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"pageLength" : 9, "publishedYear" : 2004, "abstractText" : "In mammals, the role of a prolactin-releasing factor (PRF) in the acute\nchanges of prolactin (PRL) secretion that usually occur after\nchallenges (e.g., suckling stimulus or stress) of homeostasis has been\nsuspected for a long time. We have recently observed that\n1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, salsolinol\n(SAL), produced by the hypothalamus and the neuro-intermediate lobe\n(NIL) of the pituitary gland, can selectively release PRL from the\nanterior lobe (AL). Moreover, binding sites for SAL have been detected\nin areas like median eminence, NIL, and AL. It has been proposed that\nSAL is a putative endogenous PRF. We have also found that a structural\nanalogue of SAL, 1-methyl-3,4-dihydroisoquinoline (1MeDIQ), is able to\nblock dose-dependently SAL-, suckling-, and immobilization (IMO)\nstress-induced release of PRL without having any influence on\nalpha-methyl-p-tyrosine (alphaMpT)-induced PRL responses. Neither SAL\nnor 1MeDIQ has any effect on alpha-melanocyte-stimulating hormone\n(alphaMSH), adrenocorticotrophic hormone (ACTH), beta-endorphin\n(beta-END) and arginine-vasopressin (AVP) secretion. Moreover,\nSAL-induced PRL response was attenuated in male rats pretreated with\ndexamethasone (DEX). These results strongly suggest that SAL has an\nimportant role in the regulation of PRL release induced by physiologic\nand environmental stimuli; therefore, it can be considered as the\nstrongest candidate for being the PRF in the hypothalamo-hypophysial\nsystem. 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