Radioimmunoassay for Rat Prolactin

Niswender, Gordon D.; Chen, C.L.; Midgley, A. Rees; Meites, Joseph; Ellis, Stanley

doi:10.3181/00379727-130-33657

Cited by 365 publications

(152 citation statements)

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“…Prolactin assay.-Prolactin of individual plasma samples and pituitaries was measured by a radioimmunoassay described previously by Niswender et al (1969). Sheep antirabbit globulin was purchased from Grand Island Biological Company (Grand Island, New York).…”

Section: Methodsmentioning

confidence: 99%

Neonatal modification of endocrine functions and mammary carcinogenesis in the rat

Christakos¹,

Sinha²,

Dao³

1976

Br J Cancer

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Section: Methodsmentioning

confidence: 99%

Neonatal modification of endocrine functions and mammary carcinogenesis in the rat

Christakos¹,

Sinha²,

Dao³

1976

Br J Cancer

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“…LH and prolactin concentrations were measured by double-antibody radioimmunoassays [8,9] using materials and protocol supplied by the National Hormone and Pituitary Program (NHPP), Baltimore, Maryland, USA and are expressed in terms of NHPP rat LH-reference preparation (RP)I and prolactin-RP2. Inter-and intra-assay coefficients of variation were 10.2% and 9.4%, respectively, for LH and 10.1% and 8.9% for prolactin.…”

Section: Assaysmentioning

confidence: 99%

Feedback effects of steroids and gonatrophin control in adult rats with streptozotocin-induced diabetes mellitus

1985

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Summary. The effects of long-and short-term streptozotocininduced diabetes mellitus on the control of gonadotrophin secretion have been investigated in adult intact rats. A high dose of streptozotocin (80 mg/kg), administered intraperitoneally 3 days before experimentation, inhibited ovulation and reduced the pituitary luteinizing hormone response to luteinizing hormone releasing hormone in proestrous rats. A lower dose (40 mg/kg) did not inhibit ovulation but abolished the luteinizing hormone releasing hormone-priming effect on the pituitary which normally occurs on proestrus, prior to ovulation. Oestrous cyclicity was lost when diabetes was induced for 14 or 56 days, but there was no effect on pituitary responsiveness to luteinizing hormone-releasing hormone compared with control animals. Similar observations were made with rats placed on a food-restricted diet. In all experiments there was no difference between diabetic and control animals in the pituitary luteinizing hormone content, the hypothalamic content of luteinizing hormone-releasing hormone or the ovarian weights. Ovariectomized rats treated with streptozotocin (40 mg/kg) were used to investigate the effects of diabetes on steroid feedback mechanisms. There was an attenuated luteinizing hormone response to ovariectomy in diabetic compared with control animals, and an impaired positive feedback effect of progesterone in oestrogen-primed animals. The results show that streptozotoein-induced diabetes mellitus inhibits feedback action of gonadal steroids and this could account for both the loss of oestrous cyclicity and the reduced pituitary sensitivity to luteinizing hormone-releasing hormone.Key words: Streptozotocin, diabetes mellitus, fertility, luteinizing hormone, luteinizing hormone -releasing hormone, steroid feedback, body weight.It is well known that diabetic patients show an increased incidence of infertility [1], but the mechanisms by which diabetes mellitus impairs reproductive functions are poorly understood. Drug-induced diabetes mellitus in the female rat has frequently been used as an experimental model to investigate the causes of this association, since both alloxan-and streptozotocin-induced diabetes result in ovulatory failure [2,3]. A reduced sensitivity of the pituitary gonadotrophs to luteinizing hormone-releasing hormone (LHRH) has been observed in diabetic rats [4] but this could be attributed to an impairment of LHRH secretion since the releasing hormone regulates its own pituitary receptors [5]. Indeed, the available evidence strongly indicates that diabetes inhibits the hypothalamic regulation of gonadotrophin secretion, and this could involve a failure in the feedback action of gonadal steroids. However, a direct effect of diabetes on the pituitary gland or on the ovary cannot be excluded.The majority of studies have been carried out on the immature animal in which ovulation is stimulated by the administration of pregnant mare's serum gonadotrophin. This particular animal model has some disadvantages since it precludes the c...

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“…One postulated mechanism for the action of B-END is via inhibition of dopamine release from the tuberoinfundibular neurons, thus decreasing the chronic inhibitory influence of dopamine on prolactin (19). 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).…”

Section: Resultsmentioning

confidence: 99%

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

Voogt

Reseh

Turkington

1989

J Neuroendocrinology

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The ability of 8-endorphin (/?-END) to release prolactin and t h e ability of naloxone to block prolactin's release when delivered to specific hypothalamic areas via push-pull perfusion was studied in unrestrained, conscious, ovariectomized rats. Perfusion of either the arcuate nucleus or the preoptic area with 8-END for 15 to 30 min caused a large, brief increase in plasma prolactin levels. Perfusion for a longer time period (120 min) resulted in peak prolactin levels at 60 min, with a return to baseline by 120 min, suggesting that 8-END primarily acts to induce a sequence of events that culminates in prolactin release, but other factors are needed to maintain this release over long periods of time. Perfusion of the arcuate nucleus for two 15-min periods 90 min apart resulted in two surges of prolactin. When naloxone, the opiate receptor antagonist, was added to t h e perfusate, /-END was not capable of stimulating prolactin release. These results provide a model to answer whether endogenous 8-END has a role in t h e neuroendocrine regulation of prolactin surges and what the location is of the opiate neurons involved in this neuronal pathway.Many studies have shown that exogenously administered 8-endorphin (8-END) and opiate analogs stimulate prolactin secretion (1-4). The positive effect of opioid stimulation on prolactin is reversed by opiate receptor blockade (5, 6). There is a predominance of both p-and ic-receptor sites in the hypothalamus (7, 8), although it is not clear which receptors are more important physiologically in prolactin regulation (9). Blockade of opiate receptors has been shown to inhibit prolactin during instances in which prolactin is normally secreted in large amounts. Naloxone, which blocks all classes of opiate receptors, inhibited prolactin release during proestrus (lo), stress (11-13), and suckling (11,14,15). Thus, it appears that the opioid system plays an important role in regulating prolactin.Most studies conclude that opioids have a central site of action in regulating pituitary prolactin release. Intraventricular injection of human 8-END increased prolactin quickly (4). Intrahypothalamic injection of 8-END into male rats (16) or ovariectomized female rats (17) resulted in large increases in plasma prolactin levels. In these studies b-END was given as an injection or one rnin infusion. The present study was designed to determine the effect of administration of #?-END in specific hypothalamic sites for controlled time periods on prolactin secretion in unanesthetized, ovariectomized rats using the push-pull perfusion (PPP) technique. Secondly, the opiate antagonist naloxone was given via PPP at the site where 8-END was found to be effective in releasing prolactin. ResultsTo determine whether the addition of 8-END to the perfusate would stimulate prolactin release, the cannula tip was placed in or very near to the arcuate nucleus. The average distance between the cannula tip and the third ventricle was 0.5 mm. When a dose of 8-END of 2 pg/lOmin was perfused for 30min, ther...

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Radioimmunoassay for Rat Prolactin

Cited by 365 publications

References 0 publications

Neonatal modification of endocrine functions and mammary carcinogenesis in the rat

Neonatal modification of endocrine functions and mammary carcinogenesis in the rat

Feedback effects of steroids and gonatrophin control in adult rats with streptozotocin-induced diabetes mellitus

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

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