Hyperprolactinemia Increases and Hypoprolactinemia Decreases Tyrosine Hydroxylase Messenger Ribonucleic Acid Levels in the Arcuate Nuclei, but not the Substantia Nigra or Zona Incerta*

Arbogast, Lydia A.; Voogt, James L.

doi:10.1210/endo-128-2-997

Cited by 126 publications

(70 citation statements)

References 42 publications

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“…This boosting of dopamine tone in turn leads to enhanced dopamine receptor D 2 Rmediated inhibition of the lactotroph, halting Prl release from the pituitary. It has been shown previously that Prl stimulates activity (Arbogast and Voogt, 1995) and transcription (Arbogast and Voogt, 1991;Selmanoff et al, 1991) of TH, which would increase the stores of dopamine available for release. Combined, these effects provide powerful mechanisms for Prl autoinhibition.…”

Section: Discussionmentioning

confidence: 93%

Prolactin Regulates Tuberoinfundibular Dopamine Neuron Discharge Pattern: Novel Feedback Control Mechanisms in the Lactotrophic Axis

Lyons

Hellysaz²,

Broberger³

2012

Journal of Neuroscience

127

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Balance in the body's hormonal axes depends on feedback onto neuroendocrine hypothalamic neurons. This phenomenon involves transcriptional and biosynthetic effects, yet less is known about the potential rapid modulation of electrical properties. Here, we investigated this issue in the lactotrophic axis, in which the pituitary hormone prolactin is tonically inhibited by tuberoinfundibular dopamine (TIDA) neurons located in the hypothalamic arcuate nucleus. Whole-cell recordings were performed on slices of the rat hypothalamus. In the presence of prolactin, spontaneously oscillating TIDA cells depolarized, switched from phasic to tonic discharge, and exhibited broadened action potentials. The underlying prolactin-induced current is composed of separate low-and high-voltage components that include the activation of a transient receptor potential-like current and the inhibition of a Ca 2ϩ -dependent BK-type K ϩ current, respectively, as revealed by ion substitution experiments and pharmacological manipulation. The two components of the prolactin-induced current appear to be mediated through distinct signaling pathways as the high-voltage component is abolished by the phosphoinositide 3-kinase blocker wortmannin, whereas the low-voltage component is not. This first description of the central electrophysiological actions of prolactin suggests a novel feedback mechanism. By simultaneously enhancing the discharge and spike duration of TIDA cells, increased serum prolactin can promote dopamine release to limit its own secretion with implications for the control of lactation, sexual libido, fertility, and body weight.

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Section: Discussionmentioning

confidence: 93%

Prolactin Regulates Tuberoinfundibular Dopamine Neuron Discharge Pattern: Novel Feedback Control Mechanisms in the Lactotrophic Axis

Lyons

Hellysaz²,

Broberger³

2012

Journal of Neuroscience

127

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“…This result shows that the increase in TH activity was not due to E, per se but rather mediated by the E,-induced PRL elevation. PRL is indeed known to increase TH activity and TH mRNA levels selectively in TIDA neurons (23), DA synthesis (24) and turnover (10, [25][26][27] in the terminals of TIDA neurons as well as DA release into hypophysial portal blood (28) and from isolated hypothalamic nerve endings (29). The present data shed light on the importance of determining serum PRL levels when studying E2 effects on TIDA neurons.…”

Section: Discussionmentioning

confidence: 57%

Inhibitory Actions of Acute Estradiol Treatment on the Activity and Quantity of Tyrosine Hydroxylase in the Median Eminence of Ovariectomized Rats

