial cells. Here we engineered Opto-vTrap, a light-inducible and reversible inhibition system to temporarily trap the transmitter-containing vesicles from exocytotic release. Light activation of Opto-vTrap caused full vesicle clusterization and complete inhibition of exocytosis within 1 min, which recovered within 30 min after light off. We found a significant reduction in synaptic and gliotransmission upon activation of Opto-vTrap in acute brain slices. Opto-vTrap significantly inhibited hippocampus-dependent memory retrieval with full recovery within an hour. We propose Opto-vTrap as a next-generation optogenetic silencer to control brain activity and behavior with minimal confounding effects.
    MeSH term(s) Brain ; Exocytosis ; Hippocampus ; Optogenetics ; Synaptic Transmission/physiology
    Language English
    Publishing date 2021-11-30
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 808167-0
    ISSN 1097-4199 ; 0896-6273
    ISSN (online) 1097-4199
    ISSN 0896-6273
    DOI 10.1016/j.neuron.2021.11.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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