Effects of cortisol time-scales in a model of emotion regulation
Abstract
Stress reshapes cortico-limbic dynamics across multiple timescales, with important consequences for healthy and pathological arousal responses. We develop and analyze a Wilson-Cowan model of prefrontal-amygdala circuitry, incorporating excitatory and inhibitory populations involved in emotional regulation. The effects of stress cortisol are represented as history-dependent modulations of two stress-sensitive interactions: recurrent prefrontal excitation and inhibition of basolateral amygdala principal cells. Using numerical simulations and bifurcation analysis, we examine how this self-interacting system organizes transitions between stable activity and infra-slow oscillations, and how this structure changes with cortisol-related temporal memory. To distinguish the effects of memory temporal distribution from those of its timescale, we compare weak and strong Gamma kernels with a discrete-delay limit, representing progressively different ways in which past activity can influence current coupling. Introducing temporal memory reshapes the parameter region supporting oscillations and alters their persistence. Weak and strong Gamma kernels produce remarkably similar global dynamics, whereas the discrete-delay limit generates a substantially richer bifurcation structure, including quasiperiodic activity. Together, these results suggest that the dynamical effects of cortisol depend not only on the characteristic timescale of its action, but also on the shape of the temporal memory through which past neural activity influences the present. Different forms of temporal integration may provide a mechanism by which neural systems implement distinct functional dynamics, while changes in this integration could promote atypical or pathological rhythmic regimes.
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BibTeX
@misc{buccino2026effects,
title = {{Effects of cortisol time-scales in a model of emotion regulation}},
author = {Michael Buccino and Joshua Ginart and Eva Kaslik and Anca Radulescu},
howpublished = {arXiv},
year = {2026},
month = oct,
doi = {10.48550/arxiv.2610.19282},
eprint = {2610.19282},
archivePrefix = {arXiv},
url = {https://arxiv.org/abs/2610.19282},
note = {CC BY 4.0},
}
RIS
TY - UNPB
TI - Effects of cortisol time-scales in a model of emotion regulation
AU - Michael Buccino
AU - Joshua Ginart
AU - Eva Kaslik
AU - Anca Radulescu
PY - 2026
DA - 2026/10/13
PB - arXiv
DO - 10.48550/arxiv.2610.19282
UR - https://arxiv.org/abs/2610.19282
AB - Stress reshapes cortico-limbic dynamics across multiple timescales, with important consequences for healthy and pathological arousal responses. We develop and analyze a Wilson-Cowan model of prefrontal-amygdala circuitry, incorporating excitatory and inhibitory populations involved in emotional regulation. The effects of stress cortisol are represented as history-dependent modulations of two stress-sensitive interactions: recurrent prefrontal excitation and inhibition of basolateral amygdala principal cells. Using numerical simulations and bifurcation analysis, we examine how this self-interacting system organizes transitions between stable activity and infra-slow oscillations, and how this structure changes with cortisol-related temporal memory. To distinguish the effects of memory temporal distribution from those of its timescale, we compare weak and strong Gamma kernels with a discrete-delay limit, representing progressively different ways in which past activity can influence current coupling. Introducing temporal memory reshapes the parameter region supporting oscillations and alters their persistence. Weak and strong Gamma kernels produce remarkably similar global dynamics, whereas the discrete-delay limit generates a substantially richer bifurcation structure, including quasiperiodic activity. Together, these results suggest that the dynamical effects of cortisol depend not only on the characteristic timescale of its action, but also on the shape of the temporal memory through which past neural activity influences the present. Different forms of temporal integration may provide a mechanism by which neural systems implement distinct functional dynamics, while changes in this integration could promote atypical or pathological rhythmic regimes.
ER -