The Effect of Transient Dopamine Antagonism on Thyrotropin-Releasing Hormone-Induced Prolactin Release in Pregnant Rats*

Haisenleder, Daniel J.; Moy, Jadine A.; Gala, Richard R.; Lawson, David M.

doi:10.1210/endo-119-5-1980

Cited by 23 publications

(19 citation statements)

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“…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.…”

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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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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“…OVX rats are practically devoid of sex steroids, whereas the pregnant rat has high levels of both estradiol and progesterone (20). The transient decrease in dopamine interaction at the receptor not only releases the cell from dopamine inhibition, but also may augment the cell's response to PRL-releasing factors, such as thyrotropin-releasing hormone (21). Injection of domperidone was done at 0300 h, normally the time of the nocturnal surge of PRL in pregnant rats.…”

Section: Discussionmentioning

confidence: 99%

Prolactin Implants in the Hypothalamus Inhibit Prolactin Surges During Pregnancy and Alter Prolactin Release in Response to Dopamine Receptor Blockade

Vidal¹,

Mathiasen²,

Voogt³

1991

J Neuroendocrinology

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The purpose of this study was to determine whether prolactin (PRL) could exert a negative feedback on it's own secretion during pregnancy and following ovariectomy, and to determine t h e possible mechanism by which this feedback acts. Implantation of ovine PRL into t h e arcuate nucleus-median eminence area of t h e hypothalamus completely inhibited the nocturnal PRL surge during pregnancy in t h e rat, and lowered baseline PRL to almost undetectable levels in t h e ovariectomized rat. W h e n ovariectomized rats implanted with ovine PRL in the hypothalamus were injected with the dopamine receptor blocker domperidone the PRL response was significantly lower than in control rats implanted with albumin. Pregnancy increased t h e ability of domperidone to cause PRL release following ovine PRL implantation compared to what occurred in ovariectomized rats. These results suggest that PRL implantation increases the secretion of dopamine from the tuberoinfundibular n e u r o n s , resulting in a decrease in PRL secretion.Prolactin (PRL) exerts a negative shortloop feedback on its own secretion. This has bccn best demonstrated during physiological states in which there is a surge or elevation of PRL secretion. Ovine PRL (oPRL) given either systemically ( I ) or directly into the hypothalamus (2) inhibited the proestrous rise in PRL secretion, although acute inhibitory effects of intracerebroventricular (icv) PRL on circulating PRL was minimal (3). Stress-induced PRL increases were greatly attenuated by icv rat PRL (4). Sucking-induced PRL release was totally inhibited by long-term hypothalamic implants of oPRL (2), whereas increases in circulating oPRL were only minimally effective ( I , 5). Hypothalamic implants of oPRL terminated pseudopregnancy (6) and reduced PRL levels (7).Mating induces two daily PRL surges for the first half of pregnancy, a diurnal surge occurring in the late afternoon and a nocturnal surge occurring between midnight and 0600 h (8, 9). When oPRL was implanted into the hypothalamus of pregnant rats before Day 7, pregnancy was terminated (10). The present study was designed to answer two questions. 1) Does implantation of oPRL into the arcuate nucleus-median eminence area terminate the nocturnal PRL surge of pregnant rats and reduce baseline PRL levels in ovariectomized (OVX) rats? 2) Does the oPRL implant alter the PRL response to doniperidone, a dopamine receptor antagonist? The rationale for the second question comes from numerous observations that PRL increases the release of dopamine from tuberoinfundibular neurons, which in turn directly influences PRL secretion ( 1 I , 12). Results E j k t of oPRL implunted intothe uraiutiJ nucleus-median eminence ureu on nocturnal PRL surges in pregnant rats und baseline PRL levels in OVX ruts Implantation of either 25 or 250 pg of oPRL on Day 7 o r 8 of pregnancy completely inhibited the nocturnal PRL surge 1 day later. Since there was no difference in the response due to the day of implantation, the data were combined and are shown in Fig. 1. Cont...

