Estrogen receptor expression in lumbosacral dorsal root ganglion cells innervating the female rat urinary bladder

Bennett, Haley L.; Gustafsson, Jan Åke; Keast, Janet R.

doi:10.1016/s1566-0702(03)00044-4

Cited by 71 publications

(60 citation statements)

References 56 publications

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“…Also, the ganglional sections with FB-labelled perikarya were incubated with antisera against ER subtype α (polyclonal rabbit against the C-terminus of ERα of mouse origin, sc-542, Santa Cruz Biotechnology, Santa Cruz, CA, USA, dilution 1:1000) and antisera against ER subtype β (monoclonal mouse against the human C-terminus region of the ERβ 1 isoform, MCA1974, AbD Serotec, Raleigh, NC, USA, dilution 1:20). According to previous reports, immunocytochemical detection revealed the nuclear as well as cytoplasmatic localization of ERs in the studied tissues [12,14,17,18].…”

Section: Methodssupporting

confidence: 64%

“…In turn, prepubertal β-estradiol-17-cypionate treatment increased the neuronal size in the rat celiac ganglion [12]. In female rats, DRG sensory neurons in L6-S1 segments that innervate the uterus [16,17] and urinary bladder [18] also express ER subtypes α and β. In rats, an increase in the content of ERα in L6-S1 DRG neurons projecting to the uterine cervix near term is thought to occur in parallel with augmentation of plasma estrogens.…”

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confidence: 95%

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Long-term Estradiol-17.BETA. Administration Decreases the Number of Neurons in the Caudal Mesenteric Ganglion Innervating the Ovary in Sexually Mature Gilts

Koszykowska

Całka

Szwajca

et al. 2011

Journal of Reproduction and Development

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Abstract. The effect of estradiol-17β (E2) on the number and distribution of neurons in the caudal mesenteric ganglion (CaMG) supplying the ovary of adult pigs was investigated. Also, the numbers of ovarian dopamine-β-hydroxylase (Dβ H -), neuropeptide Y (NPY-), somatostatin (SOM-), galanin (GAL-) and estrogen receptor (ER)-immunoreactive perikarya as well as the density of the intraganglionic nerve fibers containing Dβ H and/or NPY, SOM, GAL were determined. E2 was administered i.m. from day 4 of the first studied estrous cycle to the expected day 20 of the second studied cycle. Injections of E2 (1) increased the E2 level in the peripheral blood approximately 4-5 fold, (2) decreased the number of small-sized Fast Blue-positive postganglionic neurons in the CaMG, (3) decreased the number of small perikarya in the ventral, dorsal and central regions of the CaMG, (4) decreased the number of large perikarya in the dorsal and central regions, (5) [6]. Virtually all ovary-projecting postganglionic CaMG neurons in immature and adult pigs are noradrenergic; that is, they express enzymes participating in the synthesis of noradrenaline-tyrosine hydroxylase (TH) and dopamine-β-hydroxylase (Dβ H) [3,4]. Moreover, sympathetic perikarya and nerve fibers within this ganglion have also been found to be immunoreactive to other active substances in a number of mammals, including adult cats [7], immature rats [8], fetal and adult guinea-pigs [9] and prepubertal pigs [3,4]. The reactive substances include neuropeptide Y (NPY), somatostatin (SOM), galanin (GAL), calcitonin gene-related peptide (CGRP), cholecystokinin, bombesin/gastrin-releasing peptide, substance P (SP), vasoactive intestinal polypeptide (VIP), opioid peptides and enkephalins. The abundance of bioactive substances expressed in postganglionic sympathetic CaMG perikarya innervating the ovary correlates with a variety of the ovarian sympathetic actions including regulation of steroidogenesis, blood supply as well as development and ovulation of follicles (as reviewed by Kotwica et al. [10] and Jana et al.[11]).In rats, a close relationship was found between estrogens and sympathetic and sensory neurons supplying the genitourinary system. Estrogen receptor (ER) subtypes α and β are localized in preand paravertebral (at thoracolumbar neuromeres) sympathetic neurons projecting to the ovary and uterus [12,13] and proximal urethra [14]. The number of celiac ganglion neurons innervating the rat ovary and the content of ERs in these cells decreased after prenatal diethylstilbestrol exposure [15]. In turn, prepubertal β-estradiol-17-cypionate treatment increased the neuronal size in the rat celiac ganglion [12]. In female rats, DRG sensory neurons in L6-S1 segments that innervate the uterus [16,17] and urinary bladder [18] also express ER subtypes α and β. In rats, an increase in the content of ERα in L6-S1 DRG neurons projecting to the uterine cervix near term is thought to occur in parallel with augmentation of plasma estrogens. The expressions of ERs, SP [19], CGRP [20] a...

