A perfusion system was developed in which isolated median eminences (ME) were stimulated in vitro by depolarizing agents such as potassium and veratridine. Potassium concentrations between 30 and 80 mm released increasing amounts of luteinizing hormone\x=req-\ releasing hormone (LRH) from the MEs of starved and control rats. Veratridine at a concentration of 50 \ g=m\ m caused a more prolonged LRH release in both starved and control animals. LRH secretion in vitro was slightly, though not under all conditions, significantly greater in rats starved for 5days. The testosterone ((T)-LHck was studied by castra¬castra-ting the animals and substituting various doses of throuT implantation of T-releasT-reldifferent. The Tconcentration in plasma, which can prevent the castration-induceds much smaller in starved than in control rats. The in vitro release of LRH evoked by 80 mM potassium was not different for starved and fed rats under various feedback conditions. Both groups revealed decreased in vitro release of LRH when castrated animals were not substitutT.The effect of castration was studied from 1to 28 days.The plasma LH values rapidly increased in starved and control animals, indicating that the hypothalamic responsestration is not delayed by starvation. The release in vitro of LRH decreased from the firsthe fifthand remained constant thereafter. No significant difference between starved and fed rats was observed. The experiments indicate that the 'releasable pool' of LRH in vitro is greater under conditions of reduced LH release in vivo. The basic mechanism of depolarization-inducedm the ME is intact in starved animals.

In man and other mammals, starvation is accompanied by a severe suppression of luteinizing hormone-releasing hormone (LHRH) and luteinizing-hormone (LH) secretion, which is caused by unknown alterations in hypothalamic functions. Prostaglandin E₂ (PGE₂), endorphins and testosterone (T) are know to be strongly involved in the regulation of LHRH release. The present study examined whether the influence of these substances on LHRH and LH secretion was affected by starvation. In vitro experiments checked the release of PGE₂ and LHRH from median eminences (ME) of fed male rats and ones starved for 5 days. Stimulation with potassium (80 mM) induced an equally strong release of PGE₂ and LHRH from the MEs of both fed and starved rats. When PGE₂ (10 ⁴M) was added to the superfusion medium, the potassium-stimulated release of LHRH was significantly enhanced in both groups of animals. The results clearly showed that in the terminal region of the hypothalamic LHRH system the release of this hormone and the action of PGE₂ were not altered by starvation. In vivo experiments tested whether the effects of LHRH, PGE₂, naloxone (NAL), or T on LH secretion were different in intact or castrated male’rats fed or starved for 3 and 5 days. LHRH (250 ng/kg) stimulated the same amount of LH secretion in fed and starved rats. The starvation-induced LH suppression was not due to a dysfunction at the pituitary level. The stimulatory action of PGE₂ (1 mg/kg) on LH was gradually reduced throughout the starvation period. NAL (5 mg/kg) had little, respectively, no effect on LH release on the 3rd or 5th day of starvation. When given simultaneously, NAL did not affect the action of PGE₂ in any of the three nutritional states. The interference of factors other than endorphins or PGE₂ is assumed for starvation-induced suppression of LH secretion. Starvation did not alter the influence of T (ca. 3 ng/ml plasma) on LH secretion at the pituitary level. The stimulatory effect of PGE2 on LH release was completely suppressed by T in fed, as well as in castrated rats starved for 3 or 5 days.

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The regulation of gonadotropin secretion was studied in anorexia nervosa, in voluntarily starving healthy subjects, and in the starved rat. In all cases, a hypothalamic disturbance is observed, resulting in an impaired ability to secrete gonadotropin‐releasing hormone (CnRH) from the median eminence. This effect is weight‐dependent in man and animals. The central neurotransmitters noradrenaline, dopamine, dynorphin, and prostaglandin E2 are involved in the regulation of GnRH release. A decreased activity of the catecholaminergk system and an increased activity of the endorphinergic system may be responsible for the impaired GnRH release.