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STUDIES ON THE MECHANISM OF STIMULATION OF ACTH SECRETION WITH THE AID OF MORPHINE AS A BLOCKING AGENT<sup>1</sup>
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1955
Year
Anesthetic MechanismAnterior PituitaryMolecular PharmacologyAdrenal GlandPituitary GlandNeuroendocrine MechanismHypothalamic PeptidePituitary DiseaseAnesthetic PharmacologyHealth SciencesPsychoactive DrugPituitary FunctionHypothalamusNeuropharmacologyNervous SystemEndocrinologyPharmacologyNeurophysiologyNeuroanatomyPhysiologyNeuroscienceCentral Nervous SystemAnesthesiaMedicine
The rapidity with which the pituitary can release adrenocorticotropic hormone (ACTH) in response to various stimuli (Gray and Munson, 1951; Sydnor and Sayers, 1954) suggests that the nervous system must play a role in regulating pituitary function. The hypothalamus is particularly implicated in this regulatory process. Stimulation of selected hypothalamic centers (de Groot and Harris, 1950; Hume, 1952; Porter, 1953) has been shown to provoke increased secretion of ACTH while lesions in specific areas of the hypothalamus prevent the usual response of the anterior pituitary (Harris, 1951; Hume, 1952; Porter, 1953; Laqueur et al., 1953; McCamm, 1953). Hypothalmic influence is considered to be mediated by release of a neurohormone from the median eminence into the portal blood which carries it to the adenohypophysis (Harris and Jacobsohn, 1952). An alternate method for studying the role of the central nervous system is through the use of depressant drugs. In contrast to electrolytic lesions which indiscriminately destroy vascular as well as nervous tissue,