Department of Neurosciences and Movement Sciences, Section of Medicine, Faculty of Sciences and Medicine, Fribourg Center of Cognition, University of Fribourg, Chemin du Musée 5, CH-1700 Fribourg, Switzerland.
Department of Neurosciences and Movement Sciences, Section of Medicine, Faculty of Sciences and Medicine, Fribourg Center of Cognition, University of Fribourg, Chemin du Musée 5, CH-1700 Fribourg, Switzerland
J Neurosci. 2018 Dec 12;38(50):10644-10656. doi: 10.1523/JNEUROSCI.0904-18.2018. Epub 2018 Oct 24.
A restricted lesion of the hand area in the primary motor cortex (M1) leads to a deficit of contralesional manual dexterity, followed by an incomplete functional recovery, accompanied by plastic changes in M1 itself and in other cortical areas on both hemispheres. Using the marker SMI-32 specific to pyramidal neurons in cortical layers III and V, we investigated the impact of a focal unilateral M1 lesion (hand representation) on the rostral part (F6) and caudal part (F3) of the supplementary motor area (SMA) in both hemispheres in nine adult macaque monkeys compared with four intact control monkeys. The M1 lesion induced a consistent interhemispheric asymmetry in density of SMI-32-positive neurons in F3 layer V (statistically significant in 8 of 9 lesioned monkeys), highly correlated with the lesion volume and with the duration of functional recovery, but not with the extent of functional recovery itself. Such interhemispheric asymmetry was neither present in the intact monkeys, as expected, nor in F6 in all monkeys. In addition, the M1 lesion also impacted on the basal dendritic arborization of F3 layer V neurons. Neuronal density was clearly less affected by the M1 lesion in F3 layer III compared with layer V. We interpret the remote effect of M1 lesion onto the density of SMI-32-positive neurons and dendritic arborization in the SMAs bilaterally as the consequence of multiple factors, such as changes of connectivity, diaschisis and various mechanisms involved in cortical plasticity underlying the functional recovery from the M1 lesion. The motor system of macaque monkeys, in addition to be similarly organized as in humans, is a good candidate to study the impact of a focal lesion of the main contributor to voluntary movements, the primary motor cortex (M1), on non-primary motor cortical areas also involved in manual dexterity, both at behavioral and structural levels. Our results show that a unilateral permanent lesion of M1 hand area in nine monkeys affects the interhemispheric balance of the number of SMI-32-positive pyramidal neurons in the cortical layer V of the supplementary motor area, in a way strongly correlated to the lesion volume and duration of the incomplete functional recovery.
初级运动皮层（M1）手部区域的受限损伤导致对侧手灵活性缺陷，随后功能恢复不完全，伴随着 M1 本身和两个半球的其他皮质区域的塑性变化。使用针对皮质层 III 和 V 中的锥体神经元的标记物 SMI-32，我们在九只成年猕猴的对侧补充运动区（SMA）的额部（F6）和尾部（F3）部分以及四只完整的对照猕猴中研究了单侧 M1 损伤（手部代表区）对其的影响。M1 损伤导致 F3 层 V 中 SMI-32 阳性神经元密度的一致的半球间不对称（在 9 只损伤猴中有 8 只具有统计学意义），与损伤体积和功能恢复持续时间高度相关，但与功能恢复本身的程度无关。这种半球间不对称性既不存在于预期的完整猴子中，也不存在于所有猴子的 F6 中。此外，M1 损伤还影响了 F3 层 V 神经元的基底树突分支。与 F3 层 V 相比，神经元密度明显较少受到 M1 损伤的影响。我们将 M1 损伤对双侧 SMA 中 SMI-32 阳性神经元密度和树突分支的远程影响解释为多种因素的结果，例如连接变化、失神经支配和皮质可塑性涉及的各种机制，这些机制是 M1 损伤后功能恢复的基础。除了组织方式与人类相似外，猕猴的运动系统也是研究对主要贡献者的单侧局灶性损伤的一个很好的候选者自愿运动，初级运动皮层（M1），对也参与手灵活性的非主要运动皮质区域，在行为和结构水平上。我们的研究结果表明，九只猴子的 M1 手部区域单侧永久性损伤会影响补充运动区皮质层 V 中 SMI-32 阳性锥体神经元数量的半球间平衡，这种影响与损伤体积和不完全功能恢复的持续时间密切相关。
