The Endocrine System: Glands, Hormones & the Stress Response

The endocrine system is often tested alongside the nervous system — so start by being clear on the key contrast: neural signalling is fast, targeted, and brief; endocrine signalling is slow, diffuse, and sustained. The key concept connecting them is the hypothalamus, which acts as the neuroendocrine interface — converting neural signals into hormonal output.

The most examined content in biopsychology is the stress response. There are two axes to know in depth: - SAM (sympatho-adrenal medullary) axis: the fast arm — sympathetic activation + adrenaline from the adrenal medulla. Peaks in seconds. - HPA (hypothalamic-pituitary-adrenocortical) axis: the slow arm — CRH → ACTH → cortisol. Peaks at 20–30 minutes.

For the major glands, focus on the hypothalamus-pituitary axis as the master regulator, the adrenal glands (cortex and medulla separately), and the pancreas (insulin and glucagon). Know the feedback mechanism: cortisol suppresses both CRH and ACTH via glucocorticoid receptors — and why this fails in chronic stress.

Signalling comparison: hormone · endocrine gland · target cell · receptor · neural vs endocrine signalling · neuroendocrine interface

Major glands: hypothalamus · anterior pituitary · posterior pituitary · thyroid (T3/T4) · adrenal cortex · adrenal medulla · pancreas (insulin/glucagon) · gonads

Stress axes: SAM axis · sympatho-adrenal · fight-or-flight (Cannon, 1932) · adrenaline · noradrenaline · catecholamines · β-receptors · α-receptors

HPA axis · CRH · ACTH · cortisol · glucocorticoid · negative feedback · glucocorticoid receptors (GR) · hippocampus · allostatic overload (McEwen)

Adrenal gland: adrenal cortex · adrenal medulla · zona fasciculata · cortisol · aldosterone · chromaffin cells

Apply to examples: Use the stress response to integrate everything. Seeing a threat → amygdala signals hypothalamus → SAM axis activates within seconds (adrenaline, ↑ heart rate, ↑ blood glucose, bronchodilation) → HPA axis activates over minutes (CRH → ACTH → cortisol, sustained energy mobilisation, immune suppression). Know what each system contributes and why both are needed.

Compare SAM and HPA: SAM is neural + hormonal, peaks in seconds, clears in minutes, uses catecholamines. HPA is purely hormonal, peaks at 20–30 minutes, effects last hours, uses steroid hormones. They're complementary: SAM handles the immediate threat, HPA sustains the response and prepares for recovery.

Compare adrenaline as hormone vs neurotransmitter: Same molecule, same receptors (α/β adrenergic), different pharmacokinetics. As a NT (sympathetic synapses), onset is milliseconds and duration is seconds. As a hormone (adrenal medulla → bloodstream), onset is seconds and effects last minutes.

Critique: The monoamine hypothesis of depression (low serotonin/noradrenaline) is derived from endocrine pharmacology but is now regarded as an oversimplification — SSRIs raise serotonin immediately but antidepressant effects take weeks. Cortisol-depression links are correlational; it's unclear whether HPA dysregulation causes depression or results from it.

The HPA axis and cortisol are central to understanding stress-related disorders — anxiety, PTSD, burnout, and depression. McEwen's concept of allostatic overload explains why chronic stress damages the hippocampus, impairs memory, and increases vulnerability to metabolic and immune disorders. Understanding the negative feedback mechanism explains why the dexamethasone suppression test (a synthetic glucocorticoid test) is used to diagnose HPA dysregulation in depression. Cortisol's role in memory consolidation explains why emotionally significant events are remembered more vividly — and why trauma memories can be so intrusive.

Mixing up the adrenal cortex and medulla: they are anatomically adjacent but functionally and embryologically separate. Cortex = steroid hormones (cortisol, aldosterone) regulated by ACTH. Medulla = catecholamines (adrenaline, noradrenaline) regulated by sympathetic nerves. Getting these confused will lose marks on almost any exam question about stress.

Getting the HPA sequence wrong: the cascade is Stressor → CRH (hypothalamus) → ACTH (anterior pituitary) → cortisol (adrenal cortex). Students often say the pituitary releases CRH, or skip a step.

Describing fight-or-flight as only neural: the SAM response has two components — direct sympathetic innervation (neural, milliseconds) *and* adrenal medulla release of adrenaline into the bloodstream (hormonal, seconds). Both are part of Cannon's fight-or-flight.

Forgetting negative feedback: no description of the HPA axis is complete without explaining that rising cortisol suppresses CRH and ACTH. This is what terminates the acute stress response — and what fails in chronic stress.