Topic
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,.
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TL;DR: This study investigates plasma baseline cortisol and prolactin secretion in relation to plasma interleukin-6 (IL-6) and soluble IL-2 receptor (sIL-2R) levels in 34 healthy controls and 56 major depressed patients to examine the immune-endocrine relationships.
Abstract: Recently, a complete bidirectional circuit between the immune and neuroendocrine systems has been documented. Previous reports from this laboratory have shown that there are complex reciprocal relationships between immune and hypothalamic-pituitary-adrenal (HPA)-axis function in major depression. To further examine the immune-endocrine relationships, this study investigates plasma baseline cortisol and prolactin secretion in relation to plasma interleukin-6 (IL-6) and soluble IL-2 receptor (sIL-2R) levels in 34 healthy controls and 56 major depressed patients. There were significant positive correlations between IL-6 or sIL-2R and plasma cortisol in major depressed subjects and in the combined group of major depressed and healthy subjects. There were also significant positive correlations between plasma prolactin and sIL-2R concentrations in major depressed subjects and in the combined groups of normal and major depressed subjects.
109 citations
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TL;DR: It is concluded that TRH and possibly a separate hypothalamic PRF have a stimulatory action upon the releasable, but not upon the depletion-transformation, phase of PRL secretion in the lactating rat.
Abstract: We have compared the effectiveness of TRH and a rat hypothalamic PRL-releasing factor (PRF; previously incubated with rat serum to destroy TRH) in stimulating the release of PRL into the plasma of conscious lactating rats when injected before and after pituitary PRL had been depleted and transformed into releasable PRL by 10 min of suckling. TRH (1.25 microgramsss) and PRF [equivalent to 2.5 stalk median eminence (SME) fragments] each caused a small increase (38 and 30 ng, respectively) in the plasma PRL concentration within 10 min when injected into nondepleted mothers. The levels then fell quickly. Suckling, by comparison, caused a sustained 175 ng/ml increase above basal levels. Though PRL depletion occurred, as expected, as a result of suckling, there was no measurable depletion within the pituitaries of TRH- or PRF-injected rats. By contrast, the iv administration of TRH (doses ranging from 2-250 ng) and hypothalamic PRF (doses ranging from 0.2-1.0 SME equivalent) after depletion-transformation had been effected by 10 min of suckling resulted in a rapid and, in most instances, a sustained elevation in the plasma PRL concentration comparable to that seen after suckling. Dose-response relationships, though, were not clearly evident with either PRF or TRH. Neither saline, 1.25 microgram TRH previously incubated in serum, 50 mU oxytocin, 1 microgram dopamine, 25 microgram LHRH, nor an extract of cerebral cortex prepared in the same manner as hypothalamic TRH caused plasma PRL to rise after PRL depletion. We conclude that TRH and possibly a separate hypothalamic PRF have a stimulatory action upon the releasable, but not upon the depletion-transformation, phase of PRL secretion in the lactating rat.
109 citations
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TL;DR: The results suggest that in anterior pituitaries exposed to elevated levels of PRL, LH secretion and pituitary responsiveness to LHRH could be impaired, and this phenomenon may contribute in part to the antigonadotropic effects ofPRL.
Abstract: In pathological or experimental hyperprolactinemia, the elevated circulating levels of PRL are the usual cause of the impairment in gonadotropic function. The present study was undertaken to determine whether PRL could suppress basal LH secretion and LHRH-stimulated LH release by a direct action at the anterior pituitary. Anterior pituitaries from ovariectomized rats were incubated in medium 199 alone or in medium 199 containing ovine PRL, and basal and the LHRH-stimulated LH release were followed for 2 or 3 h in vitro. Ovine PRL at 40 and 80 micrograms/ml suppressed basal LH release by 41% and 72%, respectively, at 2 h of incubation. This suppressive effect of both concentrations of PRL continued to the third hour of incubation. LHRH at 5 ng/ml increased the release of LH from pituitaries incubated in medium alone by 57%, 61%, and 107% at 1, 2, and 3 h of incubation, respectively. However, in the pituitaries treated with 40 micrograms/ml ovine PRL, the stimulatory effects of LHRH were diminished at all time points measured. Pretreatment of anterior pituitaries with ovine PRL for 6 h significantly inhibited by 81% the LHRH (5 ng/ml) stimulation of LH release at 2 h of incubation. On the other hand, inhibition of endogenous PRL release by 10(-6) M bromocriptine enhanced the stimulatory effects of 5 ng/ml LHRH by 2.5-fold at 2 h of incubation. The inhibitory effects of PRL on basal and stimulated LH secretion appeared unique, since neither BSA nor vasopressin could elicit similar suppressive effects on LH. These results suggest that in anterior pituitaries exposed to elevated levels of PRL, LH secretion and pituitary responsiveness to LHRH could be impaired. This phenomenon may contribute in part to the antigonadotropic effects of PRL.
109 citations
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TL;DR: It is suggested that the onset of puberty in the female rat is brought about by a gradual increase in estrogen secretion which, acting at the CNS-pituitary level, triggers a preovulatory proestrus-like surge of gonadotropins and prolactin.
Abstract: In order to study the sequence of hormonal changes that accompany the onset of puberty in the female rat, immature animals were sacrificed by decapitation between days 32 and 38, and plasma titers of gonadotropins, prolactin, and LHRH, and the hypothalamic content of LHRH were determined by specific radioimmunoassays (RIA). Animals were decapitated at 10:00 and 16:00 h throughout the pubertal period, the uterine weight was recorded, and the ovaries were inspected for signs of ovulation. Animals with the vagina closed were grouped according to the condition of the uterus as anestrus (A), early proestrus (EP) and late proestrus (LP), the uterus being unstimulated, dilated with some fluid, or ballooned, respectively. Vaginal opening was usually associated with ovulation and in most cases occurred at the end of the late proestrous phase. Animals were studied up to 3 days after vaginal opening and were grouped according to vaginal cytology. Uterine weight, taken as an index of estrogen secretion, was low durin...
109 citations
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TL;DR: The neuroendocrine mechanisms for stress hyporesponsiveness are likely to include reduced synthesis and secretion of corticotropin releasing hormone (CRH) and arginine vasopressin (AVP) from the hypothalamus as a result of enhanced glucocorticoid negative feedback and/or reduced noradrenergic stimulatory input from the brain stem.
109 citations