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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    BJOG 103 (1996), S. 0 
    ISSN: 1471-0528
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Objective To examine the relation between obstetric factors and the prevalence of urinary incontinence three months after delivery.Design 2134 postal questionnaires sent between August 1989 and June 1991.Setting Teaching hospital in Dunedin, New Zealand.Subjects All women three months postpartum who were resident in the Dunedin area.Main outcome measure Prevalence of urinary incontinence.Results 1505 questionnaires were returned (70.5% response rate). At three months postpartum 34.3% of women admitted to some degree of urinary incontinence with 3.3% having daily or more frequent leakage. There was a significant reduction in the prevalence of incontinence for women having a caesarean section, in particular in primiparous women with a history of no previous incontinence (prevalence of incontinence following a vaginal delivery 24.5%, following a caesarean section 5.2% P = 0.002). There was little difference between elective caesarean sections and those carried out in the first and second stages of labour. The odds ratios for women having a caesarean section were 0.4 (95% confidence interval (CI) 0.2–0.7) (all women and all primiparae) and 02 (95% CI 0.0–0.6) (primipara with no previous incontinence) in comparison with those having a normal vaginal delivery. The prevalence of incontinence was also significantly lower in women having had two caesarean sections (23.3%; P = 0.05) but similar in those women having three or more caesarean sections (38.9 YO) in comparison with those women who delivered vaginally (37.7%). Other significant independent odds ratios were found for daily antenatal pelvic floor exercises (PFE) (0.6, 95% CI 0.4–09), parity ≥5 (2.2, 95% CI 1.0–4.9) and pre-pregnancy body mass index (1.07, 95% CI 1.04–1.10).Conclusions Adverse risk factors for urinary incontinence at three months postpartum are vaginal delivery, obesity and multiparity (2 5). Caesarean section and daily antenatal PFE appear to be protective, although not completely so.
    Type of Medium: Electronic Resource
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  • 2
    Keywords: ESTROGEN ; estrogen receptor ; in vivo ; THERAPIES ; ESTROGEN-RECEPTOR ; mechanisms ; DISSECTION ; LIGANDS ; RECEPTOR ; IN-VIVO ; THERAPY ; VIVO ; MECHANISM ; LIGAND
    Type of Publication: Book chapter
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  • 3
    Keywords: RECEPTOR ; CELL ; Germany ; PATHWAY ; MICE ; MECHANISM ; mechanisms ; ALPHA ; virus ; MOUSE ; NERVOUS-SYSTEM ; hormone ; LINE ; REGION ; REGIONS ; BETA ; MUTANT MICE ; RAT-BRAIN ; ESTROGEN-RECEPTOR ; RE ; DEPENDENT PROTEIN-KINASE ; ESTROGEN ; estrogen receptor ; PSEUDORABIES VIRUS ; neuron ; FEMALE RAT ; LHRH NEURONS ; LUTEINIZING-HORMONE ; PREOPTIC AREA ; SURGE
    Abstract: The mechanisms through which estrogen regulates gonadotropin-releasing hormone (GnRH) neurons to control mammalian ovulation are unknown. We found that estrogen positive feedback to generate the preovulatory gonadotropin surge was normal in estrogen receptor beta knockout (ER beta) mutant mice, but absent in ER alpha mutant mice. An ER alpha-selective compound was sufficient to generate positive feedback in wild-type mice. As GnRH neurons do not express ER alpha, estrogen positive feedback upon GnRH neurons must be indirect in nature. To establish the cell type responsible, we generated a neuron-specific ERa mutant mouse line. These mice failed to exhibit estrogen positive feedback, demonstrating that neurons expressing ER alpha are critical. We then used a GnRH neuron-specific Pseudorabies virus (PRV) tracing approach to show that the ER alpha-expressing neurons innervating GnRH neurons are located within rostral periventricular regions of the hypothalamus. These studies demonstrate that ovulation is driven by estrogen actions upon ER alpha-expressing neuronal afferents to GnRH neurons
    Type of Publication: Journal article published
    PubMed ID: 17046690
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  • 4
    Abstract: Sex differences in brain function underlie robust differences between males and females in both normal and disease states. Although alternative mechanisms exist, sexual differentiation of the male mammalian brain is initiated predominantly by testosterone secreted by the testes during the perinatal period. Despite considerable advances in understanding how testosterone and its metabolite estradiol sexually differentiate the brain, little is known about the mechanism that generates the male-specific perinatal testosterone surge. In mice, we show that a male-specific activation of GnRH neurons occurs 0-2 h following birth and that this correlates with the male-specific surge of testosterone occurring up to 5 h after birth. The necessity of GnRH signaling for the sexually differentiating effects of the perinatal testosterone surge was demonstrated by the persistence of female-like brain characteristics in adult male, GnRH receptor knock-out mice. Kisspeptin neurons have recently been identified to be potent, direct activators of GnRH neurons. We demonstrate that a population of kisspeptin neurons appears in the preoptic area of only the male between E19 and P1. The importance of kisspeptin inputs to GnRH neurons for the process of sexual differentiation was demonstrated by the lack of a normal neonatal testosterone surge, and disordered brain sexual differentiation of male mice in which the kisspeptin receptor was deleted selectively from GnRH neurons. These observations demonstrate the necessity of perinatal GnRH signaling for driving brain sexual differentiation and indicate that kisspeptin inputs to GnRH neurons are essential for this process to occur.
