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RISS 인기검색어
- 검색키워드
- 저자 : Smeester, Branden A. (검색결과 2 건)
- 무료
- 기관 내 무료
- 유료
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Smeester, Branden A.,Lee, Jang-Hern,Beitz, Alvin J. Elsevier 2017 Brain research bulletin Vol.134 No.-
<P><B>Abstract</B></P> <P>Most acute and chronic animal models of pain rely heavily on reflexive assays for evaluating levels of nociception, which involves removing the animal from its normal social environment. Here, we examine and characterize the influence of social interactions on inflammatory pain-evoked changes in movement in two different mouse strains. To produce inflammatory nociception, we injected CFA bilaterally into the hind paws of Balb/c and C3H mice and then recorded exploratory locomotor activity using an automated detector system to first evaluate the effects of social behavior on nociception. Secondly, we determined if carprofen administration altered the effects of social behavior on nociceptive-evoked movement. This methodology was expanded to create a novel thermal activity assay to objectively measure the effect of heat and cold on CFA-evoked animal movement in paired animals. Paired Balb/c and C3H mice exhibited significant hyper-locomotion that lasted for 3h post-injection in Balb/c, but only 1h post-injection in C3H. Single Balb/c mice only showed increased activity for 1h post-injection, while single C3H mice showed no increase. This CFA-induced increase in activity in paired animals was highly inversely correlated with mechanical allodynia as measured using standard Von Frey filaments. Carprofen administration completely blocked this CFA-induced hyperlocomotor activity. Both heat and cold induced a significant increase in locomotor activity in paired mice injected with CFA, while having no effect on activity in control mice injected with saline. The results presented here indicate that social interactions greatly influence inflammatory pain-induced changes in locomotor activity and indicate that the use of movement-based assays to evaluate nociception in paired mice may provide an alternative and more sensitive method to quantify nociception and characterize novel analgesic effects over time in the context of social interactions in rodent models of pain.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Normal locomotion is affected by social interactions in mice. </LI> <LI> Social interactions alter nociceptive-induced changes in locomotion. </LI> <LI> Carprofen blocks the effect of social interaction on nociception. </LI> <LI> A novel thermal locomotion assay allows detection of nociception in paired mice. </LI> </UL> </P>
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Choi, Hoon-Seong,Lee, Mi-Ji,Choi, Sheu-Ran,Smeester, Branden A.,Beitz, Alvin J.,Lee, Jang-Hern Elsevier 2018 NEUROSCIENCE Vol.372 No.-
<P><B>Abstract</B></P> <P>Aromatase is a key enzyme responsible for the biosynthesis of estrogen from testosterone. Although recent evidence indicates that spinal cord aromatase participates in nociceptive processing, the mechanisms underlying its regulation and its involvement in nociception remain unclear. The present study focuses on the potential role of astrocyte aromatase in formalin-induced acute pain and begins to uncover one mechanism by which spinal aromatase activation is controlled. Following intraplantar formalin injection, nociceptive responses were quantified and immunohistochemistry/co-immunoprecipitation assays were used to investigate the changes in spinal Fos expression and the phospho-serine levels of spinal aromatase. Intrathecal (i.t.) injection of letrozole (an aromatase inhibitor) mitigated both the late phase formalin-induced nociceptive responses and formalin-induced spinal Fos expression. Furthermore, formalin-injected mice showed significantly reduced phospho-serine levels of aromatase, which is associated with the rapid activation of this enzyme. However, sigma-1 receptor inhibition with i.t. BD1047 blocked the dephosphorylation of aromatase and potentiated the pharmacological effect of letrozole on formalin-induced nociceptive responses. In addition, i.t. administration of a sub-effective dose of BD1047 potentiated the pharmacological effect of cyclosporin A (a calcineurin inhibitor) on both the formalin-induced reduction in phospho-serine levels of aromatase and nociceptive behavior. These results suggest that dephosphorylation is an important regulatory mechanism involved in the rapid activation of aromatase and that spinal sigma-1 receptors mediate this dephosphorylation of aromatase through an intrinsic calcineurin pathway.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Dephosphorylated aromatase in astrocyte is involved in the process of formalin-induced acute nociception. </LI> <LI> Activation of astrocyte sigma-1 receptors is associated with the dephosphorylation of aromatase. </LI> <LI> Calcineurin signaling pathway is involved in the sigma-1 receptor-mediated dephosphorylation of aromatase. </LI> </UL> </P>
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