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For almost all other anterior pituitary hormones (GH, TSH, ACTH, FSH, LH), the hypothalamus acts mainly through stimulatory releasing hormones. Prolactin is the exception - its secretion is controlled predominantly by a hypothalamic inhibitory hormone, prolactin-inhibitory hormone (PIH), which is now known to be the catecholamine dopamine, secreted by neurons of the arcuate nuclei - Guyton and Hall.

Dopamine is released into the primary capillary plexus in the median eminence and travels down the hypophysial portal blood vessels within the pituitary stalk to reach the anterior pituitary, where it tonically suppresses prolactin secretion by the lactotropes - Guyton and Hall.

When the pituitary stalk is cut, crushed, or compressed (e.g., trauma, surgery, or a sellar mass), the portal vessels carrying dopamine to the lactotropes are disrupted. Because prolactin secretion is normally held in check by continuous dopamine inhibition rather than driven by a releasing hormone, loss of this inhibitory signal causes the lactotropes to secrete prolactin unopposed - resulting in a paradoxical rise in prolactin, even as secretion of the other anterior pituitary hormones (which depend on stimulatory releasing hormones reaching them through the same portal vessels) falls.

Summary reasoning: Stalk transection is disinhibitory for prolactin (because control is inhibitory/dopamine-mediated) but is deficiency-producing for GH, TSH, ACTH, and gonadotropins (because their control is stimulatory/releasing-hormone-mediated) - the same anatomical lesion produces opposite hormonal effects depending on the polarity of hypothalamic control for each hormone.

This is consistent with clinical correlation seen across other texts as well - e.g., pituitary stalk compression by a non-secreting adenoma is a classic cause of mild hyperprolactinemia that can be mistaken for a prolactinoma (Bradley and Daroff's Neurology in Clinical Practice; Goldman-Cecil Medicine).