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Section: Methodssupporting

confidence: 64%

mentioning

confidence: 95%

Long-term Estradiol-17.BETA. Administration Decreases the Number of Neurons in the Caudal Mesenteric Ganglion Innervating the Ovary in Sexually Mature Gilts

Koszykowska

Całka

Szwajca

et al. 2011

Journal of Reproduction and Development

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“…Estrogen receptors are expressed throughout the LUT, as well as in bladder sensory neurons and in many central nervous system pathways involved in bladder function (Pelletier, 2000;Bennett et al, 2003). Thus, multiple targets and mechanisms may be affected by hormonal changes.…”

Section: Discussionmentioning

confidence: 99%

Effects of β₃-Adrenergic Receptor Activation on Rat Urinary Bladder Hyperactivity Induced by Ovariectomy

Kullmann¹,

Limberg²,

Artim³

et al. 2009

J Pharmacol Exp Ther

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Voiding dysfunctions, including increased voiding frequency, urgency, or incontinence, are prevalent in the postmenopausal population. ␤ 3 -Adrenergic receptor (␤ 3 AR) agonists, which relax bladder smooth muscle, are being developed to treat these conditions. We utilized the rat ovariectomy (OVX) model to investigate the effect of ovarian hormone depletion on bladder function and the potential for ␤ 3 AR agonists to treat bladder hyperactivity in this setting. OVX increased voiding frequency and decreased bladder capacity by ϳ25% in awake rats and induced irregular cystometrograms in urethane-anesthetized rats. Reverse transcription-polymerase chain reaction revealed three ␤ARs subtypes (␤ 1,2,3 ) in bladder tissue, and immunostaining indicated ␤ 3 AR localization in urothelium and detrusor. Receptor expression was not different in OVX and SHAM rats. ]amino]-6,7,8,9-tetrahydro-5H-benzocyclohepten-2-yl]oxy], ethyl ester, hydrochloride] was confirmed by examining the relative potency for elevation of cAMP in CHOK1 cells overexpressing the various rat ␤ARs. Intravenous injection of each of the ␤ 3 AR agonists (0.1-500 g/kg) in anesthetized rats decreased voiding frequency, bladder pressure, and amplitude of bladder contractions. In bladder strips, ␤ 3 AR agonists (10 Ϫ12-10 Ϫ4 M) decreased baseline tone and reduced spontaneous contractions. BRL37344 (5 mg/kg) and TAK-677 (5 mg/kg) injected intraperitoneally in awake rats decreased voiding frequency by 40 to 70%. These effects were not altered by OVX. The results indicate that OVX-induced bladder dysfunction, including decreased bladder capacity and increased voiding frequency, is not associated with changes in ␤ 3 AR expression or the bladder inhibitory effects of ␤ 3 AR agonists. This suggests that ␤ 3 AR agonists should prove effective for the treatment of overactive bladder symptoms in the postmenopausal population.Lower urinary tract (LUT) dysfunctions, including increased voiding frequency, urgency, incontinence and nocturia, increase in the elderly population and following menopause (Stewart et al., 2003). These dysfunctions could result from hormonally induced changes in bladder contractile and/or relaxing mechanisms. Bladder contractions are triggered by parasympathetic nerves, which release ACh that in turn activates postjunctional muscarinic receptors (mAChRs) in the detrusor. Bladder relaxation is induced by release of norepinephrine from sympathetic nerves, which activates ␤-adrenergic receptors (␤AR) (Fowler et al., 2008

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“…We know little about the cellular mechanisms of steroid action in the brain, especially with regard to pain/analgesia. Many of the central regions implicated in pain and analgesia (i.e., periaqueductal gray, spinal cord, dorsal root ganglion) contain receptors for both estrogens and androgens and have the ability to synthesize steroids locally [18,56,146]. Binding of specific steroids to their receptors within these central and peripheral regions is likely involved in ligand-dependent transcriptional events, thereby influencing the expression of various neurotransmitters and receptors.…”

