Long-term facilitation of ipsilateral but not contralateral phrenic output after cervical spinal cord hemisection
Long-term facilitation of ipsilateral but not contralateral phrenic output after cervical spinal cord hemisection
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DOI：
10.1016/j.expneurol.2006.01.035
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发表时间：
2006-07-01
影响因子：
5.3
通讯作者：
Fuller, D. D.
中科院分区：
文献类型：
--
作者：
Doperalski, N. J.;Fuller, D. D.
慢性C-2脊髓损伤（C2 HS）后，暴露于间歇性缺氧（IH）引起损伤同侧记录的膈输出持续增加（即，膈长期促进作用，LTF; Golder和Mitchell，J. Neurosci。25：2925-32，2005）。然而，单侧脊髓损伤诱导对侧运动神经元活动的代偿性增加，这可能降低其进一步可塑性的能力（即，“天花板效应”）。我们假设慢性C2 HS后，对侧（与同侧）膈输出的LTF会减少。双侧膈神经活动记录在三组麻醉，瘫痪，迷走神经切断，和通气大鼠：未受伤，4或8周后，组织学证实的C2 HS。在常氧期间建立基线（BL）膈神经活动，然后将大鼠暴露于IH（5 x 3 min等二氧化碳缺氧，13-14% O-2），然后等二氧化碳常氧; IH后60 min评估LTF。未受伤的动物显示出吸气爆发振幅的增加，这在左侧（44 +/- 11%BL）和右侧膈神经（39 +/- 13%BL）中是相似的。然而，在C2 HS后4周（-10 +/-7%BL）或8周（4 +/-5%BL），在C2 HS对侧记录的膈输出中未出现类似的爆发振幅LTF。相反，同侧膈神经波幅的LTF发生在C2 HS后4周（44 +/-11%BL）和8周（129 +/-30%BL，P < 0.05）。IH后膈爆发频率持续增加（即，在对照中观察到（+9 +/-3爆发/分钟，P < 0.05），但在C2 HS大鼠中没有观察到。我们的结论是，单侧颈髓损伤的代偿性反应阻止了对侧膈神经运动神经元LTF的表达。(c)2006年由Elsevier Inc.出版
After chronic C-2 spinal hernisection (C2HS), exposure to intermittent hypoxia (IH) evokes a persistent increase in phrenic output recorded ipsilateral to the injury (i.e., phrenic long-term facilitation, LTF; Golder and Mitchell, J. Neurosci. 25:2925-32, 2005). However, unilateral spinal cord injury induces compensatory increases in contralateral motoneuron activity that may reduce their capacity for further plasticity (i.e., a "ceiling effect"). We hypothesized that after chronic C2HS, LTF would be reduced in contralateral (vs. ipsilateral) phrenic output. Bilateral phrenic activity was recorded in three groups of anesthetized, paralyzed, vagotomized, and ventilated rats: uninjured, and 4 or 8 weeks following histologically verified C2HS. Baseline (BL) phrenic activity was established during normoxia and rats were then exposed to IH (5 x 3 min isocapnic hypoxia, 13-14% O-2) followed by isocapnic normoxia; LTF was assessed 60-min post-IH. Uninjured animals showed an increase in inspiratory burst amplitude that was similar in the left (44 +/- 11%BL) and right phrenic nerves (39 +/- 13%BL). However, similar burst amplitude LTF did not occur in phrenic output recorded contralateral to C2HS at 4 (-10 +/- 7% BL) or 8 weeks post-C2HS (4 +/- 5% BL). In contrast, LTF of ipsilateral phrenic amplitude occurred at both 4 (44 +/- 11% BL) and 8 weeks post-C2HS (129 +/- 30% BL, P < 0.05). A persistent increase in phrenic burst frequency after IH (i.e., "frequency LTF") was observed in control (+9 +/- 3 burst/min, P < 0.05), but not C2HS rats. We conclude that compensatory responses to unilateral cervical spinal cord injury prevent the expression of LTF in contralateral phrenic motoneurons. (c) 2006 Published by Elsevier Inc.