Evidence for the Involvement of Hypothalamic Dopamine and Thyrotrophin-Releasing Hormone in Suckling-Induced Release of Prolactin

Abstract

The changes in adenohypophysial and hypothalamic content and in hypothalamic release of dopamine and thyrotrophin-releasing hormone (TRH) into the hypophysial portal system during the suckling-induced release of prolactin were investigated. An increase in peripheral plasma levels of prolactin was induced by mammary nerve stimulation in urethane-anaesthetized and by suckling in unanaesthetized lactating rats. In the unanaesthetized rat, suckling caused a decrease of dopamine levels in hypothalamus and adenohypophysis and a short-lasting small increase in hypothalamic TRH. Mammary nerve stimulation induced a transient decrease in dopamine levels and an increase in TRH levels in hypophysial stalk blood. To assess the significance of the observed changes in dopamine and TRH levels for prolactin release, these changes in dopamine and TRH were mimicked in lactating rats anaesthetized with urethane and pretreated with α-methyl-p-tyrosine (AMpT, a competitive inhibitor of catecholamine synthesis). Reducing hypothalamic dopamine secretion by treatment with AMpT increased peripheral plasma levels of prolactin from 15 to 477 ng/ml; an infusion with dopamine, resulting in plasma levels similar to those measured in hypophysial stalk plasma, reduced plasma levels of prolactin to 127 ng/ml. Neither a 50% reduction in dopamine infusion rate for 15 min nor administration of 100 ng TRH caused an appreciable change in plasma prolactin levels. However, when dopamine infusion was reduced by 50% for 15 min just before TRH was injected, then an increase in plasma levels of prolactin from 172 to 492 ng/ml was observed. Thus, the effectiveness of TRH in releasing prolactin in the lactating rat was enhanced when a transient decrease of dopamine levels occurred before treatment with TRH. It is concluded that the changes observed in dopamine and TRH levels in hypophysial stalk blood are involved in the suckling-induced prolactin release in an important manner.

Cocaine- and amphetamine-regulated transcript (CART) expression is differentially regulated in the hypothalamic paraventricular nucleus of lactating rats exposed to suckling or cold stimulation

“…As CART is the only known peptide that coexists with TRH in the PVN (Fekete et al, 2000) it is feasible that under the appropriate circumstances, the genes for both peptides may become simultaneously activated. The paradigm of the lactating rat subject to either suckling or cold exposure, conditions when TRH neurons are rapidly activated in the PVN (Sánchez et al, 2001), exemplify in vivo situations where TRH is released but the secretion of TSH and prolactin diverge (Adels et al, 1986;Arancibia et al, 1983;de Greef and Visser, 1981;Sanchez et al, 2001;van Haasteren et al, 1996). Using this paradigm, we demonstrate herein a differential activation of CART neurons in the PVN, stimulated by cold exposure but not by suckling.…”

“…Included among the physiologic stimuli associated with activation of hypophysiotropic TRH neurons are suckling and cold exposure that induce TRH release (Arancibia et al, 1983;de Greef and Visser, 1981;Fink and Ben-Aroya, 1983;Hefco et al, 1975) and a rapid (30-60 min) and transient increase in proTRH mRNA levels in the PVN (Rage et al, 1994;Sanchez et al, 2001;Uribe et al, 1993;van Haasteren et al, 1996). However, the response of pituitary target cells is specific to the stimulus.…”

Arcuate Nucleus and Preoptic Area Involvement in Beta‐Endorphin‐lnduced Release of Prolactin in Conscious Ovariectomized Rats†

“…The typical pattern of prolactin secretion is one of continuous low levels, interrupted by large surges as seen in pregnancy (20) or during proestrus (21). There is evidence to suggest that these prolactin surges, which may last several hours, require only a brief interruption of dopamine tone, accompanied by stimulatory input from the hypothalamus, such as TRH (22)(23)(24). If this is the case, then 8-END would only be required for a short time, to decrease dopamine tone.…”

From prolactin cell to prolactinoma: implications of ontogenic mechanisms in diagnosis and management

“…Other potential PRL inhibiting factors have also been described, but their structure has not yet been completely elucidated (Molitch 1995). Superimposed on the tonic inhibition of DA are several factors that increase PRL secretion (Hazlerigg et al 1996), including thyrotropinreleasing hormone (TRH) from the hypothalamus (De Greef & Visser 1981, Plotsky & Neill 1982, Martinez de la Escalera et al 1988, Mogg & Samson 1990, vasoactive intestinal peptide (VIP) (Kato et al 1978, Abe et al 1985, Carillo et al 1985 and steroid hormones such as estrogens (Maurer & Gorski 1977). These factors may be considered as PRL-releasing factors.…”