Effects of general anesthetics on visceral pain transmission in the spinal cord.

Effects of general anesthetics on visceral pain transmission in the spinal cord.
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全身麻醉药对脊髓内脏痛传递的影响

DOI:
10.1186/1744-8069-4-50
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发表时间:
2008-10-30
期刊:
影响因子:
3.3
通讯作者:
Fang L
Fang L
中科院分区:
医学3区
文献类型:
--
作者:
Wang Y;Wu J;Lin Q;Nauta H;Yue Y;Fang L

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目前的证据表明,全身麻醉剂的脊髓作用的镇痛作用,然而,细胞群体和细胞内机制的全身麻醉剂抗内脏痛仍然不清楚。已知内脏伤害性信号通过突触后背柱(PSDC)和脊髓丘脑束(STT)神经元通路传递,并且PSDC通路在内脏伤害性感受中起主要作用。动物研究报告,在内脏疼痛刺激后观察到持续变化,包括脊髓PSDC神经元中的伤害感受相关分子表达(例如神经激肽-1(NK-1)受体)和信号转导级联(例如蛋白激酶A [PKA]-c-AMP-响应元件结合[CREB]级联)的激活。在癌症疼痛患者中中断脊髓PSDC通路的临床实践进一步支持了这组神经元在内脏痛的发展和维持中的作用。我们提出的假设是,全身麻醉剂可能会影响关键的分子靶点,如NK-1和谷氨酸受体,以及细胞内的信号转导CaM激酶II,蛋白激酶C(PKC),PKA和MAP激酶级联在PSDC神经元,这有助于内脏痛信号的神经传递。这将有助于阐明全身麻醉药在细胞和分子水平上抗内脏伤害性感受的机制,并有助于开发新的治疗策略,以改善内脏疼痛的临床管理。
Current evidence suggests an analgesic role for the spinal cord action of general anesthetics; however, the cellular population and intracellular mechanisms underlying anti-visceral pain by general anesthetics still remain unclear. It is known that visceral nociceptive signals are transmited via post-synaptic dorsal column (PSDC) and spinothalamic tract (STT) neuronal pathways and that the PSDC pathway plays a major role in visceral nociception. Animal studies report that persistent changes including nociception-associated molecular expression (e.g. neurokinin-1 (NK-1) receptors) and activation of signal transduction cascades (such as the protein kinase A [PKA]-c-AMP-responsive element binding [CREB] cascade)-in spinal PSDC neurons are observed following visceral pain stimulation. The clinical practice of interruption of the spinal PSDC pathway in patients with cancer pain further supports a role of this group of neurons in the development and maintenance of visceral pain. We propose the hypothesis that general anesthetics might affect critical molecular targets such as NK-1 and glutamate receptors, as well as intracellular signaling by CaM kinase II, protein kinase C (PKC), PKA, and MAP kinase cascades in PSDC neurons, which contribute to the neurotransmission of visceral pain signaling. This would help elucidate the mechanism of antivisceral nociception by general anesthetics at the cellular and molecular levels and aid in development of novel therapeutic strategies to improve clinical management of visceral pain.
DOI: 10.1016/s0304-3959(00)00364-x
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