The Effect of Dopamine on Thyrotropin-Releasing Hormone-Induced Prolactin Secretion<i>In VitroM</i>*

Fagin, Katherine D.; Neill, J. D.

doi:10.1210/endo-109-6-1835

Cited by 66 publications

(26 citation statements)

References 30 publications

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“…The molecular basis of these regulatory actions remains to be determined. Nevertheless, it is noteworthy the parallelism between the initial period of Ca 2+ current enhancement and the reported potentiation of the PRL secretory efficacy of TRH after DA removal in various different physiological conditions [6, 7, 37, 38, 39]. Furthermore, these effects were not associated with obvious changes in the time- and voltage-dependent properties of the current, suggesting that the alterations in Ca 2+ current density might depend on changes in the state of phosphorylation of the channels.…”

Section: Discussionmentioning

confidence: 99%

Potentiation of Prolactin Secretion following Lactotrope Escape from Dopamine Action

et al. 1999

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Hypothalamic dopamine (DA) tonically inhibits prolactin (PRL) release from the anterior pituitary gland. Transient escapes from this DA tone elicit a pronounced potentiation of the PRL-releasing action of secretagogues such as thyrotropin-releasing hormone (TRH). Previous evidence has suggested that modulation of Ca²⁺ channels can be involved in this potentiation. With a lactotropic cell line (GH₄C₁) expressing human D₂-DA receptors, we tested the hypothesis that a brief escape from the tonic inhibitory action of DA triggers a facilitation of Ca²⁺ influx through Ca²⁺ channels. We initially found that in these cells, DA effectively and reversibly inhibited PRL secretion, and reversibly enhanced an inwardly rectifying K⁺ current. The effects of DA administration and withdrawal on Ca²⁺ currents were examined using the patch-clamp technique in the whole-cell configuration and Ba²⁺ as a divalent charge carrier through Ca²⁺ channels. Macroscopic Ba²⁺ currents were significantly decreased by short term (1–10 min) applications of DA (500 nM), which further declined following 24 h of constant exposure to DA. After DA removal, a biphasic facilitation of the density of Ba²⁺ currents was observed. An initial 2-fold enhancement of conductance was detected between 10 and 40 min, followed by a second facilitation of the same magnitude observed 24 h after DA withdrawal. The present results directly demonstrate that dissociation of DA from D₂-receptors expressed in GH₄C₁ lactotrope cells causes an increase of high-voltage-activated Ca²⁺ channel function, which may play an important role in the cross-talking amplification of endocrine cascades such as that involved in the TRH-induced PRL-release potentiating action of DA withdrawal.

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Section: Discussionmentioning

confidence: 99%

Potentiation of Prolactin Secretion following Lactotrope Escape from Dopamine Action

et al. 1999

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“…Failure of NMDA to stimulate PRL secretion after blockade of dopaminergic receptors with domperidone suggests that, in the absence of dopaminergic inhibition, the stimulatory effect of PRFs were masked and further increases in serum PRL concentrations could not be detected. Alternatively, the effects of PRFs might require a certain degree of dopaminergic inhibition, as the stimulatory effects of serotonin, thyrotrophin-releasing hormone or vasoactive intestinal polypeptide on PRL release were not detected in absence of dopaminergic inhibition (27)(28)(29)(30).…”

Section: Discussionmentioning

confidence: 99%

Effects of N-methyl-D-aspartic acid and kainic acid on prolactin secretion in hyper- and hypoprolactinaemic conditions

Pinilla

Tena‐Sempere

Aguilar

et al. 1998

European Journal of Endocrinology

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Objective: The stimulatory and inhibitory effects of N-methyl-D-aspartic acid (NMDA) and kainic acid on prolactin (PRL) secretion have been correlated with the serum prolactin concentrations before drug administration. In the present experiments, we analysed the role of NMDA and kainic acid in PRL secretion in females with different serum concentrations of PRL. Methods: Hypoprolactinaemic females were obtained by ovariectomy or after administration of diethyldithiocarbamate (an inhibitor of dopamine-b-hydroxylase). Chronic hyperprolactinaemia was induced by neonatal administration of testosterone or oestradiol and acute hyperprolactinaemia was induced either by administration of a-methyl-p-tyrosine (an inhibitor of tyrosine hydroxylase) or by ether exposure. To analyse the role of dopamine in the effects of NMDA, we measured pituitary concentrations of dopamine after NMDA treatment and the effects of pretreatment with domperidone. Results: (1) NMDA, but not kainic acid, stimulated PRL release in cyclic females. This effect was independent of serum PRL concentrations and was not accompanied by a decrease in pituitary concentrations of dopamine. (2) NMDA did not change PRL secretion in neonatally androgenized females, whereas NMDA and kainic acid inhibited PRL release in neonatally oestrogenized females. The inhibitory effects of NMDA and kainic acid were blocked by domperidone. (3) Kainic acid inhibited PRL secretion in prepubertal hyper-and hypoprolactinaemic rats. (4) Hyperprolactinaemia induced by ether stress was counteracted by administration of NMDA and kainic acid. Conclusions: (a) NMDA has a dual effect on prolactin secretion that is independent of prior prolactin concentrations and of dopamine activity, but kainic acid is only inhibitory. (b) The stimulatory or inhibitory effects of NMDA and kainic acid on PRL secretion were not strictly related to basal PRL concentrations and necessarily involved a change in the secretion of prolactin releasing factors, as no correlations were observed between changes in pituitary concentrations of dopamine and serum PRL concentrations. (c) Females rendered hyperprolactinaemic by neonatal administration of testosterone or oestradiol responded differently after NMDA administration. (d) NMDA and kainic acid blocked the mechanisms involved in stress-induced PRL secretion.

