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Stress triggers a coordinated physiological response involving the sympathetic nervous system (SNS) and the hypothalamic-pituitary-adrenal (HPA) axis. This dual activation ensures that the body is prepared for both immediate and prolonged stress management. The process begins with the perception of a stressor. This initial phase activates the SNS, leading to the rapid release of adrenaline (epinephrine) from the adrenal glands.
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Cortical-brainstem circuitry attenuates physiological stress reactivity.

Sebastian A Pace1, Ema Lukinic1, Tyler Wallace1

  • 1Department of Biomedical Sciences, Colorado State University, Fort Collins, CO, USA.

The Journal of Physiology
|February 14, 2024
PubMed
Summary

The ventromedial prefrontal cortex (vmPFC) directly influences stress responses by projecting to the rostral ventrolateral medulla (RVLM). This circuit activation reduces stress-induced corticosterone release in both sexes, highlighting a key pathway in stress appraisal and physiological reactivity.

Keywords:
corticosteroneglucoseoptogeneticsprefrontal cortexventrolateral medulla

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Area of Science:

  • Neuroscience
  • Stress Physiology
  • Behavioral Endocrinology

Background:

  • Stressful stimuli trigger multi-system responses to maintain homeostasis.
  • The ventrolateral medulla (VM) is crucial for sympathetic activity and physiological stress adaptation.
  • The ventromedial prefrontal cortex (vmPFC) is implicated in cognitive stress appraisal and physiological responses.

Purpose of the Study:

  • To investigate the direct neural circuit connecting the vmPFC to the rostral ventrolateral medulla (RVLM).
  • To determine the functional role of the vmPFC-RVLM circuit in mediating physiological stress responses.
  • To explore sex differences in the vmPFC-RVLM circuit's influence on stress reactivity.

Main Methods:

  • Utilized genetically encoded anterograde and retrograde tract tracers to map the vmPFC-RVLM connection in male and female rats.
  • Employed optogenetic terminal stimulation to activate vmPFC glutamatergic projections to the RVLM.
  • Assessed the impact of circuit stimulation on glycaemic, corticosterone, and affective behavioral responses during restraint stress.

Main Results:

  • Stress-activated vmPFC neurons project to catecholaminergic neurons in the ventrolateral medulla.
  • vmPFC-RVLM circuit stimulation suppressed glycaemic responses in males and corticosterone responses in both sexes during stress.
  • Circuit stimulation preferentially activated non-catecholaminergic and inhibitory neurons within the RVLM, without altering affective behavior.

Conclusions:

  • A direct vmPFC-RVLM projection exists, modulating endocrine stress responses.
  • This circuit likely reduces stress reactivity by activating local inhibitory neurons in the RVLM.
  • The excitatory/inhibitory balance of vmPFC synapses in the RVLM may be critical for regulating stress outcomes.