Induction of Prolactin and Luteinizing Hormone Release by Histamine in Male and Female Rats and the Influence of Brain Transmitter Antagonists

Abstract

The levels of prolactin and LH in the plasma of rats were determined at various times after intraventricular injection of histamine. Doses of 5 and 60 μg histamine (free base) in male rats, anaesthetized with ether, induced an increase in the level of prolactin in the plasma, whilst producing a slight decrease in the concentration of LH. Injection of 5 μg histamine at 14.00 h into female rats at all stages of the oestrous cycle caused prolactin to be released; the effect was greatest at oestrus and at day 1 of dioestrus. Histamine also gave rise to a marked increase in the level of LH in the plasma when administered to pro-oestrous rats, but had no effect when injected at the other stages of the oestrous cycle. The effect of histamine on the release of prolactin in ovariectomized, oestradiol benzoate: progesterone-primed (OVX,OB:P) rats was found to be dose-related, and the level of LH in the plasma was increased by as little as 1·25 μg. Pretreatment with adrenergic (phenoxybenzamine and propranolol) and cholinergic (atropine) antagonists failed to block the stimulatory effects of histamine on prolactin secretion, but pretreatment with methysergide (serotonin antagonist) increased the histamine-induced release of prolactin in male rats. Antagonists did not modify the response of prolactin to histamine in OVX,OB:P-primed rats. The histamine-induced release of LH in OVX,OB:P-primed rats was slightly reduced by pretreatment with phenoxybenzamine, propranolol and atropine, but not by methysergide. These results indicate that histamine facilitates the release of prolactin. The stimulatory action of histamine on both pro-oestrous and OVX,OB:P-primed but not male rats suggests that histamine may be involved in LH release in the rat. Results obtained in animals pretreated with transmitter antagonists, which were unable to prevent histamine-induced hormone release, suggest that the actions of this amine are not mediated by cholinergic, noradrenergic or serotonergic mechanisms.

Effect of Selective Blockade of Catecholaminergic Alpha and Beta Receptors on Histamine-Induced Release of Corticotropin and Prolactin

“…The additional experiments revealed that this effect was due to activation of β 1 -receptors, since Ate, but not the β 2 -receptor antagonist ICI, inhibited the PRL response. In contrast to these results, it was reported that systemic administration of the α-receptor antagonist Phb or the β-receptor antagonist Pro did not affect PRL secretion in conscious estrogen-progesterone-primed ovariectomized female rats [49]. Sex, prior steroid treatment and administration routes of the catecholaminergic compounds may explain the differences between this and the present study.…”

Modulation of Basal and LRH-Stimulated Gonadotrophin Secretion by Histamine in Normal Men

“…In male rats HA administered intraventricularly did not affect LH secretion [6,18]. In ovariectomized estrogen/progesterone primed rats and in proestrus rats HA administered intraventricular ly stimulated LH secretion [5,13]. No effect of HA was found in estrus and diestrus rats [5],…”

“…In ovariectomized estrogen/progesterone primed rats and in proestrus rats HA administered intraventricular ly stimulated LH secretion [5,13]. No effect of HA was found in estrus and diestrus rats [5],In humans, HA administered as an intravenous infusion was found to stimulate basal LH secretion in males and to inhibit basal LH secretion in females in the early follicular phase [17]. Intravenous injections of the H2-receptor anta gonists cimetidine (C) and ranitidine did not affect the go nadotrophin secretion [3,10], Long-term treatment with cimetidine has been found to increase basal as well as LRHstimulated gonadotrophin secretion [10,16,23], However, this stimulation is presumably caused by an anti-androgen effect of cimetidine rather than by a blockade of ^-recep tors [10,26].…”

Interactions between histaminergic and cholinergic systems in learning and memory

“…ACh electrically-elicited release was inhibited by systemic administration of zolantidine, an H 2 receptor antagonist [21], but not of pyrilamine, an H 1 receptor antagonist, thus indicating that activation of H 2 receptors resulted in an increase of extracellular level of hippocampal ACh [83]. Stimulation of H 2 receptors released also endogenous noradrenaline from rat hypothalamic slices [16] and prolactin [34]. The implication of endogenous histamine was further supported by the observation that administration of thioperamide, an H 3 receptor antagonist [4], increased, while that of R-amethylhistamine, an H 3 receptor agonist [4], decreased ACh spontaneous release from hippocampus [83].…”