Pasqualini

Leviel

Guibert

et al. 1991

J Neuroendocrinology

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The effects of acute estradiol (E2) treatment on both t h e activity of tyrosine hydroxylase (TH) in t h e median eminence and t h e serum level of prolactin (PRL) were investigated. Twelve-day-ovariectornized rats were injected with li'P-E, (25 pg sc) a t 1100 h and sacrificed hourly from 1200 to 2300 h. TH activity was quantified by measuring the amount of exogenous tyrosine converted to L-DOPA in vitro by aliquots of median eminence homogenates. Serum PRL levels were evaluated by radioimmunoassay. A biphasic response of TH activity to treatment was observed: an immediate decrease occurred-preceding and accompanying a rise in serum PRL-followed by an increase beyond control levels 2 h after the maximal release of PRL. The increase in TH activity could be prevented by the pretreatment of rats with a specific rat PRL antiserum, suggesting it was not due to E, per se but rather mediated by the E,-induced PRL elevation. To pin-point the process underlying the E,-induced decrease in TH activity, we evaluated the kinetic parameters of TH in t h e median eminence as well as its quantity (by Western blot analysis) in t h e median eminence and arcuate nucleus. Finally, we used a sensitive dot-blot assay to quantify specific TH messenger ribonucleic acid in the arcuate nucleus. The decrease in TH activity after E, treatment paralleled an immediate decrease in t h e affinity of TH for its pterin cofactor (6-MPH4), while V , , , remained unchanged. A decrease in the amount of TH protein in the arcuate nucleus and median eminence as well as in the TH messenger ribonucleic acid level in the arcuate nucleus was also observed, but the latency of these effects precluded a major involvement in the immediate decline of TH activity. Therefore, when observed separately from those of PRL, E, effects on TH in tuberoinfundibular dopaminergic neurons are clearly inhibitory consisting of a 'deactivation' of the enzyme together with a reduction of its synthesis. Tuberoinfundibular dopaminergic (TIDA) neurons with cell bodies in the arcuate nucleus (AN) and nerve terminals in the median eminence (ME) exert a tonic inhibitory influence on pituitary prolactin (PRL) secretion. It is known that these cells are estradiol (E2) targets (I), however the nature and mechanism(s) of the steroid actions on TIDA neurons are still controversial: long-term ( 2 to 3 weeks) treatment with E2 is invariably reported to result in a decrease in the concentration and synthesis of dopamine (DA) in the M E (2-7). In contrast, 'intermediateterm' (3 to 5 days) treatment has been reported to increase the activity of TIDA neurons, as revealed by an increase in the rate of synthesis (8) and turnover (9-12) of DA in the M E and a rise in its concentration in hypophysial portal blood (1 3). However, the activation of TIDA neurons seems not to be due to a direct action of the steroid per se but rather to be mediated by PRL whose secretion is increased by E2 (8, 10). On the other hand, recent studies (14) showed that 3 days of estrogen treatment had no effect in...

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“…16]. The content of DOPA in the supernatant was determined by HPLC with electrochemical detection (ECD) [1,15]. The pellet was analyzed for protein content by the method of Bradford [2].…”

Section: Methodsmentioning

confidence: 99%

The Different Effects of I.c.v. Injection of Pituitary Adenylate Cyclase Activating Polypeptide (PACAP) on Prolactin Secretion in Adult Male and Lactating Rats

et al. 2009

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The effects of intracerebroventricular (i.c.v.) administration of pituitary adenylate cyclase activating polypeptide38 (PACAP38) on prolactin (PRL) secretion and the activity of tyrosine hydroxylase (TH) were examined in adult male and lactating rats with or without suckling stimulus. In adult male rats and lactating rats with suckling stimulus, administration of PACAP38 (0.25 or 1 nmol) decreased PRL secretion and increased the activity of TH in the stalk-median eminence. On the other hand, the injection of PACAP38 did not affect PRL secretion and TH activity in lactating rats without sucking stimulus. Administration of PACAP6-38 (4 nmol), a specific receptor antagonist, also had no effect on PRL secretion and TH activity in adult male rats. These results suggest that i.c.v. administration of PACAP inhibits PRL secretion mediated by dopamine neuron within the hypothalamus, but the effects of PACAP differ depending on the physiological condition of animals. These observed effects of PACAP on PRL release may be pharmacological responses rather than physiological responses.

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Hyperprolactinemia Increases and Hypoprolactinemia Decreases Tyrosine Hydroxylase Messenger Ribonucleic Acid Levels in the Arcuate Nuclei, but not the Substantia Nigra or Zona Incerta*

Cited by 126 publications

References 42 publications

Prolactin Regulates Tuberoinfundibular Dopamine Neuron Discharge Pattern: Novel Feedback Control Mechanisms in the Lactotrophic Axis

Prolactin Regulates Tuberoinfundibular Dopamine Neuron Discharge Pattern: Novel Feedback Control Mechanisms in the Lactotrophic Axis

Inhibitory Actions of Acute Estradiol Treatment on the Activity and Quantity of Tyrosine Hydroxylase in the Median Eminence of Ovariectomized Rats

The Different Effects of I.c.v. Injection of Pituitary Adenylate Cyclase Activating Polypeptide (PACAP) on Prolactin Secretion in Adult Male and Lactating Rats

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