Role of defective dopaminergic inhibition of prolactin secretion in the pathogenesis of prolactinoma.
Prolactinomas pose an increasingly frequent therapeutic dilemma for the clinician. The neurosurgeon caring for the prolactinoma-bearing patient must stay abreast of the most current basic research concerning the pathogenesis of these often difficult tumors. A fascinating and dynamic line of research involves the possibility that prolactinomas arise secondary to a flaw in the normally inhibitory dopaminergic neurohypophyseal axis. The details of this hypothesis are presented, the current literature surrounding this topic is reviewed, and a brief synthesis of the available theoretical models of prolactinoma pathogenesis is provided.
D001323:Autoantibodies / Q000032:analysis; D002230:Carbidopa; D004298:Dopamine / Q000502:physiology*; D005260:Female; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology*; D007980:Levodopa; D008787:Metoclopramide; D007470:Monoiodotyrosine; D009433:Neural Inhibition; D009627:Nomifensine; D010911:Pituitary Neoplasms / Q000209:etiology / Q000378:metabolism*; D011388:Prolactin / Q000378:metabolism*; D011869:Radioligand Assay; D011954:Receptors, Dopamine / Q000032:analysis / Q000276:immunology
D001323:Autoantibodies; D011954:Receptors, Dopamine; D009627:Nomifensine; D007980:Levodopa; D011388:Prolactin; D007470:Monoiodotyrosine; D008787:Metoclopramide; D002230:Carbidopa; D004298:Dopamine