Melanophore stimulating hormone (MSH) release from the vertebrate pars intermedia is under an inhibitory control by the hypothalamus. Catecholamines both inhibit and stimulate MSH release from the isolated frog neurointermediate lobe or rat (and mouse) pituitary. Classical pharmacological methods using specific adrenergic receptor agonists and antagonists reveal that inhibition of MSH release by catecholamines is mediated through either alpha adrenergic receptors and/or dopamine receptors whereas stimulation of MSH release by catecholamines is mediated through beta adrenergic receptors. These results provide the physiological correlate for the morphological evidence of pars intermedia regulation by direct neuronal innervation. Acetylcholine also stimulates MSH release from the frog neurointermediate lobe and this enhanced hormone secretion is mediated through cholinergic receptors (blocked by atrophine, but not by propranolol). The possible interactions of adrenergic and cholinergic receptor mechanisms in the control of MSH release is still to be determined. Neither boiled nor acid-treated hypothalamic extracts inhibit or stimulate MSH release in vitro thus failing to implicate (by these methods) hypothalamic inhibiting or stimulating factors, if present, in the control of MSH release. Our in vitro experiments also fail to support a so-called "auto-feedback" (mass action) regulation of MSH release in either the rat, the frog, or the toad. Numerous similarities between the mechanisms involved in the control of MSH and prolactin release are apparent.
ASJC Scopus subject areas
- Animal Science and Zoology