Spinal estrogen attenuates the exercise pressor reflex but has little effect on the expression of genes regulating neurotransmitters in the dorsal root ganglia.

Spinal estrogen attenuates the exercise pressor reflex but has little effect on the expression of genes regulating neurotransmitters in the dorsal root ganglia.
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脊髓雌激素减弱运动加压反射,但对调节背根神经节神经递质的基因表达影响不大。

DOI:
10.1152/japplphysiol.01098.2005
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发表时间:
2006
期刊:
Journal of applied physiology (Bethesda, Md. : 1985)
影响因子:
--
通讯作者:
Kaufman,MarcP
Kaufman,MarcP
中科院分区:
--
文献类型:
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作者:
Schmitt,PetraM;Gohil,Kishorchandra;Kaufman,MarcP

文献摘要

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Previously, our laboratory showed that estrogen, topically applied to the spinal cord, attenuated the exercise pressor reflex in female cats (Schmitt PM and Kaufman MP.J Appl Physiol95: 1418–1424, 2003; 98: 633–639, 2005). The attenuation was gender specific and was in part opioid dependent. Our finding that the μ- and δ-opioid antagonist naloxone was only able to partially restore estrogen’s attenuating effect on the pressor response to static contraction suggested that estrogen affected an additional pathway, involving the dorsal root ganglion (DRG). Estrogen has been described to stimulate transcription within 10 min of its application to the DRG, raising the possibility that rapid genomic effects on neurotransmitter production may have contributed to estrogen’s effect on the exercise pressor reflex. This prompted us to test the hypothesis that estrogen modulated the pressor response to static contraction by influencing gene expression of the neurotransmitters released by the thin-fiber muscle afferents that evoke the exercise pressor reflex. We confirmed in decerebrated female rats that topical application of estrogen (0.01 μg/ml) to the lumbosacral spinal cord attenuated the pressor response to static muscle contraction (from 10 ± 3 to 1 ± 1 mmHg;P< 0.05). DRG were then harvested postmortem, and changes in mRNA expression were analyzed. GeneChip analysis revealed that neither estrogen nor contraction alone changed the mRNA expression of substance P, the neurokinin-1 receptor, CGRP, NGF, the P2X3 receptor, GABAAand GABAB, the 5-HT3Aand 5-HT3Breceptor,N-methyl-d-aspartate and non-N-methyl-d-aspartate receptors, opioid receptors, and opioid-like receptor. Surprisingly, however, contraction stimulated the expression of neuropeptide Y in the DRG in the presence and absence of estrogen. We conclude that estrogen does not attenuate the exercise pressor reflex through a genomic effect in the DRG.