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Suckling induces a GH surge simultaneously to that of prolactin, so we tested whether salsolinol, a dopamine derivative (1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline), participates in the regulatory process of GH secretion in lactating sheep. A series of intracerebroventricular (i.c.v.) infusions of salsolinol, in two doses, was performed in nursing sheep, without suckling, during the fifth week of lactation. In other suckling sheep, we infused i.c.v. a structural analogue of salsolinol – 1-methyl-3,4-dihydroisoqinoline (1-MeDIQ), which is able to antagonize salsolinol’s action. Intracerebroventricular treatment of nursing sheep with a lower dose of salsolinol (total 50 ng) significantly increased plasma GH concentration, as compared with the concentrations noted before the infusion and in nursing controls. A higher dose of salsolinol (total 5 μg) did not affect GH release significantly. Intracerebroventricular treatment with 1-MeDIQ (total 300 μg) significantly reduced basal GH release, not affecting a pattern of GH surge in response to suckling. In conclusion, salsolinol may affect the regulatory process of GH secretion in lactating sheep, but its role seems not to be major.
Salsolinol with its derivatives has been considered as a potential neurotoxin for the dopaminergic system in the human and rat brain. Investigating a sheep model for studies on the action of salsolinol within the central nervous system we examined whether this compound is able to affect the hypothalamic neuroendocrine dopaminergic (NEDA) system during its high seasonal activity, when sheep entered to anestrus under the long day conditions. Therefore, salsolinol was infused into the third ventricle of the brain in combination with the in vivo push-pull perfusion of the mediobasal hypothalamus/median eminence (MBH/ME). The effects of this drug on either perfusate noradrenaline (NA) or plasma prolactin concentration were also studied. The infusion of salsolinol resulted in rapid and permanent diminution in dopamine (DA) release into the extracellular spaces of the MBH/ME up to an undetectable level and in the 57% decrease in DA metabolite 3,4- dihydroxyphenylacetic acid concentration, compared to the control. This effect of salsolinol was accompanied by the significant enhancement of the pituitary prolactin release into circulation. The concentration of other DA metabolite, homovanillic acid, as well as NA in the MBH/ME was not affected. Thus, our results in the anestrous sheep underline the role played by salsolinol as a neuromodulator for the hypothalamic NEDA system and as a signal transmitter for the pituitary prolactin release. We suggest that the hypothalamic NEDA system of anestrous sheep during its high secretory activity may be set as a model for studies on the salsolinol-dopamine relationship.
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