Section: Future Directionsmentioning

confidence: 99%

Studying sex and gender differences in pain and analgesia: A consensus report

Greenspan

Craft

LeResche

et al. 2007

Pain

871

633

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In September 2006, members of the Sex, Gender and Pain Special Interest Group of the International Association for the Study of Pain met to discuss the following: (1) what is known about sex and gender differences in pain and analgesia; (2) what are the "best practice" guidelines for pain research with respect to sex and gender; and (3) what are the crucial questions to address in the near future? The resulting consensus presented herein includes input from basic science, clinical and psychosocial pain researchers, as well as from recognized experts in sexual differentiation and reproductive endocrinology. We intend this document to serve as a utilitarian and thought-provoking guide for future research on sex and gender differences in pain and analgesia, both for those currently working in this field as well as those still wondering, "Do I really need to study females?" Keywords Sex differences; Gonadal hormones; Estrogens The case for studying sex and gender differences in pain and analgesiaThe pain field has moved from debating whether sex differences in pain exist to recognizing the importance of these differences. Attention is now directed toward understanding (1) what conditions lead to the expression of sex and gender differences in pain experience and reactivity, (2) what mechanisms underlie these differences, and (3) how these differences can inform clinical management of pain.As noted in a recent review, at least 79% of animal studies published in Pain over the preceding 10 years included male subjects only, with a mere 8% of studies on females only, and another 4% explicitly designed to test for sex differences (the rest did not specify) [142]. Given the substantially greater prevalence of many clinical pain conditions in women vs. men [20,199], and growing evidence for sex differences in sensitivity to experimental pain and to analgesics [21,41,213], we recommend that all pain researchers consider testing their hypotheses in both sexes, or if restricted by practical considerations, only in females. It is invalid to assume that data obtained in male subjects will generalize to females, and the best non-human model of the modal human pain sufferer -a woman -is a female animal. If only males are examined in a given study, it is important that a rationale for exclusion of females be provided and that the potential limitation in generalizability of the findings be addressed in the discussion, particularly when examining a pain phenomenon that occurs with greater prevalence or severity in females. In both preclinical and clinical studies, a comparison of both sexes will further our understanding of individual differences in sensitivity to pain and analgesia, thus improving our ability to treat and prevent pain in all people. General considerationsTwo issues of terminology are important. First, the term "sex" refers to biologically based differences, while the term "gender" refers to socially based phenomena. Although biological sex exerts a major influence on one's gender identity, sex and gender a...

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Estrogen receptor expression in lumbosacral dorsal root ganglion cells innervating the female rat urinary bladder

Cited by 71 publications

References 56 publications

Long-term Estradiol-17.BETA. Administration Decreases the Number of Neurons in the Caudal Mesenteric Ganglion Innervating the Ovary in Sexually Mature Gilts

Long-term Estradiol-17.BETA. Administration Decreases the Number of Neurons in the Caudal Mesenteric Ganglion Innervating the Ovary in Sexually Mature Gilts

Effects of β₃-Adrenergic Receptor Activation on Rat Urinary Bladder Hyperactivity Induced by Ovariectomy

Studying sex and gender differences in pain and analgesia: A consensus report

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Estrogen receptor expression in lumbosacral dorsal root ganglion cells innervating the female rat urinary bladder

Cited by 71 publications

References 56 publications

Long-term Estradiol-17.BETA. Administration Decreases the Number of Neurons in the Caudal Mesenteric Ganglion Innervating the Ovary in Sexually Mature Gilts

Long-term Estradiol-17.BETA. Administration Decreases the Number of Neurons in the Caudal Mesenteric Ganglion Innervating the Ovary in Sexually Mature Gilts

Effects of β3-Adrenergic Receptor Activation on Rat Urinary Bladder Hyperactivity Induced by Ovariectomy

Studying sex and gender differences in pain and analgesia: A consensus report

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Product

Resources

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Effects of β₃-Adrenergic Receptor Activation on Rat Urinary Bladder Hyperactivity Induced by Ovariectomy