    Type of Publication: Journal article published
    PubMed ID: 25392497
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  • 5
    Keywords: EXPRESSION ; RAT ; MOUSE ; MUTANT MICE ; Reproduction ; KISS-1 MESSENGER-RNA ; HORMONE NEURONS ; HYPOTHALAMIC CONTROL ; MEDIAN-EMINENCE ; RECEPTOR GPR54
    Abstract: Signaling between kisspeptin and its receptor, G-protein-coupled receptor 54 (Gpr54), is now recognized as being essential for normal fertility. However, the key cellular location of kisspeptin-Gpr54 signaling is unknown. Here we create a mouse with a GnRH neuron-specific deletion of Gpr54 to assess the role of gonadotropin-releasing hormone (GnRH) neurons. Mutant mice are infertile, fail to go through puberty and exhibit markedly reduced gonadal size and follicle-stimulating hormone levels alongside GnRH neurons that are unresponsive to kisspeptin. In an attempt to rescue the infertile phenotype of global Gpr54(-)/(-) mutants, we use BAC transgenesis to target Gpr54 to the GnRH neurons. This results in mice with normal puberty onset, estrous cyclicity, fecundity and a recovery of kisspeptin's stimulatory action upon GnRH neurons. Using complimentary cell-specific knockout and knockin approaches we demonstrate here that the GnRH neuron is the key site of kisspeptin-Gpr54 signaling for fertility.
    Type of Publication: Journal article published
    PubMed ID: 24051579
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  • 6
    ISSN: 1432-1106
    Keywords: γ-aminobutyric acid ; Bicuculline ; Medial preoptic area ; Microdialysis ; Luteinising hormone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The role of GABA neurones in the medial preoptic area (MPOA) in regulating the activity of the luteinising hormone-releasing hormone (LHRH) neurones projecting to the median eminence was investigated in the conscious ovariectomised rat. Plasma luteinising hormone (LH) concentrations were measured while (1) endogenous GABA release from the MPOA was monitored with the technique of microdialysis, or (2) activity at the GABA receptor was modulated by local infusions into the MPOA. Microdialysis studies revealed a fluctuating level of GABA release in the MPOA which did not correlate with pulsatile LH secretion. Infusion of 10 μM GABA (n=8) or bicuculline methiodide (BMI, n=6) into the MPOA, at a rate of l μ1/30 min, significantly inhibited mean LH concentrations (P〈 0.05-0.001) and LH pulse frequency (P〈 0.05-0.001) compared with controls (n = 8). LH pulse amplitude was not significantly altered by infusion of GABA (P〉 0.05) while too few pulses were found after BMI treatment to enable statistical analysis. Infusions of GABA into the ventral half of the MPOA had a more significant inhibitory effect upon LH secretion compared with dorsal infusions (P=0.012). A similar relationship did not exist for BMI infusions. These results show that acute changes in preoptic GABA receptor occupancy result in disruption of pulsatile LH secretion in the ovariectomised rat. This suggests that GABA neurones provide a tonic input important for the functional integrity of the neural network controlling LH secretion. However, as changes in extracellular GABA concentrations in the MPOA do not correlate with pulsatile LH release, the preoptic GABA population, as a whole, is unlikely to be directly responsible for the pulsatile activity of the LHRH neurones in the ovariectomised rat.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1433-3023
    Keywords: Conservative treatment ; Pelvic floor muscle exercises ; Postnatal urinary incontinence ; Randomized controlled trial
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A randomized controlled trial was carried out to evaluate the extent to which a program of reinforced pelvic floor muscle exercises (PFME) reduces urinary incontinence 1 year after delivery. Two hundred and thirty women who were incontinent 3 months postpartum were randomized to either a control group doing standard postnatal pelvic floor muscle exercises (n=117) or to an intervention group (n=113) who saw a physiotherapist for instruction at approximately 3, 4, 6 and 9 months postpartum. Results collected 12 months after delivery included prevalence and frequency of incontinence and PFME, sexual satisfaction, perineometry measurements and pad tests. Twenty-six (22%) of the control group and 59 (52%) of the intervention group withdrew before the final assessment. The prevalence of incontinence was significantly less in the intervention group than in the control group (50% versus 76%,P=0.0003), and this group also did significantly more PFME. There were no significant differences between the groups as regards sexual satisfaction, perineometry measurements or pad test results.