Persistence of Low Hypothalamic Dopaminergic Activity after Removal of Chronic Estrogen Treatment

Gottschall, Paul E.; Sarkar, Dipak K.; Meites, Joseph

doi:10.3181/00379727-181-42227

Cited by 18 publications

(15 citation statements)

References 14 publications

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“…The radioimmunoassay method for PRL, using NIDDK radioimmuno-assay kits, has been previously described (Gottschall et al, 1986). The standard used in this assay was rPRL-RP-3.…”

Section: Radioimmunoassay For Prlmentioning

confidence: 99%

Ethanol and Estradiol Modulate Alternative Splicing of Dopamine D2 Receptor Messenger RNA and Abolish the Inhibitory Action of Bromocriptine on Prolactin Release From the Pituitary Gland

Oomizu

Boyadjieva

Sarkar

2003

Alcoholism Clin & Exp Res

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“…The radioimmunoassay method for PRL, using NIDDK radioimmuno-assay kits, has been previously described (Gottschall et al, 1986). The standard used in this assay was rPRL-RP-3.…”

Section: Radioimmunoassay For Prlmentioning

confidence: 99%

Ethanol and Estradiol Modulate Alternative Splicing of Dopamine D2 Receptor Messenger RNA and Abolish the Inhibitory Action of Bromocriptine on Prolactin Release From the Pituitary Gland

Oomizu

Boyadjieva

Sarkar

2003

Alcoholism Clin & Exp Res

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“…This result directly indicates that the longer the period of estradiol treatment is the smaller the enhance ment of dopamine release from TIDA neurons by estradiol withdrawal becomes. The controversy whether the TIDA neuronal functions are stimulated after the withdrawal of es trogen [9,12,13,28] or inhibited [30,31] might be accounted for by this difference in response of TIDA neurons to estro gen treatment by its duration and dose. The reason why the function of TIDA neurons was unchanged after repetitive in jections even though serum PRL concentrations showed high levels in the absence of estradiol and whether this phe nomenon is specific for F344 rats remain to be investigated.…”

Section: Effects O F Hyperprolactinemia On In Vitro Dopamine Releasementioning

confidence: 99%

Changes in the Function of Tuberoinfundibular Dopaminergic Neurons after Long-Term Estradiol Treatment in Fischer 344 Rats

Ai¹,

Kojima

Kimura³

1990

Neuroendocrinology

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The functions of tuberoinfundibular dopaminergic (ΗDA) neurons after long-term estradiol treatment were investigated in Fischer 344 (F344) rats which have high susceptibility to estradiol-induced prolactin (PRL)-secreting pituitary tumors. Dopamine synthesis in and release from TTDA neurons were determined in vitro by 3,4-dihydroxyphenylalanine (DOPA) accumulation in the median eminence following incubation with a DOPA decarboxylase inhibitor and endogenous dopamine release from the median eminence, respectively. The concentration of serum PRL and the weight of the anterior pituitary in ovariectomized F344 rats were markedly increased 3 weeks after a single injecction of 2 mg estradiol valerate (EV) and decreased thereafter, but still showed higher levels at 15 and 24 weeks than control ovariectomized rats. Dopamine contents in the median eminence were decreased 3 weeks and unchanged 24 weeks after EV treatment. DOPA accumulation and basal dopamine release in the median eminence of F344 rats were decreased 3 weeks and increased 15 and 24 weeks after EV treatment, similarly to those of Wistar rats as reported previously. However, EV treatment, which caused similar increases in the concentrations of serum PRL and estradiol in F344 and Wistar rats, decreased KCl-induced dopamine release in Wistar rats at 3 weeks, but failed to do so in F344 rats. KC1-induced dopamine release 24 weeks after a single EV injection in F344 rats was greater than that in control rats, whereas the dopamine release 24 weeks after the last treatment of 4 injections at 3-week intervals was not different from that in control rats. Sustained high levels of serum PRL for 3 weeks achieved by pituitary transplants under the kidney capsule increased basal and KCl-induced dopamine release in F344 rats. These results suggest that (1) estradiol is less effective in inhibiting KCl-induced release of dopamine from ΗDA neurons in F344 rats, and (2) extension of the period of estradiol treatment suppresses the enhancement of ΗDA function by estradiol withdrawal.

