Hormonal Activation of Female Sexual Behavior is Accompanied by Hypothalamic Norepinephrine Release

Vathy, Ilona; Etgen, Anne M.

doi:10.1111/j.1365-2826.1989.tb00133.x

Cited by 79 publications

(46 citation statements)

References 21 publications

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“…Changes in VMN NE levels are most likely re lated to induction of lordosis. Vathy and Etgen [10], using in vivo dialysis techniques, found that NE is increased in VMN dialysates from estrogen-and progesterone-treated females who exhibit lordosis. The proestrous amplifica tion of the day/evening increase in NE levels in the MCG suggest that NE in this area may also contribute to induc tion of lordosis.…”

Section: Ne and Lordosismentioning

confidence: 99%

“…In addition, because of advances in methods for electrochemical measurement of monoamines, catecholamines and some metabolites were also measured in the same microdissected brain regions. Both NE and dopamine have also been linked to some aspects of sexual receptivity [10][11][12][13]. Several studies have already investigated hypothalamic catecholamines during the estrous cycle and on proestrus [14,15], but these stud ies were conducted in relation to catecholaminergic in volvement in the proestrous LH surge.…”

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confidence: 99%

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Serotonin, Catecholamines and Metabolites in Discrete Brain Areas in Relation to Lordotic Responding on Proestrus

Luine¹

1993

Neuroendocrinology

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Levels of serotonin (5-HT) and metabolite, 5-hydroxyindole-acetic acid (5-HIAA), dopamine and metabolites, dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), and norepinephrine (NE) were measured in microdissected brain areas at 14.30 and 19.30 h on diestrus and proestrus in rats. Lordosis, sexual behavior, was exhibited only by proestrous females at 19.30 h. The content of monoamines and/or metabolites changed from afternoon to early evening of diestrus in a number of brain regions. On proestrus, during the time when females became sexually receptive, additional changes appeared and many diestrous changes were reversed or amplified. Proestrus-specific changes were found in areas provinding the descending circuit for regulation of lordosis, the medial preoptic nucleus (mPOA), ventromedial nucleus of the hypothalamus (VMN) and midbrain central gray (MCG), and in areas outside of endocrine control centers such as parietal cortex (Ctx) and dorsal raphe nucleus (DR). Thus, these data are consistent with previous studies showing functional changes in monoaminergic transmitters during the day/night cycle and during hormonal induction of neuroendocrine events. NE levels increased between 14.30 and 19.30 h on proestrus in most brain areas, ranging from 20% increases in mPOA and Ctx to a 220% increase in the DR. NE levels decreased on proestrus in the VMN. The direction of proestrous changes in NE were reversed in some, but not all of the areas, between the afternoon and evening of diestrus. Dopamine was detectable in all areas sampled, and the metabolites HVA and DOPAC were detectable in some but not all areas. In the mPOA, DOPAC increased 100% during proestrus but was unchanged during the same period on diestrus suggesting a facilitatory effect of dopamine on lordosis in this area. Dopamine terminals in the MCG may inhibit behavior since HVA increased 150% between 14.30 and 19.30 h on diestrus and decreased 40% during the same interval on proestrus. For the serotonergic system, 5-HIAA levels increased 45% in the mPOA and 200% in the MCG from the afternoon to evening of proestrus but did not change on diestrus. In the VMN, 5-HIAA increased 60% between 14.30 and 19.30 h on diestrus but did not change during the same time on proestrus. 5-HIAA also increased 580% in the DR nucleus and 70% in the Ctx during proestrus but not diestrus. These data are consistent with previous studies suggesting that 5-HT terminals regulate lordosis responding on proestrus through hormone-dependent modulations at both facilitatory and inhibitory sites. In the VMN, where 5-HT inhibits lordosis, gonadal hormones appear to decrease the availability of 5-HT, and in the mPOA and MCG, where 5-HT may facilitate lordosis, gonadal hormones appear to increase the availability of 5-HT.

