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- Author: E. O. ALVAREZ x
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The purpose of the present work was to determine the possible role of the histamine receptors located in the rostral zone of the hypothalamus in the control of the prolactin surge induced by ether stress. Cannulae were implanted into the preoptic anterior hypothalamic area or the third ventricle of several groups of adult male rats under ether anaesthesia. On the following day the rats were cannulated in the jugular vein so that they could be bled frequently. Twenty-four hours later saline, metiamide (an antagonist of H2 histamine) or pyrilamine (an antagonist of H1 histamine) were injected into the brain. Fifteen minutes after the injection all rats were subjected to an ether stress. Blood samples were taken at regular times after the stress and prolactin levels determined by radioimmunoassay. A prolactin surge was observed in rats injected with saline which extended up to 15–30 min after the stress. When the histamine antagonists were administered directly in the rostral hypothalamus both pyrilamine and metiamide inhibited the prolactin surge. When the histamine antagonists were administered into the third ventricle only metiamide was able to block the prolactin response completely.
The present results suggest that histamine receptors in the rostral hypothalamus of the rat are involved in the control of prolactin secretion induced by stress.
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The levels of prolactin in the plasma of conscious male rats were determined at various times after an acute administration of histamine or a histamine releasing agent, compound 48/80, in three brain regions. The brain structures that were examined were, the caudal part of the preoptic area and anterior part of the anterior hypothalamic area (POA–AHA), the arcuate nucleus–ventromedial nucleus region (ARC–VMN) and the medial–basal amygdaloid nucleus of the limbic system (AME).
A marked increase in plasma levels of prolactin was observed when implants of histamine were in the POA–AHA region. A more consistent increase was found when 1 μg histamine was injected in the same region; values of prolactin were about 3·6 times greater than in their controls injected with 0·9% saline. Such increased hormone levels lasted up to 2 h. A similar rise in prolactin level was found when the implants of histamine were located in the ARC–VMN region. When compound 48/80 or empty cannulae were placed in those brain regions that were examined, no changes in plasma levels of prolactin were induced.
Both histamine and compound 48/80 elicited a delayed and long-lasting decrease of the high plasma level of prolactin present in rats bearing cannulae in the AME region.
The results suggest that in the male rat, histaminergic sites, located in rostral and mediobasal hypothalamus and in the central area of the amygdala, are involved in the mechanisms controlling prolactin secretion.
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The purpose of the present work was to investigate whether the administration of a dopamine agonist (2-bromo-α-ergocryptine) was able to interfere with the normal change in uterine sensitivity to oestrogen that occurs around the onset of puberty in the rat.
To determine the change in uterine sensitivity groups of rats at 25, 30 or 35 days of age were killed (to find the initial uterine weight) or ovariectomized with or without oestrogen replacement therapy (0·05 μg/100 g body wt, daily for 5 days) and then killed to determine the final uterine weight. Comparisons were made between initial and final uterine weights. Five days before the animals reached 25, 30 or 35 days of age, one group was injected with 2-bromo-α-ergocryptine (0·5 mg/100 g body wt daily for 5 days) and another one with solvent (control rats). At the ages specified (25, 30 and 35 days of age) both groups were subjected to the ovariectomy schedule. Results showed that the bromocriptine treatment was effective in blocking the normal uterine change in sensitivity that occurs at 30 days of age. At 35 days of age the dopamine agonist was able to counteract the action of oestrogen in maintaining the uterine weight 5 days after ovariectomy. The results are interpreted as suggesting that the mechanism of change in uterine responsiveness to oestrogen in maturing rats is mediated by prolactin.
