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Physiological Foundation of Stress

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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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Related Experiment Video

Updated: Jun 21, 2026

Restraint to Induce Stress in Mice and Rats

Restraint to Induce Stress in Mice and Rats

Published on: December 6, 2024

[Stress: a neurobiological perspective].

¹Sectie Medische Farmacologie van het Leiden/Amsterdam Center for Drug Research, Leids Universitair Medisch Centrum, Leiden. e.kloet@lacdr.leidenuniv.nl

Tijdschrift Voor Psychiatrie

|August 7, 2009

Summary

This summary is machine-generated.

Chronic stress increases psychopathology risk. An imbalance between mineralocorticoid (MR) and glucocorticoid (GR) receptor actions in the brain, influenced by genetics and experience, heightens this vulnerability.

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Area of Science:

Neurobiology
Endocrinology
Psychiatry

Context:

Chronic stress impacts health and resilience.
Excessive or prolonged stress elevates psychopathology risk.
The hypothalamic-pituitary-adrenal (HPA) system is central to stress neurobiology.

Purpose:

Review the literature on the HPA system's role in stress.
Focus on cortisol's action in the brain.
Examine the neurobiological underpinnings of stress-related psychopathology.

Summary:

Cortisol, regulated by mineralocorticoid (MR) and glucocorticoid (GR) receptors in the hippocampus, amygdala, and prefrontal cortex, plays a key role in the stress response.
MR and GR mediate defense, recovery, and memory consolidation during stress.
Imbalances between MR-activating and GR-suppressing pathways increase vulnerability to psychopathology.

Impact:

Understanding MR and GR roles clarifies stress-related disorders.
Identifies potential targets for therapeutic interventions.
Highlights the interplay of genetics and experience in stress coping.