Effect of pharmacological blockade of ACTH and TSH secretion on the acute stimulation of prolactin release by exposure to cold and ether stress.
Acute exposure of male rats to cold (5C)leads to a rapid increase of plasma levels of thyrotropin (TSH), prolactin (PRL), corticosterone, and L-thyroxine. Exposure to ether is similarly followed by a rapid increase of plasma levels of PRL and corticosterone, while TSH release is inhibited. Acute treatment with dexamethasone (500 mug) inhibits almost completely the PRL response to both exposure to cold and ether stress, while the plasma TSH response to cold is only delayed and the decrease of plasma TSH observed after ether stress is unchanged. Basal plasma levels of both TSH and PRL are lowered after treatment with the steroid. Thyroxine treatment lowers the plasma TSH concentration to undetectable levels without affecting the plasma PRL response to cold or ether exposure. The present data suggest that the rise of plasma PRL observed after cold exposure is not related to TRH and may suggest that common mechanisms control ACTH and PRL secretion during acute stress exposure.
D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000818:Animals; D003080:Cold Temperature; D003907:Dexamethasone / Q000494:pharmacology; D004986:Ether / Q000494:pharmacology*; D005019:Ethyl Ethers / Q000494:pharmacology*; D008297:Male; D011388:Prolactin / Q000378:metabolism*; D051381:Rats; D013312:Stress, Physiological; D013972:Thyrotropin / Q000378:metabolism; D013973:Thyrotropin-Releasing Hormone / Q000502:physiology*; D013974:Thyroxine / Q000097:blood / Q000494:pharmacology; D014284:Triiodothyronine / Q000494:pharmacology
D005019:Ethyl Ethers; D014284:Triiodothyronine; D004986:Ether; D013973:Thyrotropin-Releasing Hormone; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D013972:Thyrotropin; D013974:Thyroxine