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“…Estrogens stimulate the synthesis and the release of prolactin (PRL) in rats and other species by acting at both adenohypophysis and hypothalamus [1], At the hypotha lamic level, estrogens principally decrease the inhibitory dopaminergic activity [2,3], It has been shown [4] that the arcuate is the most important nucleus in the mediation of estrogen action on the endocrine regulation of the adeno hypophysis. Neurons expressing estrogen receptors are especially abundant in this nucleus [5],…”

Section: Introductionmentioning

confidence: 99%

Participation of Opioid and Serotoninergic Systems in Prolactin Secretion Induced by Hypothalamic Action of Estradiol

Carón

Deis²

1996

Neuroendocrinology

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The aim of the present study was to determine the central effect of estradiol (E₂) on the pattern of secretion of prolactin (PRL) in virgin rats and the participation of opioid and serotoninergic systems in the regulation of this secretion. Bilateral cannulae containing E₂ (group E) or cholesterol (group C) were implanted in the arcuate nucleus on the day of estrus (day 0). Blood samples were obtained at 09.00, 14.00, or 18.00 h on days 1, 3, 6, or 9. All rats were blood sampled once. In group E, the PRL levels at 09.00 h on days 1 and 3 were similar to those from group C. However, higher values were obtained at 14.00 and 18.00 h, thus showing a diurnal rhythm with low levels in the morning and high values during the afternoon. No rhythm in PRL secretion was observed on days 6 and 9 in group E in which serum PRL was similarly increased with respect to group C at all times. The progesterone (P) levels paralleled PRL concentration, being significantly higher in group E at 18.00 h on day 1 at 14.00 and 18.00 h on day 3, and at all three times on days 6 and 9; the P measurements were consistent with luteotropic actions of PRL. Naloxone (NAL; 2 mg/kg i.p.) was injected at 17.30 h on days 3, 6, or 17, and 30 min later the animals were blood sampled. P-Chlorophenylalanine (pCPA; 200 mg/ kg s.c.) was administered at 07.00 h on days 2, 5, or 16, and blood samples were taken 35 h later. Control E rats were injected with vehicle and blood sampled at 18.00 h on days 3, 6, or 17. The PRL increase induced by E₂ at 18.00 h on days 3 and 6 was not modified by pretreatment with NAL or pCPA. Serum P was significantly reduced after pCPA administration on days 3 and 6 and after NAL only on day 6. The increase in PRL at 18.00h on day 17 induced by E₂ was dramatically enhanced by NAL or pCPA, while these treatments did not significantly modify serum P levels. Our results indicate an inhibitory influence from both opioid and serotoninergic systems on PRL secretion induced by the long-term application of E₂ in the arcuate nucleus.

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Persistence of Low Hypothalamic Dopaminergic Activity after Removal of Chronic Estrogen Treatment

Cited by 18 publications

References 14 publications

Ethanol and Estradiol Modulate Alternative Splicing of Dopamine D2 Receptor Messenger RNA and Abolish the Inhibitory Action of Bromocriptine on Prolactin Release From the Pituitary Gland

Ethanol and Estradiol Modulate Alternative Splicing of Dopamine D2 Receptor Messenger RNA and Abolish the Inhibitory Action of Bromocriptine on Prolactin Release From the Pituitary Gland

Changes in the Function of Tuberoinfundibular Dopaminergic Neurons after Long-Term Estradiol Treatment in Fischer 344 Rats

Participation of Opioid and Serotoninergic Systems in Prolactin Secretion Induced by Hypothalamic Action of Estradiol

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