CorpusHuman Anatomy
EndocrineBrain region

Supraoptic nucleus

Nucleus supraopticus

Also known as: SON

A paired cluster of large (magnocellular) neurosecretory neurons straddling the optic tract that synthesises mainly antidiuretic hormone (vasopressin) for release from the posterior pituitary.

Show on body map Hypothalamic–Pituitary Axis

Overview

The supraoptic nucleus lies at the base of the anterior hypothalamus, draped over the beginning of the optic tract lateral to the optic chiasm. Its magnocellular neurons synthesise ADH (predominantly) and oxytocin as large precursors (prepropressophysin, prepro-oxyphysin) that are cleaved inside secretory granules into the hormone and its carrier protein, neurophysin II (with ADH) or neurophysin I (with oxytocin).

Their unmyelinated axons form the supraopticohypophyseal (hypothalamo-hypophyseal) tract, which runs down the pituitary stalk to terminate on fenestrated capillaries in the posterior lobe. Firing is driven by osmoreceptor neurons in the OVLT and by the neurons' own intrinsic osmosensitivity: a 1–2 % rise in plasma osmolality increases firing and ADH release. Baroreceptor input (via the nucleus of the solitary tract) increases firing when blood volume falls substantially.

Location

Anterior hypothalamus, above and lateral to the optic chiasm, overlying the optic tract.

Function

  • Synthesises ADH (and some oxytocin) and transports it down axons to the posterior pituitary.
  • Translates plasma osmolality and volume signals into ADH release.
Physiology

Granules travel by fast axonal transport (kinesin on microtubules) and accumulate in axonal swellings (Herring bodies). Action potentials invading the terminals open voltage-gated Ca²⁺ channels and trigger exocytosis; bursts of firing are most efficient at releasing hormone.

Clinical significance

Central diabetes insipidus (AVP deficiency)

Destruction of supraoptic and paraventricular neurons or their axons (surgery, trauma, tumours) causes polyuria of dilute urine; symptoms appear once ≈80–90 % of magnocellular neurons are lost. A low stalk transection may cause only transient DI because axons regenerate and release ADH higher up.

Compiled from standard anatomy and physiology references — see the Endocrine System sources. For education only; not medical advice.