Liu Y, Rouiller E M
Institute of Physiology and Program in Neuroscience, Faculty of Sciences, University of Fribourg, Rue du Musée 5, CH-1700 Fribourg, Switzerland.
Exp Brain Res. 1999 Sep;128(1-2):149-59. doi: 10.1007/s002210050830.
The mechanisms of recovery of manual dexterity after unilateral lesion of the sensorimotor cortex in adult primates remain a matter of debate. It has been proposed that the cortical zone adjacent to the lesion may take over part of the function of the damaged cortex. To investigate further this possibility, two adult (4-5 years old) macaque monkeys were trained to perform a natural precision-grip task to assess hand dexterity. Intracortical microstimulations (ICMS) were used to map the hand area in M1 on both hemispheres. Ibotenic acid was then injected intracortically to damage the representation in M1 of the preferred hand. Subsequent histological analysis indicated that the hand representation in M1 was indeed lesioned, but, due to a spread of ibotenic acid, the lesion encroached a significant extent of the hand representation in the primary somatosensory cortex. A few minutes after infusion of ibotenic acid, there was a complete loss of dexterity of the preferred hand, which lasted for 1-2 months. Later, a progressive functional recovery of the affected hand took place over a 3- to 4-month period, reaching a stable level corresponding to 30% of the pre-lesion behavioral score. ICMS remapping, conducted nine months after the lesion, revealed that stimulation of the intact or lesioned M1 did not induce any visible movement of the recovered hand. The M1 hand representation on the intact hemisphere was similar to that observed before the lesion. Transient inactivation of the M1 hand/arm areas or of the dorsal and ventral premotor cortical areas (PM) on both hemispheres was undertaken by using microinjections of the GABA-agonist muscimol. Inactivations of M1 had no effect. Inhibition of PM in the damaged hemisphere suppressed the recovered manual dexterity of the affected hand. These results suggest that PM plays a significant role in the incomplete functional recovery of hand dexterity following unilateral damage of the sensorimotor cortex in adult monkeys.
成年灵长类动物感觉运动皮层单侧损伤后手动灵活性恢复的机制仍存在争议。有人提出，损伤附近的皮质区域可能会接管受损皮质的部分功能。为了进一步研究这种可能性，对两只成年（4 - 5岁）猕猴进行训练，使其执行自然精确抓握任务以评估手部灵活性。采用皮层内微刺激（ICMS）来绘制两侧大脑半球M1区的手部区域。然后向皮层内注射鹅膏蕈氨酸以损伤优势手在M1区的表征。随后的组织学分析表明，M1区的手部表征确实受到了损伤，但由于鹅膏蕈氨酸的扩散，损伤侵入了初级体感皮层中相当大一部分的手部表征区域。在注入鹅膏蕈氨酸几分钟后，优势手的灵活性完全丧失，这种情况持续了1 - 2个月。之后，受影响的手在3至4个月的时间里逐渐出现功能恢复，达到了相当于损伤前行为评分30%的稳定水平。在损伤九个月后进行的ICMS重新映射显示，刺激完整或受损的M1区均未引起恢复后手部的任何可见运动。完整半球上的M1区手部表征与损伤前观察到的相似。通过微量注射GABA激动剂蝇蕈醇对两侧大脑半球的M1区手部/手臂区域或背侧和腹侧运动前皮层区域（PM）进行短暂失活。M1区失活没有效果。抑制受损半球的PM区会抑制受影响手已恢复的手动灵活性。这些结果表明，PM区在成年猴子感觉运动皮层单侧损伤后手灵活性的不完全功能恢复中起重要作用。