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“…Others have shown that a decrease in DAergic tone con ditions the pituitary to respond to TRH in its capacity as a PRL-releasing hormone [e.g. 4,15,[37][38][39][40]. Various reports have proven the involvement of TRH in the mediation of the normal PRL surge [e.g.…”

Section: Trh Effects On Da and Prlmentioning

confidence: 99%

Semicircadian Rhythm of Dopamine Release in the Mediobasal Hypothalamus in Awake Rats during Pseudopregnancy: Evidence that a Thyrotropin-Releasing Hormone Analogue Stimulates Dopamine Release and thereby Inhibits Prolactin Secretion

Timmerman

Poelman²,

Westerink³

et al. 1995

Neuroendocrinology

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The release of dopamine (DA) from tuberoinfundibular (TIDA) neurons during prolactin (PRL) surge and nonsurge periods and the effects of the thyrotropin-releasing hormone (TRH) analogue CG 3703 on DA and PRL secretion were studied in awake pseudopregnant (PSP) rats by simultaneous measurement of extracellular DA levels in the mediobasal hypothalamus (MBH) by means of microdialysis and of plasma PRL concentrations by radioimmunoassay of PRL in blood sampled from a permanent heart cannula. Since basal DA levels were low, the experiments were performed under local infusion of the reuptake inhibitor nomifensine (5 µmol/l), which increased extracellular DA levels 5-fold around the probe, but did not affect the occurrence of the nocturnal PRL surge on day 7–8 of PSP. Under nomifensine conditions, during the interphase (18.00–1.00 h), plasma PRL levels were low (<50 ng/ml), while the DA release from TIDA neurons was elevated (∼250%) relative to the DA values measured during the phase when the nocturnal PRL surge occurred (100%; 1.00–12.00 h; plasma PRL levels were elevated to ∼300 ng/ml). Thus, semicircadian rhythms were detected both for DA and PRL, which were broadly reciprocal in timing. The TRH analogue CG 3703 (100 and 500 µg/ animal i.v.), when administered at 00.00 h, dose-dependently increased extracellular DA levels (to 300 and 500% of pretreatment values, respectively) and postponed the PRL surge in a corresponding manner (for ∼2 and 3 h, respectively). Thus, in addition to its PRL-releasing effects, TRH can also suppress the PRL secretion by stimulating the release of DA from TIDA neurons, thereby increasing the inhibitory DAergic tone on lactotrophs. During the interphase, when DA levels were relatively elevated, administration of the DA blocking agent HA 966 (100 mg/kg body weight i.p.) at 20.00 h resulted in a short-lasting decrease in extracellular DA levels (to ∼60% of pretreatment values for 30 min) accompanied by an immediate, short-lasting increase in PRL levels (to 400 ng/ml for ∼1 h). Administration of CG 3703 (500 µg/ animal i.v.) in combination with HA 966 (100 mg/kg body weight i.p.) at 20.00 h prevented the decrease in DA levels and the rise in plasma PRL values. Thus, the TRH analogue and HA 966 counteracted each other regarding the DAergic system, which again illustrates the stimulatory effect of the TRH analogue on the release of DA from TIDA neurons. Moreover, our results suggest that the interphase and the phase during which the nocturnal PRL surge occurs under the condition of PSP differ with regard to the DAergic inhibition of the PRL secretion; during the interphase the DAergic inhibitory tone prevents the rise in PRL secretion, while during the nocturnal PRL surge period another factor in addition to a decrease in DA levels appears necessary to increase plasma PRL levels.

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The Effect of Transient Dopamine Antagonism on Thyrotropin-Releasing Hormone-Induced Prolactin Release in Pregnant Rats*

Cited by 23 publications

References 0 publications

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

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

Prolactin Implants in the Hypothalamus Inhibit Prolactin Surges During Pregnancy and Alter Prolactin Release in Response to Dopamine Receptor Blockade

Semicircadian Rhythm of Dopamine Release in the Mediobasal Hypothalamus in Awake Rats during Pseudopregnancy: Evidence that a Thyrotropin-Releasing Hormone Analogue Stimulates Dopamine Release and thereby Inhibits Prolactin Secretion

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