Castro-Moure F, Goshgarian H G
Department of Anatomy and Cell Biology, Wayne State University, School of Medicine, Detroit, Michigan 48201, USA.
Exp Neurol. 1997 Nov;148(1):293-8. doi: 10.1006/exnr.1997.6649.
Interruption of the main descending respiratory drive to phrenic motoneurons by cold block or spinal cord hemisection results in morphological modifications of the ipsilateral phrenic nucleus in the rat. The modifications consist of an increase in the number of multiple synapses and dendrodendritic appositions and elongation of the asymmetric and symmetric synaptic active zones. Hemisection and hemispinalization by cold block cause not only "functional deafferentation" of the ipsilateral phrenic neurons (i.e., a loss of ipsilateral descending respiratory drive), but also an increase in the remaining contralateral descending respiratory drive. The contralateral respiratory pathways connect with phrenic motoneurons ipsilateral to cold block or hemisection by decussating collateral axons which cross the spinal cord midline below the hemisection/cold block site. Thus, the phrenic nucleus synaptic plasticity could possibly be induced by functional deafferentation or by an increase of the descending respiratory drive. To differentiate between these two possible inducers of the plasticity, we assessed the synaptic morphology of the phrenic nucleus of nonoperated rats exposed to 48 h of hypoxia in an atmosphere chamber. The hypoxia exposure produces an increased descending respiratory drive without functional deafferentation. The quantitative data extracted from electron micrographs of the phrenic nucleus from four experimental rats were compared with the data from four normal breathing animals. Phrenic nucleus morphometric analysis showed that there was no significant difference in the mean number of single synapses between the samples from control animals (141 +/- 12.12) and the experimental animals (156 +/- 26.73). Similarly, no significant difference was detected in the total number of synaptic active zones of control animals (178.25 +/- 11.13) and experimental animals (195.05 +/- 5.35). Furthermore, the length of synaptic active zones of asymmetrical synapses (0.21 +/- 0.024 micron) or symmetrical synapses (0.22 +/- 0.022 micron) did not change significantly compared to the synaptic active zone length in control animals (0.21 +/- 0.018 micron for asymmetrical and 0.21 +/- 0.010 micron for symmetrical). We conclude that no synaptic plasticity occurs in the phrenic nucleus without functional deafferentation in spite of an increase in descending respiratory drive. Therefore functional deafferentation may be the primary inducer of phrenic nucleus synaptic plasticity occurring after hemisection or cold block.
通过冷阻断或脊髓半横断来中断向膈运动神经元的主要下行呼吸驱动，会导致大鼠同侧膈核的形态学改变。这些改变包括多突触和树突 - 树突并置数量的增加以及不对称和对称突触活性区的延长。冷阻断造成的半横断和半脊髓化不仅导致同侧膈神经元的“功能性传入神经阻滞”（即同侧下行呼吸驱动丧失），还使剩余的对侧下行呼吸驱动增加。对侧呼吸通路通过在半横断/冷阻断部位下方穿过脊髓中线的交叉侧支轴突，与冷阻断或半横断同侧的膈运动神经元相连。因此，膈核突触可塑性可能是由功能性传入神经阻滞或下行呼吸驱动增加所诱导的。为了区分这两种可能的可塑性诱导因素，我们评估了在大气舱中暴露于48小时缺氧环境的未手术大鼠膈核的突触形态。缺氧暴露会导致下行呼吸驱动增加，但没有功能性传入神经阻滞。从四只实验大鼠的膈核电子显微照片中提取的定量数据与四只正常呼吸动物的数据进行了比较。膈核形态计量分析表明，对照动物样本（141±12.12）和实验动物样本（156±26.73）之间单突触的平均数量没有显著差异。同样，对照动物（178.25±11.13）和实验动物（195.05±5.35）的突触活性区总数也没有检测到显著差异。此外，与对照动物的突触活性区长度相比，不对称突触（0.21±0.024微米）或对称突触（0.22±0.022微米）的突触活性区长度没有显著变化（对照动物中不对称突触为0.21±0.018微米，对称突触为0.21±0.010微米）。我们得出结论，尽管下行呼吸驱动增加，但在没有功能性传入神经阻滞的情况下，膈核不会发生突触可塑性。因此，功能性传入神经阻滞可能是半横断或冷阻断后膈核突触可塑性发生的主要诱导因素。
