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Translational models of adaptive and excessive fighting: an emerging role for neural circuits in pathological aggression
Aggression is a phylogenetically stable behavior, and attacks on conspecifics are observed in most animal species. In this review, we discuss translational models as they relate to pathological forms of offensive aggression and the brain mechanisms that underlie these behaviors. Quantifiable escalat...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
F1000 Research Limited
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6593325/ https://www.ncbi.nlm.nih.gov/pubmed/31281636 http://dx.doi.org/10.12688/f1000research.18883.1 |
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author | Covington, Herbert E. Newman, Emily L. Leonard, Michael Z. Miczek, Klaus A. |
author_facet | Covington, Herbert E. Newman, Emily L. Leonard, Michael Z. Miczek, Klaus A. |
author_sort | Covington, Herbert E. |
collection | PubMed |
description | Aggression is a phylogenetically stable behavior, and attacks on conspecifics are observed in most animal species. In this review, we discuss translational models as they relate to pathological forms of offensive aggression and the brain mechanisms that underlie these behaviors. Quantifiable escalations in attack or the development of an atypical sequence of attacks and threats is useful for characterizing abnormal variations in aggression across species. Aggression that serves as a reinforcer can be excessive, and certain schedules of reinforcement that allow aggression rewards also allow for examining brain and behavior during the anticipation of a fight. Ethological attempts to capture and measure offensive aggression point to two prominent hypotheses for the neural basis of violence. First, pathological aggression may be due to an exaggeration of activity in subcortical circuits that mediate adaptive aggressive behaviors as they are triggered by environmental or endogenous cues at vulnerable time points. Indeed, repeated fighting experiences occur with plasticity in brain areas once considered hardwired. Alternatively, a separate “violence network” may converge on aggression circuitry that disinhibits pathological aggression (for example, via disrupted cortical inhibition). Advancing animal models that capture the motivation to commit pathological aggression remains important to fully distinguish the neural architecture of violence as it differs from adaptive competition among conspecifics. |
format | Online Article Text |
id | pubmed-6593325 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | F1000 Research Limited |
record_format | MEDLINE/PubMed |
spelling | pubmed-65933252019-07-05 Translational models of adaptive and excessive fighting: an emerging role for neural circuits in pathological aggression Covington, Herbert E. Newman, Emily L. Leonard, Michael Z. Miczek, Klaus A. F1000Res Review Aggression is a phylogenetically stable behavior, and attacks on conspecifics are observed in most animal species. In this review, we discuss translational models as they relate to pathological forms of offensive aggression and the brain mechanisms that underlie these behaviors. Quantifiable escalations in attack or the development of an atypical sequence of attacks and threats is useful for characterizing abnormal variations in aggression across species. Aggression that serves as a reinforcer can be excessive, and certain schedules of reinforcement that allow aggression rewards also allow for examining brain and behavior during the anticipation of a fight. Ethological attempts to capture and measure offensive aggression point to two prominent hypotheses for the neural basis of violence. First, pathological aggression may be due to an exaggeration of activity in subcortical circuits that mediate adaptive aggressive behaviors as they are triggered by environmental or endogenous cues at vulnerable time points. Indeed, repeated fighting experiences occur with plasticity in brain areas once considered hardwired. Alternatively, a separate “violence network” may converge on aggression circuitry that disinhibits pathological aggression (for example, via disrupted cortical inhibition). Advancing animal models that capture the motivation to commit pathological aggression remains important to fully distinguish the neural architecture of violence as it differs from adaptive competition among conspecifics. F1000 Research Limited 2019-06-25 /pmc/articles/PMC6593325/ /pubmed/31281636 http://dx.doi.org/10.12688/f1000research.18883.1 Text en Copyright: © 2019 Covington III HE et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution Licence, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Covington, Herbert E. Newman, Emily L. Leonard, Michael Z. Miczek, Klaus A. Translational models of adaptive and excessive fighting: an emerging role for neural circuits in pathological aggression |
title | Translational models of adaptive and excessive fighting: an emerging role for neural circuits in pathological aggression |
title_full | Translational models of adaptive and excessive fighting: an emerging role for neural circuits in pathological aggression |
title_fullStr | Translational models of adaptive and excessive fighting: an emerging role for neural circuits in pathological aggression |
title_full_unstemmed | Translational models of adaptive and excessive fighting: an emerging role for neural circuits in pathological aggression |
title_short | Translational models of adaptive and excessive fighting: an emerging role for neural circuits in pathological aggression |
title_sort | translational models of adaptive and excessive fighting: an emerging role for neural circuits in pathological aggression |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6593325/ https://www.ncbi.nlm.nih.gov/pubmed/31281636 http://dx.doi.org/10.12688/f1000research.18883.1 |
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