Peripheral estradiol induces temporomandibular joint antinociception in rats by activating the nitric oxide/cyclic guanosine monophosphate signaling pathway

Fávaro-Moreira, Nadia Cristina; Torres-Chávez, Karla Elena; Fischer, Luana; Tambeli, Cláudia Herrera

doi:10.1016/j.neuroscience.2009.08.012

Cited by 20 publications

(22 citation statements)

References 46 publications

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“…Chronic neuronal iNOS inhibition decreased nociception in chronic carrageenan‐induced TMD in rats (Tesser‐Viscaino et al, ). In contrast to the study by Kishimoto et al (), blocking NO synthesis by administration of nitro‐1‐arginine in the TMJ blocked the antinociceptive effect of high physiologic estradiol, as did the inhibition of the guanylate cyclase activity (Favaro‐Moreira, Torres‐Chavez, Fischer, & Tambeli, ). On the other hand, nonphysiologic doses of estrogen given to OVX rats injected with CFA dose dependently upregulated expression of pro‐inflammatory iNOS and repressed M2‐associated genes such as IL‐10 and arginase (Kou et al, ).…”

Section: High Physiologic Concentrations Of Estrogen Leads To Reducedcontrasting

confidence: 79%

Estrogenic effects on temporomandibular disorder and pain

Stinson¹,

Bellinger²,

Puri³

et al. 2019

J Appl Biobehavioral Res

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Purpose It has become more apparent that studies focusing on the effect of sex steroids on orofacial pain in humans and animals require careful attention to the methods of hormone replacement. As a result, the purpose of this review is to highlight differences in estrogen concentration and its effects on temporomandibular joint (TMJ) pain and behavior. Methods This literature review searched keywords TMJ, orofacial, pain, nociception sex steroids, estrous cycle, menstrual cycle estradiol, and progesterone. Results In the case of estrogen, the change in concentration was a consideration, as a rise in estrogen can lead to protective effects and a decrease in estrogen appears to exacerbate the pain response. The dosage and timing was important when administering sex steroids as many orofacial pain studies conducted on animals have used large pharmacologic dosages and/or have given the hormone in a nonphysiologic way that does not mimic natural secretion patterns. Conclusions The results demonstrate that when performing studies or experiments these factors can result in alteration of the pain or behavioral response, as well as, joint structure and inflammatory response. Therefore, these factors must be considered when designing experiments focused on determining the mechanisms of action for sex steroids.

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Section: High Physiologic Concentrations Of Estrogen Leads To Reducedcontrasting

confidence: 79%

Estrogenic effects on temporomandibular disorder and pain

Stinson¹,

Bellinger²,

Puri³

et al. 2019

J Appl Biobehavioral Res

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“…ICI 182780 as well as acute inhibition of either nitric oxide synthase or guanylate cyclase eliminates antinociceptive effects of estradiol applied directly to the TMJ [67]. This confirms mediation of estradiol antinociceptive effects via a non-genomic membrane-generated second messenger mechanism.…”

Section: Plasma Membrane Ers and Nociception/antinociceptionmentioning

confidence: 74%

Importance of sex to pain and its amelioration; relevance of spinal estrogens and its membrane receptors

Gintzler

Liu

2012

Frontiers in Neuroendocrinology

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Estrogens have a multitude of effects on opioid systems and are thought to play a key role in sexually dimorphic nociception and opioid antinociception. Heretofore, classical genomic actions of estrogens are largely thought to be responsible for the effects of these steroids on nociception and opioid antinociception. The recent discovery that estrogens can also activate estrogen receptors that are located in the plasma membrane, the effects of which are manifest in seconds to minutes instead of hours to days has revolutionized our thinking concerning the ways in which estrogens are likely to modulate pain responsiveness and the dynamic nature of that modulation. This review summarizes parameters of opioid functionality and nociception that are subject to modulation by estrogens, underscoring the added dimensions of such modulation that accrues from rapid membrane estrogen receptor signaling. Implications of this mode of signaling regarding putative sources of estrogens and its degradation are also discussed.

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“…It has been reported that 17␤-E 2 delivered directly into the temporomandibular joint of anesthetized OVX rats reduced the nocifensive response (rubbing and flinching) to intrajoint injection of formalin measured over 45 min (Fá varo-Moreira et al, 2009). A nongenomic mechanism was suggested on the basis of the effectiveness of a membrane-impermeable form of 17␤-E 2 (conjugated to BSA).…”

Section: Discussionmentioning

confidence: 99%

“…Estrogen receptors (ERs) are expressed in nociceptors of the trigeminal ganglia (TG) and dorsal root ganglia (DRG) (Yang et al, 1998;Bereiter et al, 2005), and treatment with 17␤-estradiol (17␤-E 2 ) influences a variety of functions and cellular processes in nociceptors such as expression of trkA mRNA (Liuzzi et al, 1999), expression of calcitonin generelated peptide mRNA and protein (Gangula et al, 2000), extracellular signal-regulated kinase activity (Liverman et al, 2009), calcium mobilization (Chaban and Micevych, 2005), and transient receptor potential cation channel V1 (TRPV1) function (Xu et al, 2008). Furthermore, local 17␤-E 2 injection into the temporomandibular joint reduces nociceptive behavioral responses to intrajoint administration of formalin (Fá varo-Moreira et al, 2009), suggesting estrogen's effect on nociceptors is functionally relevant.…”

Section: Introductionmentioning

confidence: 99%

17β-Estradiol Rapidly Enhances Bradykinin Signaling in Primary Sensory Neurons In Vitro and In Vivo

Rowan¹,

Berg²,

Milam³

et al. 2010

J Pharmacol Exp Ther

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Many studies have demonstrated that premenopausal women are at increased risk for various pain disorders. Pain-sensing neurons, termed "nociceptors," in the trigeminal ganglia (TG) and dorsal root ganglia (DRG) express receptors for inflammatory mediators and noxious physical stimuli and transmit signals for central processing of pain sensation. Estrogen receptors (ERs) are also expressed on nociceptors in the TG and DRG, and there is ample literature to suggest that activation of ERs can influence pain mechanisms. However, the mechanism for ER modulation of nociceptor activity is incompletely understood. The aim of this study was to characterize the effect of 17␤-estradiol (17␤-E 2 ) on signaling of the inflammatory mediator bradykinin (BK) in primary cultures of rat sensory neurons and a behavioral model of thermal allodynia in rats. Here, we show that exposure to 17␤-E 2 rapidly (within 15 min) enhanced responses to BK in vitro and in vivo. The 17␤-E 2 -mediated enhancement of BK signaling was not blocked by the transcription inhibitor anisomycin and was mediated by a membraneassociated ER. The effect of 17␤-E 2 to enhance BK responses required activation of ␤1-containing, RGD-binding integrins. These data show that 17␤-E 2 rapidly enhances inflammatory mediator responses both in vitro and in vivo and suggest that 17␤-E 2 acting at primary sensory pain neurons may participate in regulating the sensitivity of women to painful stimuli.

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Peripheral estradiol induces temporomandibular joint antinociception in rats by activating the nitric oxide/cyclic guanosine monophosphate signaling pathway

Cited by 20 publications

References 46 publications

Estrogenic effects on temporomandibular disorder and pain

Estrogenic effects on temporomandibular disorder and pain

Importance of sex to pain and its amelioration; relevance of spinal estrogens and its membrane receptors

17β-Estradiol Rapidly Enhances Bradykinin Signaling in Primary Sensory Neurons In Vitro and In Vivo

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