GREATER SPLANCHNIC EXCITATION OF PRIMATE T1-T5 SPINOTHALAMIC NEURONS
GREATER SPLANCHNIC EXCITATION OF PRIMATE T1-T5 SPINOTHALAMIC NEURONS
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DOI：
10.1152/jn.1984.51.3.592
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发表时间：
1984-01-01
影响因子：
2.5
通讯作者：
FOREMAN, RD
中科院分区：
文献类型：
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作者：
AMMONS, WS;BLAIR, RW;FOREMAN, RD
观察电刺激左侧内脏大神经(SPL)对T1-T5脊髓丘脑(STT)神经元的影响。在36只麻醉猕猴(猕猴)上，对85个STT神经元进行了研究。所有神经元均通过操纵其躯体感受野和电刺激心肺(CP)交感纤维而兴奋。刺激SPL可兴奋63个(74%)STT神经元。在更多的尾段和更深的板层，SPL输入的细胞所占比例增加。SPL和CP交感神经刺激均可引起早反应或早反应和晚反应。CP交感神经刺激的细胞激活潜伏期通常比SPL刺激的短(5.4±-)。0.8比11.3。+-。2.0ms用于早期响应，44.2.+-。4.2vs.111.0+-。延迟响应为6.6毫秒)。测定每个CP交感刺激SPL的最大峰数。在T2和T3节段，对CP交感神经刺激的早期反应明显更强。在更多的尾段，对CP交感神经输入的反应减少，而对SPL输入的反应增加，直到T4时两者的反应没有差异。在T5阶段，对SPL输入的反应更强。在任何节段中都没有观察到迟发反应的大小差异。对左胸迷走神经施加一系列条件性刺激可抑制6个细胞对SPL刺激的反应。最大抑制发生在50ms的CT间期，而当CT间期长达200ms时，测试反应显著减少。双侧迷走神经切断术消除了抑制作用。切断T5和T6交感支之间的左侧交感神经链，可消除对刺激SPL的27%的反应。更多的尾部切割进一步降低了反应，直到在T8和T9之间的切割取消了71%的反应。损毁脊髓背外侧柱对上述反应影响不大，而损毁侧柱和腹外侧柱则使上述反应减弱或消失。刺激SPL通过脊髓外和脊髓内通路兴奋T1-T5 STT神经元。SPL信息与来自各种其他内脏和躯体来源的信息整合在一起。SPL输入到胸区有躯体区域的细胞，可以解释与腹部疾病相关的胸痛的临床现象。
Effects of electrical stimulation of the left greater splanchnic nerve (SPL) on T1-T5 spinothalamic (STT) neurons were determined. STT neurons (85) were studied in 36 anesthetized monkeys (Macaca fascicularis). All neurons were excited by manipulation of their somatic receptive fields and by electrical stimulation of cardiopulmonary (CP) sympathetic fibers. SPL stimulation excited 63 (74%) STT neurons. There was an increasing percentage of cells with SPL input at more caudal segments and in deeper laminae. Both SPL and CP sympathetic stimulation elicited early or both early and late responses. Latencies to cell activation were usually shorter for CP sympathetic stimulation than for SPL stimulation (5.4 .+-. 0.8 vs. 11.3 .+-. 2.0 ms for early responses and 44.2 .+-. 4.2 vs. 111.0 .+-. 6.6 ms for late responses). The maximum number of spikes per SPL of CP sympathetic stimulus was determined. In the T2 and T3 segments, early responses to CP sympathetic stimulation were significantly greater. At more caudal segments, responses to CP sympathetic input decreased while responses to SPL input increased until at T4 there was no difference in the 2 responses. In T5, responses to SPL input were greater. No differences in the magnitudes of late responses were observed in any of the segments. The response of 6 cells to SPL stimulation was inhibited by a train of conditioning stimuli applied to the left thoracic vagus nerve. Maximum inhibition occurred at a CT interval of 50 ms and test responses were significantly reduced at CT intervals as great as 200 ms. Bilateral vagotomy eliminated the inhibitory effect. Cutting the left sympathetic chain between the T5 and T6 rami communicantes eliminated 27% of the response to SPL stimulation. More caudal cuts reduced the response further until 71% of the response was abolished by a cut between T8 and T9. Lesions in the dorsolateral column of the spinal cord had little effect on the responses, while lesions of the lateral and ventrolateral columns reduced or abolished the responses. SPL stimulation excites T1-T5 STT neurons by way of extraspinal and intraspinal pathways. SPL information is integrated with information from a variety of other visceral and somatic sources. SPL input to cells with somatic fields in the chest region may explain the clinical phenomenon of chest pain associated with abdominal disorders.