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Section: Ne and Lordosismentioning

confidence: 99%

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confidence: 99%

Serotonin, Catecholamines and Metabolites in Discrete Brain Areas in Relation to Lordotic Responding on Proestrus

Luine¹

1993

Neuroendocrinology

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“…Biol. 109, 1341(1989 DARPP-32, a dopamine-and adenosine 3Ј,5Ј-monophosphate (cAMP)-regulated phosphoprotein (32 kilodaltons in size), is an obligate intermediate in progesterone (P)-facilitated sexual receptivity in female rats and mice. The facilitative effect of P on sexual receptivity in female rats was blocked by antisense oligonucleotides to DARPP-32.…”

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confidence: 99%

Requirement for DARPP-32 in Progesterone-Facilitated Sexual Receptivity in Female Rats and Mice

Mani

Fienberg

O’Callaghan

et al. 2000

Science

126

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adhesion were not significantly reduced by the loss of PI3K␥. Teflon-coated 12-well glass slides (Marienfeld) were coated with fibronectin (20 g/ml; Sigma) solution. Calcein-AM (Molecular Probes)-loaded PMNs (20 l) were applied to the glass slides. After stimulation, nonadherent cells were removed by washing. Fluorescence of attached cells was measured in a Bio-Tek FL600 fluorescence plate reader (excitation, 485 nm, 20-nm slit; emission, 530 nm, 25-nm slit). 12. M. Romano et al., Immunity 6, 315 (1997). 13. C. Nathan et al., J. Cell. Biol. 109, 1341(1989 DARPP-32, a dopamine-and adenosine 3Ј,5Ј-monophosphate (cAMP)-regulated phosphoprotein (32 kilodaltons in size), is an obligate intermediate in progesterone (P)-facilitated sexual receptivity in female rats and mice. The facilitative effect of P on sexual receptivity in female rats was blocked by antisense oligonucleotides to DARPP-32. Homozygous mice carrying a null mutation for the DARPP-32 gene exhibited minimal levels of P-facilitated sexual receptivity when compared to their wild-type littermates. P significantly increased hypothalamic cAMP levels and cAMP-dependent protein kinase activity. These increases were not inhibited by a D 1 subclass dopamine receptor antagonist. P also enhanced phosphorylation of DARPP-32 on threonine 34 in the hypothalamus of mice. DARPP-32 activation is thus an obligatory step in progestin receptor regulation of sexual receptivity in rats and mice.Progesterone (P) and dopamine (DA) facilitation of sexual receptivity in female rats requires intact, intracellular progestin receptors (PRs) (1). Wild-type female mice exhibit high levels of P-and DA-facilitated lordosis, whereas homozygous females carrying a null mutation for the PR gene show minimal reproductive behavior (2, 3). These observations substantiate a critical role for the PR as a transcriptional mediator for the signal transduction pathways initiated by P and DA. DA, signaling through the D 1 subclass of receptors in the neostriatum, induces increases in the levels of adenosine 3Ј,5Ј-monophosphate (cAMP) and activates cAMP-dependent protein kinase (PKA) (4). Dopamineand cAMP-regulated phosphoprotein-32 (DARPP-32) is phosphorylated by PKA. In its phosphorylated state, this molecule, by inhibiting the activity of protein phosphatase-1 (PP-1), increases the state of phosphorylation of many substrate proteins, leading to the induction of physiological responses (4). To determine whether DARPP-32 might be involved in P and DA actions on the hypothalamus, we examined its role in the facilitation of sexual receptivity in female rats and mice (5).Antisense oligonucleotides to the PR inhibit P-facilitated lordosis in female rats (6, 7). We used a similar strategy to examine the role of DARPP-32 in P-and DA-facilitated sexual receptivity. Ovariectomized, estradiol benzoate (EB)-primed, Sprague-Dawley female rats with stereotaxically implanted stainless steel cannulae in the third cerebral ventricle (5) exhibited high levels of P-facilitated lordosis in the presence of males (Fig...

