Responses of thoracic spinal neurons to activation and desensitization of cardiac TRPV1-containing afferents in rats.
Responses of thoracic spinal neurons to activation and desensitization of cardiac TRPV1-containing afferents in rats.
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DOI：
10.1152/ajpregu.00231.2006
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发表时间：
2006-12
期刊：
影响因子：
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通讯作者：
C. Qin;J. Farber;K. Miller;R. Foreman
中科院分区：
文献类型：
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作者：
C. Qin;J. Farber;K. Miller;R. Foreman
本研究的目的是检查上胸椎神经元如何对含有心脏瞬时受体电位香草酸 1 (TRPV1) 的传入纤维的激活和脱敏做出反应。在戊巴比妥麻醉、麻痹和通气的雄性大鼠中记录单个 T3 脊髓神经元的细胞外电位。 To activate cardiac nociceptive receptors, a catheter was placed in the pericardial sac to administer various chemicals: bradykinin (BK; 10 microg/ml, 0.2 ml), capsaicin (CAP, 10 microg/ml, 0.2 ml), or a mixture of algesic chemicals (AC; 0.2 ml) containing adenosine 10(-3) M, BK, serotonin, histamine,和PGE(2)，各10(-5)M。本研究中使用了对心包内 BK 和/或 CAP 做出反应的脊髓神经元。结果显示，81% (35/43) 的神经元对心包内 BK 和 CAP 均有兴奋反应，其余神经元对 BK 或 CAP 均有反应。心包内树脂毒素 (RTX)（0.2 微克/毫升，0.2 毫升，1 分钟）可使含有 TRPV1 的神经末梢脱敏，消除对 BK (n = 8) 和 CAP (n = 7) 以及对 AC (n = 5) 的兴奋反应，但不消除对躯体刺激的兴奋反应。心包内注射辣椒素（1 mg/ml，0.2 ml，3 分钟）（TRPV1 的一种特异性拮抗剂），可急剧减弱 5/5 神经元对 CAP 的兴奋反应，但维持 5/5 神经元对 BK 的反应。此外，心包内注射辣椒西平对 3/3 神经元对 AC 的兴奋反应没有显着影响。这些数据表明，心包内 BK 发起的脊髓神经元反应与含有 TRPV1 的心脏传入纤维相关，但不依赖于 TRPV1。心脏伤害感受的椎管内信号传导是通过支配心脏的 CAP 敏感传入纤维介导的。
The purpose of this study was to examine how upper thoracic spinal neurons responded to activation and desensitization of cardiac transient receptor potential vanilloid-1 (TRPV1)-containing afferent fibers. Extracellular potentials of single T3 spinal neurons were recorded in pentobarbital-anesthetized, paralyzed, and ventilated male rats. To activate cardiac nociceptive receptors, a catheter was placed in the pericardial sac to administer various chemicals: bradykinin (BK; 10 microg/ml, 0.2 ml), capsaicin (CAP, 10 microg/ml, 0.2 ml), or a mixture of algesic chemicals (AC; 0.2 ml) containing adenosine 10(-3) M, BK, serotonin, histamine, and PGE(2), 10(-5) M for each. Spinal neurons that responded to intrapericardial BK and/or CAP were used in this study. Results showed that 81% (35/43) of the neurons had excitatory responses to both intrapericardial BK and CAP, and the remainder responded to either BK or CAP. Intrapericardial resiniferatoxin (RTX) (0.2 microg/ml, 0.2 ml, 1 min), which desensitizes TRPV1-containing nerve endings, abolished excitatory responses to both BK (n = 8) and CAP (n = 7), and to AC (n = 5) but not to somatic stimuli. Intrapericardial capsazepine (1 mg/ml, 0.2 ml, 3 min), a specific antagonist of TRPV1, sharply attenuated excitatory responses to CAP in 5/5 neurons, but responses to BK in 5/5 neurons was maintained. Additionally, intrapericardial capsazepine had no significant effect on excitatory responses to AC in 3/3 neurons. These data indicated that intrapericardial BK-initiated spinal neuronal responses were linked to cardiac TRPV1-containing afferent fibers, but were not dependent on TRPV1. Intraspinal signaling for cardiac nociception was mediated through CAP-sensitive afferent fibers innervating the heart.