Differential Alterations in Dopamine Turnover Rates in the Stalk-Median Eminence and Posterior Pituitary during the Preovulatory Prolactin Surge

Changes in the concentrations of dopamine (DA) and its major metabolite, 3,4-dihydroxyphenylacetic acid (DOPAC), were characterized in the pituitary gland throughout the 4-day estrous cycle of the rat. Female rats were sacrificed at 2- to 3-hour intervals throughout each day of the 4-day estrous cycle. Pituitary glands were removed, and the concentrations of DA and DOPAC were determined by high-performance liquid chromatography coupled to electrochemical detection. The concentration of prolactin (PRL) in serum from these same animals was determined by radioimmunoassay. The concentration of DA in the anterior lobe was constant throughout most of the 4-day estrous cycle. Prior to initiation of the proestrous surge of PRL, there were significant (p <0.05) decreases in the concentrations of both DA and DOPAC in the anterior lobe which returned to elevated baseline levels just prior to the termination of the proestrous surge of PRL. The concentrations of DA and DOPAC in the intermediate lobe exhibited a daily rhythm. However, in the intermediate as well as in the anterior lobe, there were significant (p < 0.001) decreases in the concentrations of both DA and DOPAC, coincident with the initiation of the proestrous surge of PRL. Similarly, coincident with the peak of the proestrous surge of PRL, there were significant (p < 0.001) increases in the concentrations of DA and DOPAC in the intermediate lobe, followed by a return to basal levels and resumption of the daily rhythm. The pattern of the concentrations of DA and DOPAC in the neural lobe was also daily in nature, with peaks occurring between 13.00 and 15.00 h each day of the 4-day estrous cycle. These data, taken together: (1) confirm that a decrease of the concentrations of DA and DOPAC occurs in the anterior lobe prior to the proestrous surge of PRL; (2) reveal that DA is released in a daily pattern at intermediate and neural lobes, and (3) suggest an apparent role for DA released to the intermediate lobe in the regulation of the proestrous surge of PRL.

Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Characterization of the Dopaminergic Input to the Pituitary Gland throughout the Estrous Cycle of the Rat

DeMaria

Livingstone²,

Freeman³

1998

“…The short-term inhibitory effect of progesterone on TIDA neuronal activity appears to be physiologically relevant during the late afternoon and evening of proestrus, when a dopaminergic mechanism prolongs the preovulatory PRL surge [2, 5]. Dopamine turnover rates, TH activity and TH mRNA signal levels are suppressed during the preovulatory period [3, 6, 7, 8]. Acute ovariectomy on proestrous morning prevents the decline in TH activity and TH mRNA levels and progesterone, but not estradiol replacement at the appropriate time restores the decrease in TH function [3, 8].…”

Section: Introductionmentioning

confidence: 99%

Progesterone Induces Dephosphorylation and Inactivation of Tyrosine Hydroxylase in Rat Hypothalamic Dopaminergic Neurons

Arbogast

Voogt²

2002

Self Cite

After in vivo treatment, progesterone initially decreases tyrosine hydroxylase (TH) activity in the TIDA neurons, but subsequently increases TH activity with prolonged treatment. In order to explore the cellular mechanism for progesterone’s effect, this study examined the acute inhibitory action of progesterone on TH activity in rat fetal hypothalamic dopaminergic neurons in vitro. Progesterone caused a rapid decrease in TH activity within 1 h, which was sustained for at least 6 h. However, the dopaminergic cells became refractory to progesterone with continuous treatment for 12 h to 10 days. Progesterone (10–100 nM) treatment suppressed TH activity in a concentration-dependent manner. The inhibitory effect of progesterone was dependent on prior exposure to estradiol. Whereas progesterone decreased TH activity, A ring-reduced metabolites of progesterone did not alter TH activity, suggesting that the response was specific to progesterone. Progesterone decreased radiolabeled phosphate incorporation into TH protein. Okadaic acid, a phosphoprotein phosphatase inhibitor, prevented the progesterone-induced suppression of TH activity and phosphate incorporation into TH, implicating dephosphorylation of TH as the cellular mechanism. In contrast, neither TH mRNA levels nor TH protein content was altered after 1 or 12 h of progesterone treatment. Progesterone decreased TH activity after pretreatment of the hypothalamic cells for 2 or 24 h with actinomycin D, an RNA synthesis inhibitor, suggesting that increased transcription does not mediate the effect. These data indicate that the acute progesterone-induced decline in TH activity is caused by dephosphorylation of TH.

“…The PP was gently separated from the anterior pituitary, and the SME was dissected out under a microscope as described previously [25]. Individual tissues were enveloped by a fine, stainless steel mesh (No.…”

Section: Tissue Preparationmentioning

confidence: 99%

“…Catecholamines were determined by reverse-phase high-performance chromatography with electrochemical detection as described previously [25], with some modifications. The buffer con sisted o f 30 m M citric acid, 50 m M dibasic sodium phosphate, 0 .1 mM EDTA, 1.4 mM sodium octyl sulfate, and 12% methanol, a ta pH o f2 .5.…”

Section: Catecholamine Determinationmentioning

confidence: 99%

Regulation of Dopamine Release in vitro from the Posterior Pituitary by Opioid Peptides

Garris¹,

Ben‐Jonathan²

1990

Self Cite

Opioid peptides are present in both the posterior pituitary (PP) and stalk-median eminence (SME). Their effects on the dopaminergic neurons in the SME are well documented, but little is known concerning their role in the regulation of dopamine (DA) release from the PP. The objectives of this study were (1) to develop an in vitro method suitable for examining the regulation of endogenous DA release from PP and SME, and (2) to describe and compare the effects of selected opioid peptides on potassium-evoked DA release from these tissues. Tissues were dissected from ovariectomized rats and incubated in media. After equilibration, two pulses of 28 mM potassium (K⁺), 3 min each, were delivered 30 min apart. Test substances were administered 20 min before the second K⁺ stimulus. DA in the media was determined by high-performance liquid chromatography. Potassium at 28 and 56 mM elicited a marked increase in DA release from the PP and SME; this was abolished by the removal of calcium. The opioid receptor antagonist, naloxone, significantly increased the release of DA from both PP and SME by 55%. Dynorphin A elicited a significant inhibition of DA release from PP and SME by 33 and 50%, respectively. In contrast, methionine enkephalinamide decreased DA release from the SME by 50%, but was without effect in the PP. The release of DA from both PP and SME was significantly inhibited by β-endorphin, and this was reversed by naloxone. However, β-endorphin was fourfold more effective in the SME. N-acetyl-β-endorphin did not alter DA release. Conclusions: (1) we have developed a simple and sensitive in vitro method for studying the effects of hormones and drugs on the release of endogenous DA from PP and SME; (2) tuberoinfundibular dopaminergic and tuberohypophyseal dopaminergic nerve terminals are subjected to a similar inhibitory control by endogenous opioid peptides, and (3) exogenously applied opioid peptides exert differential effects on the release of DA from SME and PP which could be attributable to a dissimilar distribution of opioid receptor subtypes in these two tissues.