Central Inhibitory Action of TRH on Prolactin Secretion in the Rat

Ohta, Hikaru; Kato, Yuzuru; Matsushita, Norio; Shimatsu, Akira; Kabayama, Yasuhiro; Imura, Hiroo

doi:10.3181/00379727-179-42056

Cited by 15 publications

(10 citation statements)

References 10 publications

(12 reference statements)

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“…Similarly, NPY has been shown to have effects on LH release in vitro that are dependent on gonadal steroid milieu (23,24). The opposite effects of orexin A on the HPG at the pituitary and hypothalamus are not unusual and have been reported for other peptides (25). We were unable to detect orexin A peptide in whole pituitaries using our RIA, which would be expected if orexin The effect of estrous cycle stage on orexin A content of different brain regions.…”

Section: Discussionmentioning

confidence: 67%

Orexin A Interactions in the Hypothalamo-Pituitary Gonadal Axis

et al. 2001

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The distribution of orexin A-immunoreactive neurons and orexin type I receptors in the CNS suggests important roles in regulating the hypothalamo-pituitary gonadal (HPG) axis and sexual behaviors. We examined orexin A interactions in the HPG axis in vivo and in vitro.Orexin A stimulated LH-releasing hormone (LHRH) release in hypothalamic explants harvested from male rats (؉133%) and from females at proestrus (؉233%), with no effect at estrus or metestrus. Orexin A dose dependently inhibited LHRH-stimulated LH release in dispersed pituitaries from proestrous females only. A selective NPY1-receptor antagonist abolished in vitro release of LHRH by orexin A. Hyperestrogenization in female rats reduced orexin A content in hypothalamus (؊28%), midbrain (؊26%), medulla (؊40%), thalamus (؊36%), olfactory tubercles (؊25%), and cortex (؊35%), brain regions that are important in HPG control and sex-cycle specific behaviors. Orexin A content was lower in hypothalamus (؊20%) and higher in midbrain (؉40%), medulla (؉31%), and thalamus (؉33%) at late proestrus vs. other cycle stages. Orexin A release after administration of 56 mM KCl was significantly greater in hypothalamic explants harvested on the morning of proestrus than at estrus or metestrus, and orexin A release was stimulated by estradiol (E2) in explants from males. These results reveal important interactions for orexin A in the HPG axis. (Endocrinology 142: -5302, 2001)O REXIN A, ALSO known as hypocretin-1, is a 33-amino acid peptide synthesized almost exclusively in the posterolateral hypothalamus (1). Orexin A immunoreactive fibers project to a number of CNS sites involved in hypothalamopituitary gonadal (HPG) axis control. Within the hypothalamus, orexin A immunoreactive fibers project to the septal preoptic and arcuate nucleus median eminence region (2, 3). These areas are directly involved in the control of the HPG axis via LH-releasing hormone (LHRH) neuronal projections to the median eminence (4). Orexin A immunoreactive neurons also project to the medulla and midbrain dorsal raphe and the pontine locus coeruleus (2, 3). These areas are involved in the control of the HPG through noradrenergic, adrenergic, and serotoninergic projections to the preoptic hypothalamus and via the paraventricular hypothalamus (4, 5). Orexin A immunoreactive neurons and LHRH neurons project to areas that are important in the control of sexual behavior, including the amygdala, olfactory bulbs, and central gray matter (4). Furthermore, the orexin receptor (type 1) is expressed in the medial preoptic area and at high levels in the monoaminergic locus coeruleus and dorsal/median raphe (6). The distribution of orexin A immunoreactive neurons and orexin type I receptors suggest potentially important roles in the regulation of the HPG axis and sexual behaviors.Previous studies have shown that injection of orexin A into the lateral cerebral ventricle stimulates plasma LH in ovariectomized (OVEX) steroid-replaced rats (7). By contrast, orexin A inhibits plasma LH when injected into the later...

