Prolactin

About: Prolactin is a research topic. Over the lifetime, 22356 publications have been published within this topic receiving 609537 citations. The topic is also known as: lactotropin, & PRL,.

Endogenous opiates block dopamine inhibition of prolactin secretion in vitro.

Abstract: OPIATES stimulate prolactin secretion in vivo; plasma prolactin levels are increased by morphine administration in normal1 and steroid-primed male rats2, as well as in immature3 and oestrogen-treated female rats4. Met-enkephalin and β-endorphin were also stimulatory1–6 as were enkephalin analogues3,7,8. Naloxone or naltrexone, specific opiate antagonists, reduce basal prolactin levels when given alone1,3,9, and block, at least partially, the effect of opiate agonists1–4,7,8. None of these drugs is active in vitro when tested alone on anterior pituitaries3 or dispersed pituitary cells2,4. However, as we have previously shown in a preliminary experiment, the inhibitory effect of dopamine on prolactin secretion in vitro was antagonised by the addition of morphine to the incubation medium10. In the present work, we have attempted to clarify further the mode of interaction of opiates with prolactin secretion. We confirmed that morphine, Met-enkephalin and β-endorphin do not affect the spontaneous release of prolactin in vitro, but found that they suppress the inhibitory effect of dopamine on prolactin release. We have also characterised the specificity and the kinetics of this interaction.

Diurnal Variation in Neuroendocrine Response to Stress in Rats: Plasma ACTH, β-Endorphin, β-LPH, Corticosterone, Prolactin and Pituitary Cyclic AMP Responses

Abstract: The effects of restraint stress applied at different times of the day on levels of five stress-responsive plasma hormones (ACTH, β-endorphin, β-LPH, corticosterone and prolactin) and pituitary cyclic AMP levels were assessed. Different groups of rats were subjected to 15 min of restraint stress at 2-hour intervals over a 24-hour period. Rats were sacrificed immediately upon removal from their home cage (controls) or immediately following restraint (stressed). The time of day of stress exposure markedly affected the stress responses measured. Generally, responses to stress applied at the beginning of the dark cycle (18.00) were less than those seen following stress applied at the beginning of the light cycle (06.00). Stress at 06.00 increased levels of pituitary cyclic AMP 10-fold, while stress applied at 18.00 did not significantly increase pituitary cyclic AMP levels. In stressed rats, high correlations were seen among levels of hormones derived from the common precursor, proopiomelanocortin (ACTH, β-endorphin, β-LPH) and between these hormones and levels of pituitary cyclic AMP. These findings support the hypothesis that pituitary cyclic AMP is involved in the stress-induced release or synthesis of the pituitary hormones ACTH, β-endorphin, and β-LPH.

Hormone interactions regulating energy balance during pregnancy.

Abstract: Appetite and food intake are increased during pregnancy, comprising an adaptive response that facilitates energy storage in preparation for the high metabolic demands of pregnancy and subsequent lactation. To maintain the increased energy intake in the face of increased adiposity and rising leptin levels, pregnant females become resistant to the central anorectic actions of leptin. In rats, pregnancy-induced leptin resistance is characterised by elevated neuropeptide Y and reduced pro-opiomelanocortin expression in the arcuate nucleus, reduced leptin receptor mRNA levels and suppression of leptin-induced phosphorylated signal transducer and activator of transcription-3 protein in the ventromedial hypothalamic nucleus, as well as a loss of anorectic responses to both leptin and alpha-melantocyte-stimulating hormone. Our recent data suggest that this leptin-resistance may also cause central insulin resistance and an altered peripheral glucose homeostasis. The specific hormone changes during pregnancy that might mediate these effects on leptin signalling are a current focus of investigation. In pseudopregnant rats, chronic i.c.v. infusion of ovine prolactin to mimic patterns of placental lactogen secretion that occur during pregnancy completely blocked the ability of leptin to suppress food intake. These data suggest that placental lactogen secretion may mediate the hormone-induced loss of response to leptin during pregnancy. This action of prolactin/placental lactogen appears to be mediated downstream of the primary leptin-responsive neurones in the mediobasal hypothalamus, possibly in the paraventricular nucleus. Our studies show complex hormone-induced adaptations in the normal hypothalamic pathways regulating body weight homeostasis during pregnancy.

Anterior pituitary hormone control by interleukin 2.

Abstract: Several monokines, proteins secreted by monocytes and macrophages, alter release of hormones from the anterior pituitary. We report here the ability of femtomolar concentrations of interleukin 2 (IL-2), a lymphokine released from T lymphocytes, to alter directly pituitary hormone release. The effects of concentrations of IL-2 ranging from 10(-17) to 10(-9) M on anterior pituitary hormone release were evaluated in vitro. Hemipituitaries were preincubated in 1 ml of Krebs-Ringer bicarbonate buffer (KRB) followed by incubation for 1 or 2 hr with KRB or KRB containing different concentrations of IL-2. This was followed by incubation for 30 min in 56 mM potassium medium to study the effect of pretreatment with IL-2 on subsequent depolarization-induced hormone release. Prolactin (PRL), luteinizing hormone (LH), follicle-stimulating hormone (FSH), corticotropin (ACTH), growth hormone (GH), and thyrotropic hormone (TSH) released into the incubation medium were measured by radioimmunoassay. IL-2 stimulated the basal release of PRL at 1 or 2 hr but suppressed the subsequent depolarization-induced PRL release, perhaps because the readily releasable pool of PRL was exhausted. The minimal effective dose (MED) was 10(-15) M. Conversely, IL-2 significantly suppressed the basal release of LH and FSH at 1 or 2 hr, with a MED of 10(-16) M, thus demonstrating a reciprocal action of the cytokine on lactotrophs and gonadotrophs. The subsequent depolarization-induced release of LH and FSH was suppressed, indicative of a persistent inhibitory action of IL-2. IL-2 stimulated ACTH and TSH release at 1 hr and the MEDs were 10(-12) and 10(-15) M, respectively. Conversely, IL-2 significantly lowered the basal release of GH at 1 hr, with a MED of 10(-15) M. The release of GH was not altered at 2 hr. The high potassium-induced release of ACTH, TSH, and GH was not affected. The results demonstrate that IL-2 at picomolar concentrations affects the release of anterior pituitary hormones. This cytokine may serve as an important messenger from lymphocytes exerting a direct paracrine action on the pituitary by its release from lymphocytes in the gland or concentrations in the blood that reach the gland may be sufficient to activate it.