Differential expression of estrogen receptor alpha and beta in rat dorsal root ganglion neurons

Taleghany, N.; Sarajari, S.; DonCarlos, Lydia L.; Gollapudi, Lakshmi Asritha; Oblinger, Monica M.

doi:10.1002/(sici)1097-4547(19990901)57:5<603::aid-jnr3>3.0.co;2-r

Cited by 134 publications

(72 citation statements)

References 60 publications

(30 reference statements)

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“…For example, the presence of estrogen in ovariectomized rats has been reported to either up-or downregulate the neuronal estrogen receptors in a region-specific manner (12,26). Long-term estrogen treatment of ovariectomized rats decreased levels of estrogen receptor-␣ mRNA in the dorsal root ganglion, whereas this treatment increased levels of estrogen receptor-␤ (27). This last finding raises the possibility that the estrogen-dependent mechanism that we found in gonadally intact female cats involved estrogen receptor-␤.…”

Section: Discussionmentioning

confidence: 99%

Estrogen’s attenuating effect on the exercise pressor reflex is more opioid dependent in gonadally intact than in ovariectomized female cats

Schmitt¹,

Kaufman²

2005

Journal of Applied Physiology

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Schmitt, Petra M., and Marc P. Kaufman. Estrogen's attenuating effect on the exercise pressor reflex is more opioid dependent in gonadally intact than in ovariectomized female cats. J Appl Physiol 98: 633-639, 2005. First published September 24, 2004 doi:10.1152/ japplphysiol.00788.2004.-Using gonadally intact female cats, we showed previously that estrogen, applied topically to the spinal cord, attenuated the exercise pressor reflex. Although the mechanism by which estrogen exerted its attenuating effect is unknown, this steroid hormone has been shown to influence spinal opioid pathways, which in turn have been implicated in the regulation of the exercise pressor reflex. These findings prompted us to test the hypothesis that opioids mediate the attenuating effect of estrogen on the exercise pressor reflex in both gonadally intact female and ovariectomized cats. We therefore applied 200 l of 17␤-estradiol (0.01 g/ml) with and without the addition of 1,000 g naloxone, a -and ␦-opioid antagonist, to a spinal well covering the L 6-S1 spinal cord in decerebrated female cats that were either gonadally intact or ovariectomized. The exercise pressor reflex was evoked by electrical stimulation of the L 7 or S1 ventral root, a maneuver that caused the hindlimb muscles to contract statically. We found that, in gonadally intact cats, the attenuating effect of estrogen was more pronounced than that in ovariectomized cats. We also found that, in gonadally intact female cats, naloxone partly reversed the attenuation of the pressor response to static contraction caused by spinal estrogen application. For example, in intact cats, the pressor response to contraction before estrogen application averaged 39 Ϯ 4 mmHg (n ϭ 10), whereas the pressor response 60 min afterward averaged only 18 Ϯ 4 mmHg (P Ͻ 0.05). In contrast, the pressor response to contraction before estrogen and naloxone application averaged 33 Ϯ 5 mmHg (n ϭ 11), whereas afterward it averaged 27 Ϯ 6 mmHg (P Ͻ 0.05). In ovariectomized cats, naloxone was less effective in reversing the attenuating effect of estrogen on the exercise pressor reflex. sex hormones; static contraction; blood pressure; neural control of circulation; autonomic nervous system THE EXERCISE PRESSOR REFLEX consists of increases in mean arterial pressure, heart rate and ventilation that are evoked by static contraction of the hindlimb muscles in anesthetized or decerebrated animals (19). Recently, spinally applied estrogen was found to attenuate the arterial pressure component of the exercise pressor reflex in decerebrated cats. This attenuation was shown to be gender specific because the threshold concentration of estrogen needed to attenuate the pressor response to contraction was 1,000 times more dilute in female cats than it was in male cats (24,25).The mechanism by which spinally applied estrogen attenuated the reflex pressor response to static contraction is unknown. Nevertheless, -opioid receptors and ␦-opioid receptors have been implicated in the spinal regulation of the exercise pressor ...

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Section: Discussionmentioning

confidence: 99%

Estrogen’s attenuating effect on the exercise pressor reflex is more opioid dependent in gonadally intact than in ovariectomized female cats

Schmitt¹,

Kaufman²

2005

Journal of Applied Physiology

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“…According to the available reports, this E2 blood concentration accompanies pathological states, such as ovarian cysts [24,27] and tumors [31]. It has also been found that estrogen application results in significant decreases in ERs peripheral sympathetic [15] and sensory [32] neurons. Moreover, for determination of the E2 level, blood samples were collected from gilts of both groups through out the whole period of E2/oil administration (twice a day-0900 and 2100 h).…”

Section: Methodsmentioning

confidence: 99%

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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“…ERβ is widely expressed on small-sized nociceptive DRG neurons and the colon, suggesting modulation in peripheral pain signal transduction [38][39][40]. Reports have shown that the selective ERβ agonist ERB-131 regulated nociception during the inflammatory state [18,19,41].…”

Section: Estrogen Modulates Inflammatory Pain Via Erβmentioning

confidence: 99%

Inhibitory effect of estrogen receptor beta on P2X3 receptors during inflammation in rats

Jiang

Sun

et al. 2016

Purinergic Signalling

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Estrogen receptor beta (ERβ) has been shown to play a therapeutic role in inflammatory bowel disease (IBD). However, the mechanism underlying how ERβ exerts therapeutic effects and its relationship with P2X3 receptors (P2X3R) in rats with inflammation is not known. In our study, animal behavior tests, visceromotor reflex recording, and Western blotting were used to determine whether the therapeutic effect of ERβ in rats with inflammation was related with P2X3R. In complete Freund adjuvant (CFA)-induced chronic inflammation in rats, paw withdrawal threshold was significantly decreased which were then reversed by systemic injection of ERβ agonists, DPN or ERB-041. In 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in rats, weight loss, higher DAI scores, increased visceromotor responses, and inflammatory responses were reversed by application of DPN or ERB-041. The higher expressions of P2X3R in dorsal root ganglia (DRG) of CFA-treated rats and those in rectocolon and DRG of TNBS-treated rats were all decreased by injection of DPN or ERB-041. DPN application also inhibited P2X3R-evoked inward currents in DRG neurons from TNBS rats. Mechanical hyperalgesia and increased P2X3 expression in ovariectomized (OVX) CFA-treated rats were reversed by estrogen replacements. Furthermore, the expressions of extracellular signal-regulated kinase (ERK) in DRG and spinal cord dorsal horn (SCDH) and c-fos in SCDH were significantly decreased after estrogen replacement compared with those of OVX rats. The ERK antagonist U0126 significantly reversed mechanical hyperalgesia in the OVX rats. These results suggest that estrogen may play an important therapeutic role in inflammation through downregulation of P2X3R in peripheral tissues and the nervous system, probably via ERβ, suggesting a novel therapeutic strategy for clinical treatment of inflammation.

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Differential expression of estrogen receptor alpha and beta in rat dorsal root ganglion neurons

Cited by 134 publications

References 60 publications

Estrogen’s attenuating effect on the exercise pressor reflex is more opioid dependent in gonadally intact than in ovariectomized female cats

Estrogen’s attenuating effect on the exercise pressor reflex is more opioid dependent in gonadally intact than in ovariectomized female cats

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

Inhibitory effect of estrogen receptor beta on P2X3 receptors during inflammation in rats

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