Temporal and frontal lobe initiation and regulation of the top-down escalation of anger and aggression

Michael Potegal

Research output: Contribution to journalReview articlepeer-review

50 Scopus citations


The widespread, across-species strategy of stagewise escalation of aggression in agonistic encounters can be understood in terms of resource capture and control with least risk and cost. Human anger likely follows similar principles. As an adaptive phenomenon, escalation may involve particular neural circuitry. To advance beyond a standard view that the frontal lobe tonically inhibits subcortical circuits of aggression, a model is proposed which starts with the general rostrally directed flow of information in the brain. Earlier stage processing of visual and auditory input is transmitted from posterior and middle temporal cortices to anterior temporal lobe where rudimentary appraisals of threat and provocation are developed. These directly but diffusely activate cortical/subcortical anger/aggression response systems. At the same time, the anterior temporal loci transmit the modality-specific perceptual information to orbito-frontal cortex where it is integrated with information about, e.g., the opponent's relative dominance/social status and evaluated for likelihood of potential rewards and punishments associated with different modes of responding and so forth. These frontal areas then impose an inhibitory gating or modulation and focusing of activity initiated by the anterior temporal loci through their projections to GABAergic interneurons in the same cortical/subcortical circuits. Escalation occurs as the inhibition imposed by the frontal areas is progressively lifted. Exploration of the implications, applications and hypotheses flowing from this model will improve our understanding of the biologically important and socially significant phenomena of escalation.

Original languageEnglish (US)
Pages (from-to)386-395
Number of pages10
JournalBehavioural Brain Research
Issue number2
StatePublished - Jun 1 2012

Bibliographical note

Funding Information:
This work was supported by NICHHD grant R01-HD055343 and by a grant from The Netherlands Institute for Advanced Study in the Humanities and Social Sciences (NIAS) to MP.


  • Amygdala
  • GABA
  • Hypothalamus
  • Inhibition


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