Abstract
Active responses to stressors involve motor planning, execution, and feedback. Here we identify an insular cortex to BNST (insula→BNST) circuit recruited during restraint stress-induced active struggling that modulates affective behavior. We demonstrate that activity in this circuit tightly follows struggling behavioral events and that the size of the fluorescent sensor transient reports the duration of the struggle event, an effect that fades with repeated exposure to the homotypic stressor. Struggle events are associated with enhanced glutamatergic- and decreased GABAergic signaling in the insular cortex, indicating the involvement of a larger circuit. We delineate the afferent network for this pathway, identifying substantial input from motor- and premotor cortex, somatosensory cortex, and the amygdala. To begin to dissect these incoming signals, we examine the motor cortex input, and show that the cells projecting from motor regions to insular cortex are engaged shortly before struggle event onset. This study thus demonstrates a role for the insula→BNST pathway in monitoring struggling activity and regulating affective behavior.
Highlights
Active responses to stressors involve motor planning, execution, and feedback
Rodents engage in periodic physical struggle events that are thought to underlie active stress coping[11,13]
BNSTCRF and SF-iGluSnFR sensors generated much higher average peak transient amplitudes and area under the curve (AUC) from 0–5 s compared to the eGFP control (Fig. 3l, m). (3) We identified calcium signaling in the insula that was negatively correlated with movement
Summary
We identify an insular cortex to BNST (insula→BNST) circuit recruited during restraint stressinduced active struggling that modulates affective behavior. This study demonstrates a role for the insula→BNST pathway in monitoring struggling activity and regulating affective behavior. The insula shares dense interconnections with stress-related regions, such as the bed nucleus of the stria terminalis (BST, BNST), which plays a major role in modulating the hypothalamic–pituitary–adrenal (HPA) axis and has been implicated in passive stress-coping behavior[7]. We elucidated a mid-insula:BNSTCRF neuronal circuit (insula→BNST) that reports struggling behavior during restraint stress, a potential active coping response, and show this circuit regulates subsequent affective behavior. We uncovered an unexpectedly large input from executive motor cortical regions and demonstrated that activity in these insula-projecting motor cortex neurons is time-locked to and precedes the onset of the restraint stress struggle events and insula→BNST activity
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