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The molecular and cellular characteristics of the gonadotropin-releasing hormone (GnRH) neurons have been difficult to ascertain due to their scattered distribution within the basal forebrain. Using morphological criteria coupled with single cell RT-PCR postidentification, we have developed a method for investigating native GnRH neurons in the mouse brain and used it to examine the development of GABAA receptor signalling in this phenotype. Following the harvesting of the cytoplasmic contents of individual GnRH neurons, single cell multiplex RT-PCR experiments demonstrated that GABAA receptor α1–5, β1–3 and γ2 & 3 subunit transcripts were expressed by both neonatal (postnatal day 5) and juvenile (day 15–20) GnRH neurons in a heterogeneous manner. Following puberty, this profile was reduced to a predominant α1, α5, β1, γ2 subunit complement in rostral preoptic area GnRH neurons of the adult female. Whole-cell patch-clamp recordings revealed little difference between juvenile and adult GnRH neurons in their resting membrane potential and spontaneous firing rates. All GnRH neurons were found to be subjected to a tetrodotoxin-insensitive, tonic GABAergic barrage signalling through the GABAA receptor. However, marked heterogeneity in the sensitivity of individual juvenile GnRH neurons to GABA was revealed and, in parallel with the change in subunit mRNA profile, this was dramatically reduced in the reproductively competent adult GnRH neurons. These findings provide the first electrical and molecular characterization of the GnRH phenotype and demonstrate a novel pattern of late postnatal reorganization of native GABAA receptor gene expression and signalling in the GnRH neuronal population.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Marked plasticity in GABAA receptor signalling occurs in adult oxytocin neurons of the supraoptic nucleus (SON) through the modulation of GABAA receptor α subunits during pregnancy. The present studies were undertaken to examine the potential mechanisms underlying this plasticity. In vivo microdialysis experiments in conscious rats revealed that no significant changes in extracellular GABA concentrations occurred within the SON over the last two days of pregnancy and the time of parturition itself. In situ hybridization studies examined the effects of gonadal steroid manipulation upon the GABAA receptor subunits expressed by SON neurons (α1, α2, β2 and γ2 subunits) and demonstrated that cellular levels of the α1 subunit were increased following 8 days oestrogen and progesterone treatment. Estrogen alone or allopregnanolone, the progesterone derivative, had no effect on α1 subunit mRNA expression in the SON. Immunocytochemical experiments demonstrated progesterone receptors in many neural populations but not within the SON of late pregnant rats. These studies indicate that alterations in endogenous GABA release within the SON are unlikely to be responsible for the GABAA receptor plasticity exhibited by oxytocin neurons in late pregnancy. Rather, data demonstrate that the fluctuating concentrations of progesterone during pregnancy act indirectly on SON neurons to modulate α1 subunit mRNA expression. Together, these experiments provide evidence for the ligand-independent induction of GABAA receptor plasticity in the adult brain by progesterone.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We have employed transgenic mouse models to examine the functional significance of the γ2 subunit of the GABAA (γ-aminobutyric acid) receptor to the correct development of gonadotropin-releasing hormone (GnRH) neurons in vivo. In the first experiment, the expression of γ2 subunit protein by the GnRH phenotype was determined using transgenic mice in which GnRH gene sequences direct the expression of the LacZ reporter to the nucleus of the GnRH neurons. This greatly facilitates the immunocytochemical identification of non-nuclear-located antigens within GnRH neurons and revealed that ∼ 25% of juvenile GnRH neurons were immunoreactive for the γ2 subunit and that this increased to 40% in pubertal mice. In the second experiment, GnRH mRNA expression was examined in the brains of γ2 subunit knockout mice (γ20/0) and their wild-type (γ2+/+) littermates at embryonic day 15 and postnatal days (P) 0 and 11–16 using in situ hybridization. The distribution and numbers of cells expressing GnRH mRNA in γ2+/+ and γ20/0 mice were not found to differ at any age. However, the GnRH mRNA content of medial septal cells was significantly lower in γ20/0 compared with γ2+/+ mice at P11–16 (P 〈 0.05) and the same trend was observed for preoptic area neurons. These results demonstrate that while the γ2 subunit of the GABAA receptor is expressed by postnatal GnRH neurons, their embryonic development does not require a functional γ2 subunit. In contrast, postnatal GnRH mRNA expression was found to be dependent upon signalling through the GABAA receptor.
    Type of Medium: Electronic Resource
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