Neurochemical Evidence that Estrogen-Induced Suppression of Kappa-Opioid-Receptor-Mediated Regulation of Tuberoinfundibular Dopaminergic Neurons Is Prolactin-lndependent

Wagner, Edward J.; Manzanares, Jorge; Moore, Kenneth E.; Lookingland, Keith J.

doi:10.1159/000126659

Cited by 24 publications

(11 citation statements)

References 18 publications

(26 reference statements)

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“…This is in keeping with myriad other pivotal roles of the steroid in regulating hypothalamic function. Estrogen positively modulates NMDA and negatively modulates ĸ-opioid receptor-mediated regulation of A 12 dopamine neurons [14, 15]. Estrogen also uncouples µ-opioid and GABA B receptors from their effector K + channels in ARC POMC neurons [16, 17].…”

Section: Discussionmentioning

confidence: 99%

“…In the ARC, over 50% of the neurons co-express α-amino-3-hydroxy-5-methyl-4-isoxazole-proprionate (AMPA) and estrogen receptors, and estrogen upregulates the expression of these ionotropic glutamate receptors [13]. In addition, estrogen modulates N-methyl- D -aspartate (NMDA) and ĸ-opioid receptor-mediated regulation of A 12 dopamine neuronal activity [14, 15]. Furthermore, estrogen attenuates the coupling of metabotropic µ-opioid and γ-aminobutyric acid (GABA) B receptors to their effector K + channels in ARC POMC neurons [16, 17], which is instrumental in the negative feedback effects of the steroid on the reproductive axis [18, 19], and also exerts a permissive influence on the ability of cannabinoids to alter POMC gene expression [20].…”

Section: Introductionmentioning

confidence: 99%

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Estrogen Differentially Modulates the Cannabinoid- Induced Presynaptic Inhibition of Amino Acid Neurotransmission in Proopiomelanocortin Neurons of the Arcuate Nucleus

Nguyen¹,

Wagner²

2006

Neuroendocrinology

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The present study sought to determine whether cannabinoids inhibit glutamatergic and GABAergic synaptic input onto neurons of the hypothalamic arcuate nucleus (ARC), and whether estrogen modulates this process. Whole-cell patch clamp recordings were performed in hypothalamic slices prepared from ovariectomized female guinea pigs. CB1 receptor activation reduced the amplitude of excitatory postsynaptic currents (EPSCs) evoked by electrical stimulation that were sensitive to ionotropic glutamate receptor antagonists. The CB1 receptor antagonist AM251 increased evoked EPSC (eEPSC) amplitude, and reversed the agonist-induced decrease. CB1 receptor activation similarly decreased the amplitude of evoked inhibitory postsynaptic currents (eIPSCs). The cannabinoid-induced reduction in eEPSC and eIPSC amplitude correlated with a decrease in the frequency of miniature EPSCs (mEPSCs) and IPSCs (mIPSCs) that were abolished by ionotropic glutamate and GABA_A receptor antagonists, respectively. AM251 increased mEPSC frequency, and antagonized the agonist-induced decrease. Compared to neurons obtained from vehicle-treated controls, estradiol benzoate (25 µg; s.c.) given 24 h prior to experimentation increased mEPSC frequency, and markedly decreased the potency of CB1 receptor agonists to decrease mEPSC frequency. Conversely, the steroid potentiated the cannabinoid-induced decrease in mIPSC frequency. These effects were observed in neurons subsequently identified as proopiomelanocortin (POMC) neurons. These data reveal that ARC neurons, including POMC neurons, receive glutamatergic and GABAergic synaptic inputs that are presynaptically inhibited by cannabinoids, and differentially modulated by estrogen. These opposing effects of estrogen on the cannabinoid regulation of amino acid neurotransmission excite POMC neurons, and lend additional insight into the mechanisms underlying estrogen-induced anorexia and negative feedback of the reproductive axis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Estrogen Differentially Modulates the Cannabinoid- Induced Presynaptic Inhibition of Amino Acid Neurotransmission in Proopiomelanocortin Neurons of the Arcuate Nucleus

Nguyen¹,

Wagner²

2006

Neuroendocrinology

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“…On the other hand, estrogens have been shown to inhibit adrenergic tone depending on the basal estrogenic levels of the subject [23][24][25]. Estrogens have also been shown to increase opioidergic tone [26] and to affect the serotonergic [27] and GABA-ergic [28] systems. This last effect would agree with the GABA-ergic theory of PMS [11].…”

