Doperalski N J, Fuller D D
Department of Physical Therapy, University of Florida, Gainesville, FL 32610, USA.
Exp Neurol. 2006 Jul;200(1):74-81. doi: 10.1016/j.expneurol.2006.01.035. Epub 2006 May 2.
After chronic C2 spinal hemisection (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% O2) 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.
在慢性C2脊髓半横断（C2HS）后，暴露于间歇性低氧（IH）会引起损伤同侧记录到的膈神经输出持续增加（即膈神经长期易化，LTF；Golder和Mitchell，《神经科学杂志》25:2925 - 32，2005）。然而，单侧脊髓损伤会引起对侧运动神经元活动的代偿性增加，这可能会降低它们进一步可塑性的能力（即“天花板效应”）。我们假设，在慢性C2HS后，对侧（相对于同侧）膈神经输出中的LTF会降低。在三组麻醉、麻痹、迷走神经切断和通气的大鼠中记录双侧膈神经活动：未受伤组，以及经组织学证实的C2HS后4周或8周的大鼠。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次×3分钟等碳酸血症性低氧，13 - 14% O2），随后是等碳酸血症性常氧；在IH后60分钟评估LTF。未受伤动物的吸气爆发幅度增加，左侧（44±11%BL）和右侧膈神经（39±13%BL）相似。然而，在C2HS后4周（-10±7% BL）或8周（4±5% BL），在C2HS对侧记录到的膈神经输出中未出现类似的爆发幅度LTF。相反，同侧膈神经幅度的LTF在C2HS后4周（44±11% BL）和8周（129±30% BL，P < 0.05）均出现。在对照大鼠中观察到IH后膈神经爆发频率持续增加（即“频率LTF”）（+9±3次爆发/分钟，P < 0.05），但在C2HS大鼠中未观察到。我们得出结论，对单侧颈脊髓损伤的代偿反应会阻止对侧膈神经运动神经元中LTF的表达。