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Section: Discussionmentioning

confidence: 67%

Orexin A Interactions in the Hypothalamo-Pituitary Gonadal Axis

et al. 2001

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“…In this paper an unpublished observation reportedly showed that hypothalamic extracts containing TRH altered the content of hypothalamic TRH when injected systemically into hypophysectomized-thyroidectomized animals. More recently intraventricular injections ofTRH were shown to inhibit prolac tin secretion from the anterior pituitary [2]. Since the hypotha lamic paraventricular nucleus (PVN) contains a moderately dense number ofTRH receptors [3], these actions could occur by direct effects of TRH on TRH paraventricular neurons through synaptic associations or indirectly through another chemical mediator.…”

mentioning

confidence: 99%

Thyrotropin-Releasing-Hormone-Immunoreactive Innervation of Thyrotropin-Releasing-Hormone-Tuberoinfundibular Neurons in Rat Hypothalamus: Anatomical Basis to Suggest Ultrashort Feedback Regulation

Toni

Jackson²,

Lechan³

1990

Neuroendocrinology

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Thyrotropin-releasing-hormone (TRH)-synthesizing neurons in the medial and periventricular parvocellular subdivisions of the rat hypothalamic paraventricular nucleus (PVN) are involved in regulation of the anterior pituitary. Since ultrashort feedback regulation of TRH in the hypothalamus has been suggested by physiological studies, we sought to identify the presence of TRH synaptic contacts containing TRH on TRH tuberoinfundibular neurons in the PVN. An immunocytochemical study was performed at light- and electron-microscopic levels using antiserum directed to the N-terminal cryptic sequence of the TRH precursor, preproTRH 25–50. At the light-microscopic level, contacts between TRH immunoreactive (IR) fibers and the perikarya and processes of TRH-IR neurons were observed in medial and periventricular subdivisions of the PVN. At the ultrastructural level, TRH-neurons appeared either tightly juxtaposed to TRH-immunopositive perikarya and dendrites or to establish axodendritic and axosomatic contacts suggestive of synaptic associations. These data provide a morphologic basis to support a neuroendocrine role for TRH or processed forms of proTRH in the PVN and in particular suggest their involvement as neuromodulators in an ultrashort feedback regulation of TRH tuberoinfundibular neurons.

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“…TRH does not stimulate but rather suppresses the PRL secretion [11][12][13]16]. Our experiments using the TRH analogue, CG 3703, supply strong evidence for the hypothesis that the inhibitory effect of TRH was me diated via a stimulatory effect of the drug on TIDA neu rons; the TRH analogue dose-dependentlv stimulated the extracellular DA levels in the MBH and postponed the PRL surge in a corresponding manner.…”

Section: Trh Effects On Da and Prlmentioning

confidence: 59%

“…The cell bodies of the TRH neurons are located in discrete areas of the paraventricular nucleus and their fibers project to the neurovascular zone of the ME [10]. Recently, however, evidence has been obtained that TRH, under certain conditions, suppresses rather than promotes the PRL synthesis and secretion [11][12][13], In our laboratory we studied the effects of TRH and the TRH analogue CG 3703 (6-methyl-5-oxothio-morpholinyl-3-carbonyl-His-ProNHs) on plasma PRL levels in pseudo pregnant (PSP) rats, which under standard lighting condi tions (i.e. lights off at 18.00 until 6.00 h) generate two peaks of PRL daily for 10 days; a diurnal peak between 13.00 and 18.00 h and a nocturnal peak between 1.00 and 12.00 h, with an interphase between 18.00 and 1.00 h, during which the PRL levels in the blood are low [14,15], Both TRH and CG 3703 were able to postpone the noc turnal PRL surge [13.…”

Section: Introductionmentioning

confidence: 98%

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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Central Inhibitory Action of TRH on Prolactin Secretion in the Rat

Cited by 15 publications

References 10 publications

Orexin A Interactions in the Hypothalamo-Pituitary Gonadal Axis

Orexin A Interactions in the Hypothalamo-Pituitary Gonadal Axis

Thyrotropin-Releasing-Hormone-Immunoreactive Innervation of Thyrotropin-Releasing-Hormone-Tuberoinfundibular Neurons in Rat Hypothalamus: Anatomical Basis to Suggest Ultrashort Feedback Regulation

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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