Section: Discussionmentioning

confidence: 99%

Lack of Plasma Norepinephrine Cyclicity, Increased Estradiol during the Follicular Phase, and of Progesterone and Gonadotrophins at Ovulation in Women with Premenstrual Syndrome

et al. 2004

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In healthy women, plasma norepinephrine (NE) has a cycle with the highest levels occurring at ovulation and early luteal phase. We examined plasma NE cyclicity in premenstrual syndrome (PMS) patients as compared to controls, its relation to estradiol (E₂), progesterone (P), luteinizing hormone and follicle-stimulating hormone, and the correlation of these parameters with the PMS symptoms. Lack of NE cyclicity was observed in PMS patients. In controls, peak NE levels occurred at ovulation and early luteal phase. In PMS, serum E₂ was higher during the follicular phase, while P and gonadotrophins were higher especially at ovulation and the luteal phase. In the late luteal phase, E₂ levels were lower in PMS patients than in controls. A negative correlation was observed between the area under the curve for E₂ in the luteal phase and PMS somatic and mental scores. Plasma NE showed a negative correlation with abrupt mood swings, impatience, nervousness, tiredness, weakness, apathy, and headache. These data suggest that lack of NE cyclicity characterizes PMS, some symptoms being related to low E₂ levels during the late luteal phase and decreased noradrenergic activity at ovulation and the luteal phase.

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“…The κ ‐opioid receptor mediated increase in prolactin secretion is thought to involve TIDA neuronal inhibition because U50 488 decreases TIDA neuronal activity and norBNI reverses the effect in males and females (46). Moreover, norBNI increases TIDA neuronal activity in ovariectomized rats (47). These studies support our findings that prolactin secretion during pregnancy and lactation is enhanced by opioid‐mediated inhibition of TIDA neurones acting at κ ‐opioid receptor.…”

Section: Discussionmentioning

confidence: 99%

Opioid Receptor Subtypes Involved in the Regulation of Prolactin Secretion During Pregnancy and Lactation

Andrews

Grattan

2003

J Neuroendocrinology

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Afferent endogenous opioid neuronal systems facilitate prolactin secretion in a number of physiological conditions including pregnancy and lactation, by decreasing tuberoinfundibular dopamine (TIDA) inhibitory tone. The aim of this study was to investigate the opioid receptor subtypes involved in regulating TIDA neuronal activity and therefore facilitating prolactin secretion during early pregnancy, late pregnancy and lactation in rats. Selective opioid receptor antagonists nor-binaltorphimine (kappa-receptor antagonist, 15 micro g/5 micro l), beta funaltrexamine (mu-receptor antagonist, 5 microg/5 microl) and naltrindole (delta-receptor antagonist, 5 microg/5 microl) or saline were administered intracerebroventricularly (i.c.v.) on day 8 of pregnancy during a nocturnal prolactin surge, on day 21 of pregnancy during the ante partum prolactin surge or on day 7 of lactation before the onset of a suckling stimulus. Serial blood samples were collected at regular time intervals, via chronic indwelling jugular cannulae, before and after drug administration and plasma prolactin was determined by radioimmunoassay. TIDA neuronal activity was measured using the 3,4-dihydroxyphenylacetic acid (DOPAC) : dopamine ratio in the median eminence 2 h 30 min after i.c.v. drug injection. In each experimental condition, plasma prolactin was significantly inhibited by both kappa- and mu-receptor antagonists, whereas the delta-receptor antagonist had no effect compared to saline-injected controls. Similarly, nor-binaltorphimine and beta funaltrexamine significantly increased the median eminence DOPAC : dopamine ratio during early and late pregnancy, and lactation whereas naltrindole had no effect compared to saline-injected controls. These data suggest that TIDA neuronal activity, and subsequent prolactin secretion, is regulated by endogenous opioid peptides acting at both kappa- and mu-opioid receptors during prolactin surges of early pregnancy, late pregnancy and lactation.

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Neurochemical Evidence that Estrogen-Induced Suppression of Kappa-Opioid-Receptor-Mediated Regulation of Tuberoinfundibular Dopaminergic Neurons Is Prolactin-lndependent

Cited by 24 publications

References 18 publications

Estrogen Differentially Modulates the Cannabinoid- Induced Presynaptic Inhibition of Amino Acid Neurotransmission in Proopiomelanocortin Neurons of the Arcuate Nucleus

Estrogen Differentially Modulates the Cannabinoid- Induced Presynaptic Inhibition of Amino Acid Neurotransmission in Proopiomelanocortin Neurons of the Arcuate Nucleus

Lack of Plasma Norepinephrine Cyclicity, Increased Estradiol during the Follicular Phase, and of Progesterone and Gonadotrophins at Ovulation in Women with Premenstrual Syndrome

Opioid Receptor Subtypes Involved in the Regulation of Prolactin Secretion During Pregnancy and Lactation

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