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“…In contrast, DAMGO has no effect on KClstimulated NE release in slices from EB-treatcd females. In female rats, estradiol priming is known to be essential for the display of female reproductive behavior, and in a previous microdialysis study, we showed that the display of this behavior in hormone-treated females correlates with increased hypothalamic NE release [18], Thus, it is possible that one of the mechanisms by which estradiol priming facilitates female reproductive behavior is by removing or attenuating tonically active, inhibitory ef fects of endogenous p-opioids on hypothalamic NE re lease. In support of this interpretation is evidence that ovarian steroids facilitate gonadotropin-releasing hor mone secretion by removing the inhibitory influence of endogenous opioid peptides on NE transmission [ 16,20].…”

Section: Discussionmentioning

confidence: 99%

“…There is now a great deal of evidence supporting the hypothesis that estradiol facilitation of female reproduc tive behavior involves enhancement of hypothalamic NE release [18,19]. Neuroendocrine studies also suggest that a major action of estradiol is to decrease the inhibitory influences of endogenous opioid peptides on hypothalam ic NE systems, in part by decreasing hypothalamic (3-endorphin levels [5,[20][21][22][23][24][25][26], Interestingly, our recent work on p-opioid receptor binding demonstrated that gesta tional morphine alters hypothalamic p-opioid receptor density in adult female progeny [27], In ovariectomized (OVX) females, prenatal morphine reduced the density of p-receptor binding sites.…”

Section: Introductionmentioning

confidence: 99%

Effects of Prenatal Morphine and Adult Estrogen Administration on μ-Opioid Inhibition of Norepinephrine Release from Hypothalamic Slices

Vathy

Etgen²

1996

Neuroendocrinology

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The present study tested the hypotheses that exposure to morphine in utero (10 mg/kg twice a day on gestation days 11–18) and acute estrogen treatment in adulthood alter µ-opioid regulation of hypothalamic norepinephrine (NE) release in sexually mature rats. Both basal and KCl-stimulated NE releases were measured in superfused hypothalamic and preoptic area (POA) slices preloaded with ³H-NE. The µ-opioid receptor agonist D-Ala², MePhe⁴-Gly-ol⁵-enkephalin (DAMGO; 10 or 100 nM) or the opioid antagonist naloxone (1 µM) was applied to some slices 15 min prior to KC1 stimulation. Prenatal morphine had no effect on basal or KCl-stimulated release of preloaded ³H-NE from hypothalamic and POA slices from adult male progeny. Neither the µ-opioid agonist DAMGO nor the nonspecific antagonist naloxone significantly affected KCl-evoked overflow of ³H-NE in slices from either brain region of male rats. Adult female offspring were ovariectomized (OVX), and some were injected with a replacement dose of estrogen 48 h prior to sacrifice. Prenatal morphine had no effect on basal or KCl-stimulated release of ³H-NE from hypothalamic or POA slices or on the response of slices to opioid drugs. Estrogen treatment modestly increased KCl-evoked release of ³H-NE from POA slices from females. Moreover, there was a significant interaction between opioid drugs and estrogen treatment on KCl-evoked overflow of ³H-NE. In hypothalamic and POA slices from OVX females, DAMGO reduced KCl-evoked efflux of ³H-NE. This inhibitory effect of DAMGO was not apparent in slices from estrogen-treated females. In addition, naloxone increased KCl-stimulated NE release in slices from both hypothalamus and POA of estrogen-treated female rats but not control OVX females. Thus, prenatal exposure to morphine does not alter basal, KCl-evoked or µ-opioid modulation of NE efflux from hypothalamic or POA slices in adult progeny of either sex. However, treatment of adult, OVX females with estrogen attenuates µ-opioid inhibition and promotes the appearance of naloxone facilitation of KCl-evoked ³H-NE release from hypothalamic and POA slices.

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Hormonal Activation of Female Sexual Behavior is Accompanied by Hypothalamic Norepinephrine Release

Cited by 79 publications

References 21 publications

Serotonin, Catecholamines and Metabolites in Discrete Brain Areas in Relation to Lordotic Responding on Proestrus

Serotonin, Catecholamines and Metabolites in Discrete Brain Areas in Relation to Lordotic Responding on Proestrus

Requirement for DARPP-32 in Progesterone-Facilitated Sexual Receptivity in Female Rats and Mice

Effects of Prenatal Morphine and Adult Estrogen Administration on μ-Opioid Inhibition of Norepinephrine Release from Hypothalamic Slices

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