Formation of new synapses in the cat motor cortex following lesions of the deep cerebellar nuclei.
Formation of new synapses in the cat motor cortex following lesions of the deep cerebellar nuclei.
复制标题
小脑深部核损伤后，猫运动皮层中新突触的形成。
DOI：
10.1007/bf00228843
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发表时间：
1990
影响因子：
2
通讯作者：
Asanuma,H
中科院分区：
文献类型：
--
作者：
Keller,A;Arissian,K;Asanuma,H
本文应用电生理和电镜方法，研究了单侧损毁猫小脑深核对皮层体感区向运动区投射的影响。轴突终末在运动皮层属于CC传入标记的变性引起的病变的躯体感觉皮层，在运动皮层的神经元标记的高尔基体/EM方法。在每只猫中，比较了小脑病变对侧（实验）和同侧（对照）运动皮层（MCx）的数据。小脑病变产生明显的运动缺陷，逐渐消退，并在30至40天后消失。随后病变的躯体感觉皮层（区2）对侧小脑病变导致小脑症状的再现。实验组MCx单位面积CC突触数显著高于对照组。CC突触数量的增加在MCx的II-V层中是明显的，但在II/III层中最为突出。实验MCx中CC突触数量的增加主要是由于与锥体神经元树突棘突触的轴突终末增加。相比之下，CC突触与棘，非锥体神经元从实验和对照MCx的数量和空间分布是相似的。场电位在实验MCx，引起的刺激区2，改变小脑病变。在实验MCx，极性的早期组成部分的场电位逆转在皮层深度对应于层II-III，而这种逆转没有观察到在控制MCx。这些结果表明，小脑核病变诱导发芽的轴突终末MCx建立一个新的功能。结果提供了第一个解剖学证据，证明成年中枢神经系统中新突触的产生不是由消除现有突触引起的。
The effects of unilateral lesions of the deep cerebellar nuclei on the corticocortical (CC) projection from the somatosensory to the motor cortex were studied in adult cats, utilizing electrophysiological and electron microscopical methods. Axon terminals in the motor cortex belonging to CC afferents were labeled by degeneration induced by lesions of the somatosensory cortex; neurons in the motor cortex were labeled by the Golgi/EM method. In each cat, data from the motor cortex (MCx) contralateral (experimental) and ipsilateral (control) to the cerebellar lesion were compared. Cerebellar lesions produced marked motor deficits, which receded gradually and disappeared after 30 to 40 days. Subsequent lesions of the somatosensory cortex (area 2) contralateral to the cerebellar lesions resulted in the reappearance of the cerebellar symptoms. The number of CC synapses per unit area in experimental MCx was significantly higher than in control MCx. The increase in the number of CC synapses was apparent throughout layers II–V of the MCx, but was most prominent in layers II/III. The increase in the number of CC synapses in experimental MCx was due mainly to an increase of axon terminals synapsing with dendritic spines belonging to pyramidal neurons. In comparison, the numbers and spatial distribution of CC synapses with aspinous, nonpyramidal neurons from both experimental and control MCx were similar. Field potentials in the experimental MCx, evoked by stimulation of area 2, were altered following cerebellar lesions. In experimental MCx, the polarity of the early component of the field potentials reversed at cortical depths corresponding to layers II–III, whereas this reversal was not observed in control MCx. These findings suggest that lesions of the cerebellar nuclei induced sprouting of axon terminals in the MCx to establish a new function. The results provide the first anatomical evidence for the generation of new synapses in the adult CNS which is not induced by elimination of existing synapses.