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“…These data are in line with results from experiments in male rats showing that pretreatment with -methyl-p-tyrosine (an inhibitor of DA biosynthesis) blocked the inhibitory effect of AMPA on PRL secretion (our unpublished results), and with our previous data showing that in prepubertal females activation of NMDA and KA receptors increased dopamine release, which in turn reduced prolactin secretion (Pinilla et al 1996b(Pinilla et al , 1998. However, it has to be considered that, in our experimental model, removal of dopaminergic regulation resulted in a dramatic increase in PRL secretion, and thus the possibility remains that activation of AMPA receptors resulted, in addition, in decreased secretion of PRFs such as vasointestinal peptide, thyrotropin-releasing hormone or the newly characterized PRL-releasing peptide (Kato et al 1978, Fagin & Neill 1981, Hinuma et al 1998. Assessment of the effects of AMPA on secretion of PRL-inhibitory and -stimulatory factors will shed further light on this matter.…”

Section: Discussionmentioning

confidence: 80%

Role of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptors in the control of prolactin, growth hormone and gonadotropin secretion in prepubertal rats

Gonzalez

Pinilla²,

Tena‐Sempere³

et al. 1999

Journal of Endocrinology

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Excitatory amino acids, such as glutamate, constitute a major transmitter system in the control of hypothalamicpituitary secretion. Different subtypes of glutamate receptors, such as NMDA (N-methyl--aspartic acid) and KA (kainate) receptors, are involved in the control of anterior pituitary secretion. Other receptor subtypes, such as AMPA (activated by -amino-3-hydroxy-5-methylisoxazole-4-propionic acid) and metabotropic receptors, have been identified, although their role in the control of neuroendocrine function remains largely unknown. Recent reports have demonstrated the involvement of AMPA receptors in the control of the steroidinduced luteinizing hormone (LH) surge in female and growth hormone (GH) secretion in male rats. The aim of this study was to assess the potential role of AMPA receptors in the control of GH, prolactin (PRL), LH and follicle-stimulating hormone (FSH) secretion in prepubertal 23-day-old rats. To this end, prepubertal female rats were injected with AMPA (2·5 or 5 mg/kg i.p.) or the antagonist of AMPA receptors 1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-benzo (f ) quinoxaline-7-sulfonamide (NBQX; 0·25 or 0·50 mg/kg i.p.). Serum LH and FSH concentrations and hypothalamic LH-releasing hormone (LHRH) content remained unchanged after AMPA or NBQX administration. In contrast, serum PRL levels significantly decreased 15, 30 and 60 min after i.p. administration of AMPA and increased 120 min after NBQX treatment, whereas serum GH levels increased after AMPA treatment and decreased after NBQX administration. Considering that AMPA has been shown to activate a subset of kainate receptors, its effects were compared with those elicited by 2·5 mg/kg KA in prepubertal female rats. At this age, however, KA was unable to reproduce the effects of AMPA on PRL and GH secretion, thus suggesting that the actions observed after AMPA administration were carried out specifically through AMPA receptors. In addition, as the effects of AMPA on LH secretion in adult females have been proved to be steroid-dependent, the effects of AMPA (2·5 mg/kg) and NBQX (0·5 mg/kg) were tested in prepubertal animals with different gonadal backgrounds, i.e. intact males, and intact and ovariectomized (OVX) females. The effects of AMPA in prepubertal females appeared to be modulated by ovarian secretion, as the inhibition of PRL secretion disappeared and LH secretion was partially suppressed by AMPA in OVX animals whereas the stimulatory effect on GH release was enhanced by ovariectomy. Furthermore, in male rats, AMPA administration significantly decreased PRL secretion and increased serum GH levels, the amplitude of the GH response being higher than in prepubertal females. To ascertain the pituitary component for the reported actions of AMPA, hemi-pituitaries of male rats were incubated in the presence of AMPA (10 8 -10 6 M). The results obtained showed no effect of AMPA on PRL, GH and gonadotropin secretion in vitro. Finally, we investigated the involvement of the dopaminergic (DA) system in the inhibitory action of AMPA on PR...

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The Effect of Dopamine on Thyrotropin-Releasing Hormone-Induced Prolactin SecretionIn VitroM*

Cited by 66 publications

References 30 publications

Potentiation of Prolactin Secretion following Lactotrope Escape from Dopamine Action

Potentiation of Prolactin Secretion following Lactotrope Escape from Dopamine Action

Effects of N-methyl-D-aspartic acid and kainic acid on prolactin secretion in hyper- and hypoprolactinaemic conditions

Role of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptors in the control of prolactin, growth hormone and gonadotropin secretion in prepubertal rats

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